standardizednomenclaturefor inbredstrainsof …...[cancer research 45, 945-977, march 1985]...

[CANCER RESEARCH 45, 945-977, March 1985]

StandardizedNomenclaturefor InbredStrainsof Mice:EighthListing1

Joan Staats

The Jackson Laboratory, Bar Harbor, Maine 04609

For the International Committee on Standardized Genetic Nomenclature for Mice

ABSTRACT

This paper presents a list of inbred strains of mice with theirorigins and characteristics, and a list of standard subline designations.

INTRODUCTION

Previous listings of Standardized Nomenclature for InbredStrains of Mice appeared in Cancer Research in 1952, 1960,1964,1968,1972,1976, and 1980 (5). Between issues, additionsand deletions to strain holdings appear in Mouse News Letter (4)and Inbred Strains of Mice (3).

Most fostered and otherwise manipulated lines, named geneson inbred backgrounds, and congenie histocompatibility strainshave been omitted, to keep the list to a manageable size. Listsof congenie and segregating inbred strains and recombinantinbred strains can be found in two new publications (1,2). Sincecomprehensive revised rules for nomenclature of strains, genes,and chromosome anomalies are presented in both these books,they are not included here.

Appendix 1 is the list of inbred strains and some clearly definedsubstrains. It contains 233 entries, compared with 299 in theseventh listing and 124 in the first. Several strains have beendropped since the seventh listing, either because they are known

1Preparation of this paper was supported in part by Grant DEB 79-26708 from

the National Science Foundation. Address requests for reprints to: Library, TheJackson Laboratory. Bar Harbor, ME 04609.

Received October 30,1984; accepted November 8,1984.

to be extinct or because they were not reported. Appendix 2 isa list of standard abbreviations for the names of persons orinstitutions maintaining inbred strains. The principal use of thesymbols is in designating sublines. For example, strain AU/Ssupon transfer from Silvers to The Jackson Laboratory becomesAU/SsJ or AU/J.

The Committee stresses the importance of using full strain orsubstrain designations in publications, and also of spelling outthe source of the animals. The brief symbol C57, for example,could stand for seven or eight different strains. The many differences among substrains emphasize the importance of using fulldesignations. For example, CBA/J carries the gene for retinaldegeneration whereas CBA/Ca has the normal alÃele;the twodiffer in radiosensitivity, they are not histocompatible, and theyvary in at least five polymorphic loci. We also stress the importance of identifying the sex of the parents when listing hybrids.It is customary to list the female first. Thus, C57BL/6J 9 x DBA/2J a is B6D2F,, and DBA/2J 9 x C57BL/6J a is D2B6F,.

REFERENCES

1. Foster, H. L, Small, J. D., and Fox, J. G. (eds ) The Mouse in BiomÃ©dicalResearch, Vol. 1. New York: Academic Press, Inc., 1981.

2. Green, M. C. (ed.). Genetic Variants and Strains of the Laboratory Mouse.Stuttgart: Gustav Fischer Verlag, 1981.

3. Inbred Strains of Mice: an informal biennial document listing laboratoriesmaintaining inbred strains of mice; the companion document to Mouse NewsLetter. ISM No. 13 appeared in July 1983.

4. Mouse News Letter: an informal semiannual document carrying information onmutant genes, research stocks of mice, and research news. MNL is currentlyedited by Dr. J. Peters; No. 71 appeared in July 1984.

5. Staats, J. Standardized nomenclature for inbred strains of mice: seventh listing.Cancer Res., 40: 2083-2128,1980.

APPENDIX

List of inbred strains of mice and their clearly defined sub-strains.

Abbreviations

Inbr = number of generations of brother x sisterinbreeding. The substrain on which the figure is based is indicated in parentheses. Ifa line has been produced by appropriatecrosses to an inbred strain, the number ofgenerations is preceded by N.

Genet

Origin

= genetic constitution,and eye colors.

mainly mutant coat

origin. In some cases references are given.A table in Chap. 1 of BLM-2 gives moreextensive information.

BLM-2

Charac

Maintained by

b x s

Green, E. L. (ed.) Biology of the LaboratoryMouse, Ed. 2. New York: McGraw-Hill,1966.

characteristics. In some cases journal references are given. Letters in parenthesesindicate specific contributions to InbredStrains of Mice. The key to the letters willbe found in Appendix 2. In a few casesinformation has been obtained by correspondence or personal communication.

persons or laboratories maintaining eachstrain, insofar as information is available,are indicated by substrain symbols.

brother x sister inbreeding.

CANCER RESEARCH VOL. 45 MARCH 1985

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STANDARDIZED NOMENCLATURE FOR INBRED STRAINS OF MICE

SNISM-7

SPF

A/He

A/He

A/J

Staats, J. Standardized nomenclature forinbred strains of mice: seventh listing. Cancer Res., 40: 2083-2128,1980.

specific-pathogen-free.

Inbr: 195. Genet: abc. Origin: Strong,1921, from cross of Cold Spring Harboralbino and Bagg albino. Majority of sublinestrace to a stock that Bittner obtained fromStrong in 1927. Charac: mammary tumorincidence varies with colony and breedingstatus, from 0 to 80% (SNISM-7); some

reticular tissue neoplasms; few skeletal variants (Gr); 40% of ?9 have positive LE cellsor antinuclear antibodies (Umc); 84% neo-

natally thymectomized develop runting syndrome; high incidence of hyperplastic alveolar nodules correlated with pregnancy (Ki);cleft lip with or without deft palate occurssporadically, cleft palate is easily inducedwith a variety of agents (H. Kalter, Teratology, 20: 213, 1979); highly susceptible tomeasles virus (B. Rager-Zisman, Fed.Proc., 35: 391, 1976); susceptible to Plas-

modium chabaudi (M. M. Stevenson ef al.,Infect. Immun., 3d: 80, 1982); resistant toLeishmania infection (D. J. Bradley, Clin.Exp. Immunol., 30:130, 1977). Maintainedby: Crc, Cv, Dv, Fre, Icrf, Imr, Ki, Man, Ok,Ola, Ph, Ros, Ss, Sy, Tru, Tu, Y, Zgr.

Inbr (N): 215. Strong to Heston 1938, He toJ 1948. Charac: low incidence of mammaryand lung tumors (SNISM-7); high incidence

of renal disease in older animals, some cleftlip observed in young (J); cleft palate iseasily induced with a variety of agents; lungtissue very susceptible to methylcholan-

threne (J); most susceptible to ectromeliavirus of 8 strains tested (S. M. Ermolaevaet al., Sov. Genet. (Eng. TransÃ.Genetika),8: 681,1972); relatively susceptible to Op-

isthorchis felineus (A. G. Zelentsov, Med.Parazitol. Parazitamye Bolezni, 43: 95,1974); susceptible to rabies virus infection(D. L. Lodmell, Fed. Proc., 41: 566, 1982);hematocrit 48%, systolic blood pressure 82mm Hg (G. Schlager and R. S. Weibust, J.Hered., 67: 295, 1976); serum Â«t-antitryp-

sin lowest of 34 strains tested (S. K. Chan,Arch. Environ. Health, 27:271,1973). Maintained by: Cr, Cum, Gh, Hok, Han, 1er, J,Kun, Mob, N, Novosibirsk, Rl, Ros, Sf, Sv.

Inbr (J): 196. Origin: Strong to Cloudman1928; survivors of Bar Harbor fire to Jax1947 at F73. Charac: mammary tumorsmoderate (J); renal disease in older animals(Umc); lower percentage of granulocytes

AB/Jena

than other sublines (E. S. Russell et al.,Proc. Soc. Exp. Biol. Med., 78: 761,1951)hematocrit 48%, systolic blood pressure 81mm Hg (G. Schlager and R. S. Weibust, J.Hered., 67: 295, 1976); cleft lip with orwithout cleft palate occurs sporadically (H.Kalter, Teratology, 20:213,1979); cleft palate is easily induced with a variety ofagents; very sensitive to X-irradiation (BLM-

2); some heart disease in old breeders(BLM-2); moderately susceptible to audi-

ogenic seizures over a long period up to245 days (E. Vicari, J. Psycho!., 43: 111,1957); low alcohol preference (C. L. Good-

rick, J. Stud. Alcohol, 39:19,1978); lowestactivity level of liver arylsulfatase C of 24Jax strains tested [K. Nelson and W. D.Daniel, Experientia (Basel), 35: 309,1979];protein kinase C activity one-half that found

in 7 other strains (A. M. Malkinson et al.,Biochem. Biophys. Res. Commun., 722:492, 1984); resistant to Salmonella typhi-

murium C5 (V. Hormaeche, Immunology,37: 311, 1979); intermediate susceptibilityto rabies virus (D. L. Lodmell, Fed. Proc.,41:566,1982); susceptible to Ustoria mon-ocytogenes (E. Skamene and P. A. L. Kong-

shaven, J. Reticuloendothel. Soc. 24(Suppl.): 32a, 1978); resistant to BacillusCalmette-Guerin (A. Forget et al., Fed.

Proc., 41: 730,1982); most susceptible toPseudomonas aeruginosa of 16 strainstested (J. E. Pennington and R. M. Williams,J. Infect. Dis., Ã•39:396,1979); sensitive toCryptococcus neoformans due to the He"

alÃele(J. C. Rhodes er a/., Infect. Immun.,29:494,1980); for other susceptibilities seeN. N. Nesbitt and E. Skamene. J. Leuk.Biol., 36: 357, 1984. resistant to inductionof amyloid (M. A. Scheinberg and E. S.Cathcart, Immunology, 37: 443, 1976).Maintained by: Ao, Cr, Gh, Han, Ibg, J, Odn,Ola, Ori, Pt, Scr, Sg, Sx, Ucsd, Univ. Helsinki (O. MÃ¤kelÃ¤),Yok

Inbr (Jena): 70. Genet: AB DC Hbb". Origin:

from Agnes Bluhm to P. Hertwig in 1934,to J. Fortner in 1945, to H. RÃ¶hrerin 1949,to Jena in 1952; 1945-1959 random bred,

new start of b x s in Jena in 1959 (Z.Versuchstierk Nd., 11: 241,1969). Charac:av. litter size at birth 7.3 Â±0.15 (S.D.), av.litter size at weaning 6.5 Â±0.10; sex ratio49.2% do at weaning; body weight at weaning (21 days) 10.2 Â±0.28 g ?$, 10.9 Â±0.30g <5(Ã®;mean life span in Jena 18.1 mo $$;fetal retentions and accompanying purulentpanmetritis in a small number of breeding9$; in animals older than 1 year more than80% amyloidosis mostly affecting, in de-


946




ABP

AE

AEJ/Gn

AG/Cam

AKR

scending order of frequency, the liver, kidneys, spleen, adrenals, and intestine; in virgins 25% lymphomas, less than 10% lungtumors, 6% uterine leiomyosarcomas, fewsarcomas of soft tissue, but no mammarytumors; susceptible to chronic interstitialnephritis; highly susceptible to mousepox,Sindbis-, MM, Mengo, encephalomyocardi-tis, and Columbia S. K. viruses, epidemicdiarrhea of infant mice, and Plasmodiumberghei, moderately susceptible to mousepneumonia virus; strong antibody responseto sheep RBC; males are aggressive. Maintained by: Jena.

Inbr (Le):64. Genet:abbtpse wa-1. Origin:A. B. Griffen to Lane 1968, sib-mated sincethen. Charac: useful for linkage testing.Maintained by: Le, R.

Inbr (Nctr): 70. Genet: a" o ofp se. Origin:

Hollander, Iowa, 1962. Charac: mean littersize at weaning more than 9. Maintainedby: Nctr.

Inbr (Rk): 70. Genet: a". Origin: Hollander

(Schaible), Iowa State, Ames waltzer stockwith miscellaneous markers to M. C. Greenin 1963. Crossed once to C57BL/10Gn followed by cross to C57BL/6J->TJ, then b x

s. F28 to Roderick in 1972. Charac: highfertility, mean litter size 9. Maintained by:Le, Rk.

Inbr (Cam): about 155. Genet: A*/a" x A*/a", with Aâ„¢,A, A", a', a, and p, continuallybackcrossed to Ay/a" line. Origin: R. A.Fisher, "A" from GrÃ¼nebergin 1945 [a CBA

subline (J. R. Morton, personal communication)]. Various a-locus alÃelesintroducedby backcrosses, stock maintained mainlyby sib-mated sublines until 1959. Back-crossing to one Ay/a x Ay/a line started1959; central line now replaced by Ay/a" xAy/a". Charac: high penetrance of Nil, 0%

penetrance of chylous ascites in Ra (B. M.Herbertson and M. E. Wallace, J. Med. Genet., 1: 10, 1964). Maintained by: Cam,Odn.

Inbr (N): 181. Genet: a Be. Origin: a dealernamed Detwiler in Norristown, PA; carriedby Furth as a high-leukemia strain from1928 to 1936, then random-bred at Rockefeller Inst. for several generations, b x smated 9 gen. by Mrs. Rhoades and 21 byC. Lynch. Charac: lymphatic leukemia invarious colonies from 68 to 91% (SNISM-7). AKR/J and AKR/Cum reject each other's

spontaneous lymphomas (M. M. Zatz, Cell.

AL

AU

AX/Pa

BA

Immunol., 36: 251, 1978). Oslo sublinesource of adrenocortical lipiddepletion gene(K. Amesen, Acta Pathol. Microbiol. Scand.,58:212,1963); low concentration of lipid inadrenals (BLM-2); hematocrit of AKR/J47.6%, systolic blood pressure 80 mm Hg(G. Schlager and R. S. Weibust, J. Hered,67: 295,1976); resistant to Leishmania infection (D. J. Bradley, Clin. Exp. Immunol.,30:130,1977). Maintained by: A, Bkl, Bog,Cr, Crc, Cri, Cri, Cum, Dp, Fhc, Fib, Han,Hok, 1er,Icrf, J, Ki, N, Novosibirsk, Ok, Ola,Ori, Ph, Pp, Pt, Rij, Ros, Ser, Sy, W, Wn,Y.

Inbr (N): 195. Genet: a b c. Origin: believedto have originated from strain A outcrossedto unknown strain followed by b x s mating.Should not be considered a strain A subline.Charac: mammary tumor incidence 20% at15 months (N); high incidence of amyloi-dosis (J. S. Ram ef al., Proc. Soc. Exp. Biol.Med., 730: 462, 1969); expression ofXenCSA is low on thymic and high onsplenic lymphocytes (H. C. Morse III ef al.,J. Exp. Med., 122: 443, 1979); susceptibleto rabies fixed virus and Lansing strain poliovirus, young animals susceptible to toxo-plasmosis infection (N). Maintained by: la,N, Pt.

Inbr (J): ? + 69. Genet: a U. Origin: R. A.Fisher,about 1937.50% GrÃ¼neberg'sCBA,28.5% Fisher's color stocks, and 21.5%GrÃ¼neberg'swavy stock, the latter 2 being

unrelated to stocks of American origin (J.R. Morton, personal communication). ToMedawar 1947, to Silvers at F23 in 1957,to Jax 1967. Charac: 9$ do not reject disografts; unusual induction of kidney ÃŸ-glucuronidase by testosterone (Cv). Maintained by: Cv, J.

Inbr (Pa); 27. Genet: a*. Origin: L. B. Russell's balanced lethal stock Ay/a" 6PB; to

M. H. L. Snow in 1969 who separated thealÃelesby a cross to C57BL/6 and back-crossed a* mice to C57BL/6 for 4 gen.Snow to Papaioannou in 1973; sib-matedwith forced heterozygosity. Charac: embryonic lethal at the agouti locus (V. E. Papaioannou and H. Mardon, Dev. Genet., 4:21,1983). Maintained by: Pa.

Inbr (Nmg): 64. Genet: b. Origin: Falconer,noninbred obese stock. Charac: good reproductive performance; no known tumors.Poor retention in black-white discriminationlearning (J. van Abeelen ef al., Physiol. &Behav., 10: 751, 1973). Maintained by:Nmg.


947




BALB/C Inbr (Hok): 186. Genet: b c. Origin: albinostock acquired by H. Bagg in 1913. Priorinbreeding uncertain (E. C. MacDowell, J.Gen. Phystol., 11: 57,1927). MacDowell toSnell (who added the /c) in 1932 at F26;subsequently widely distributed, especiallyby Andervont. Charac: susceptible tochronic pneumonia, extremely sensitive toradiation (J. Vacha ef al., Z. Versuchs-

tierkd., 26: 157, 1984); long breeding life.Some heart lesions in old breeders, arteriosclerosis common in both sexes (BLM-2).Relatively nonaggressive. Very large retic- BBT/Ha

uloendothelial organs relative to bodyweight (T. Gotjamanos, J. Reticuloendothel.Soc., 8: 421, 1970). Mammary and lungtumor incidence varies with colony andbreeding status (SNISM-7). Susceptible to BDP

the induction of plasma cell tumors withmineral oil. Cd subline develops spontaneous bilateral adenocarcinoma of the kidney, 60-70% in both sexes at 9-15 mo;

adenocarcinoma cells inhibit body growthwhen grafted into the same or other strains(Cd). Almost all <5dsnow spleen amyloidosisby 20 mo (P. Ebbesen, J. Nati. Cancer Inst.,47:1241,1971); high level of a-fetoproteinin BALB/cJ (D. R. Pollard ef al., Can. J. BLNGenet. Cytol., 24: 343, 1982); 38% ofBALB/cJ have dorsoventral vaginal septaversus 0-8% in other sublines (T. Cunliffe-

Beamerand D. B. Feldman, Lab. Anim. Sci.,26:895,1976); highest wheel-running activ- BN/a

ity of 18 strains tested (M. F. W. Festing,Lab. Anim., 11: 257, 1977); hematocrit52.2%, systolic blood pressure 128 mm Hg,highest of 21 Jax strains tested (G. Schlager and R. S. Weibust, J. Hered., 67: 295,1976). BALB/cJ has twice the level of 3-catecholamine-synthesizing enzymes in the

adrenals as do BALB/cN; they also differ infighting behavior (R. Ciaranello ef a/., Proc.Nati. Acad. Sci. USA, 71:3006,1974); 35%of BALB/cAnN develop spontaneous monoclonal B-cell tumors at 20-21 mo (R. Keller BN/b

ef a/., Blood, 58: 161 a, 1981); relativelyresistant to Candida albicans (H. F. Hectoref al., Infect. Immun., 38: 1020, 1982); resistant to Eimeria vermlformis (M. E. Roseet al., Parasitology, 88: 45,1984); resistantto Cryptococcus neoformans due to He1

alÃele(J. C. Rhodes ef al.. Infect. Immun., BNT29: 484, 1980). Susceptible to: Salmonellatyphimurium C5 (C. E. Hormaeche, Immunology, 37: 311, 1979); measles virus (intermediate) (B. Rager-Zisman, Fed. Proc.,

35: 391, 1976); Leishmania (D. J. Bradley,Clin. Exp. Immunol., 30: 130, 1977); spotted fever group rickettsiae (L. Sammons,Lab. Anim. Sci., 27: 229, 1977); ScWsfo-

soma mansoni (M. M. Fanning, Parasite Immunol. (Oxf.), 6: 95,1984). Maintained by:A, Ani, Ao, Be, Bkl, By, Cox, Cr, Crc, Crgl,Cri, Cri, Cum, Dp, Dub, Dv, Dy, Ei, Ess,Fhc, Fib, Fnn, Ga, Gy, Han, Hf, Hok, Hsd,Ico, 1er, Imr, J, Ki, Kun, Lac, Ul, Man, Mcd,Mel, N, Nii, Odn, Ok, Ola, Ori, Pas, Ph, Pp,Pt, Rij, Rk, Rl, Ros, Saf, Ser, Sed, Sg, Sid,Sim, Stutman, Sx, Sy, Tac, Tbr, Tru, Tu,Uct, Urne, Univ. Helsinki (O. MakelÃ¡), W,Wm, Wn, Wrm, Y, Yok.

Inbr (Cv): 65. Genet: a of GUS". Origin: cross

of noninbred hr/hr Ã¶f/of x C57BL/Ha. ToChapman 1974. Charac: belted. Maintainedby: Cv.

Inbr (J): 124. Genet: a b d p rd se. Origin:W. H. Gates, inbred since 1926; dilutebrown ? from Uttte x pink-eyed d from

Strong (W. H. Gates, Genetics, 12: 295,1927). Charac: frequent mammary tumors;hemorrhagic ovaries; polycystic kidneys;hematocrit 52.2%, systolic blood pressure84 mm Hg (G. Schlager and W. S. Weibust,J. Hered., 67:295,1976). Maintained by: J.

Inbr (Nmg): 58. Genet: a B. Origin: Cpb,noninbred yellow stock. Charac: very goodreproductive performance. Maintained by:Nmg.

Inbr (W): 90. Genet: A B c D H-2*1. Origin:

Anna Dux, Gliwice, September 1950, fromunknown parents. F13 taken to WarsawJune 1956, where it was split into 2 sub-strains, inbreeding continued (A. Dux, Nowotwory, 7: 67, 1957). Charac: 35% lungtumors at 662 days; 7.1% leukemia at 647days; 23% chronic nephritis at 562 days.Used for carrying transplantable vaginal ep-ithelioma G93. Maintained by: W. (Bogmaintains the unsplit BN strain at F91.)

Inbr (W): 96. Genet, and Origin: as BN/a.Charac: lung tumors 25% at 629 days;1.8% leukemia at 512 days in $9, 13%chronic nephritis at 493 days; used for carrying transplantable vaginal epiteliomaG94. Maintained by: W.

Inbr (Le): 73. Genet: a Bn/+. Origin: mutation to bent tail arose in Navy Med. Res.Unit stock, discovered by E. D. Garber.From A. B. Griffen to Lane 1960. Inbred toF27 followed by one outcross to C57BL/6Jx CBA/Ca F,, then b x s. Charac: tails ofhemizygous males are more kinked andshorter than tails of heterozygous females.Penetrance is complete. Maintained by: Le.


948




BRSUNT

BRVR

BSVR

BSVS

BUB

BXSB

CBA/Br

CBA/Ca

Inbr (N): 158. Genet: abC. Origin: Strong,a branch of BRS (from strain NH) continuedwithout further methylcholanthrene treatment. Charac: gastric lesions; adiposity;100% incidence of periodontal disease.Maintained by: N, Y.

Genet: c. Origin: Webster 1930, at Rockefeller Inst. (L. T. Webster, J. Exp. Med., 57:793,1933). Charac: resistant to salmonella,some encephalitic viruses, and experimental allergic encephalomyelitis. Normal immune response (D. Briles et al., Eur. J.Immunol., 9:255,1979). Maintained by: Dv.

Gent: c. Origin: as above and L. T. Webster(J. Exp. Med., 65:261,1937). Charac: sus- CBA/H-T6

ceptible to salmonella, resistant to someencephalitic viruses. Maintained by: Db.

Genet: c. Origin: as above. Charac: susceptible to salmonella, some encephalitic viruses, and experimental allergic encephalitis. Immune response deficient. Maintainedby: Db, Dv, Pt.

CBA/JInbr (J): 122. Genet: a c rd. Origin: fromalbinos of unknown origin at Brown Univ.;maintained by random breeding until 1945.Charac: selected for good growth and reproductive performance; no known tumors;relatively resistant to Schistosoma mansoni(M. M. Fanning ef al.. Parasite Immunol.(Oxf.). 6:95,1984). Maintained by: J.

Inbr (Mp): 49. Origin: C57BL/6J x SB/Le-sa bg/sa bg (E. D. Murphy); selection of thesatin, non-beige recombinant followed by b

x s mating with forced heterozygosis at thesa locus (Mouse News Lett., 58:52,1978).Charac: a new recombinant inbred strain.All animals develop spontaneous autoimmune disease characterized by moderatelymphadenopathy with hypergammaglobu-linemia, splenomegaly, Coombs-positivehemolytic anemia, and immune complexglomerulonephritis with nephrotic syndrome. 9? survive an average 63 weeks, <W22 weeks. Maintained by: J, Ola, Scr.

Inbr: 150+. Origin: see C3H/St; Jax to Hal-dane and GrÃ¼neberg 1932, to Bonser CBA/N(Leeds) approx. 1933. Charac: carries H-2"

alÃelein contrast to all other CBA sublines,which are H-2". Maintained by: A, Rij.

Inbr (J): 116. Genet: +. Origin: see C3H/St.Jax to Haldane and GrÃ¼neberg1932, toCarter through Royal Cancer Hosp. andBrit. Emp. Cancer Campaign. Charac: ab

sence of lower third molars in about 18%,few skeletal variants (Gr); some mammarytumors in breeders. Do not develop antinuclear antibodies or LE cells with aging(Urne). Birmingham strain Â¿Â¿over 120weeks all have hepatomas (J. G. Sharp efal., J. Pathd., T19:211.1976). Resistant toS. typhimurium C5 (C. E. Hormaeche, Immunology, 37: 311, 1979); resistant toLeishmania infection (D. J. Bradley, Clin.Exp. Immunol., 30:130,1977). Maintainedby: Ao, Bkl, Cam, Cnb, Cr, Crc, Cum, Gy,H, Hb, J, Kw, Lac, N, Nii, Novosibirsk, Ola,Ori. Pt, Scr, Stutman, Tu, Uct, Univ. Helsinki(0. MakelÃ¤),W, Y, Zal, Zbr.

Inbr (J): N13 F88. Genet: T6/T6. Origin:T(14;15)6Ca translocation homozygoteswere backcrossed to CBA/H by M. F. Lyon,eventually sib-mated. Charac: homozygousfor small marker chromosome of T6 trans-location. Congenie with CBA/H. Maintainedby: Bkl, Cam, Crc, H, Hok, J, Lac, Pt, Rij,W, Y, Zgm.

Inbr (J): 194. Genet: rd. Origin: see C3H/St;Strong to Andervont 1947, to Jax 1948.Charac: 65% hepatomas in Â¿6(J. B. Storer,J. Gerontol., 21: 404, 1966); 24% hepatomas in da, 15% lymphomas in $9 and 33%mammary tumors in 9$ (G. S. Smith ef al.,J. Nati. Cancer Inst., 50:1195,1973). Mid-range of radiation resistance (BLM-2); renaltubulointerstitial lesions in 78% of mice 3-22 mo (U. H. Rudofsky, Am. J. Pathol., 92:333,1978); hematocrit 46.3%, lowest of 21Jax strains tested, systolic blood pressure78 mm Hg (G. Schlager and R. S. Weibust,J. Hered., 67: 295, 1976). Susceptible toamyloid induction by casein (M. A. Schein-berg and E. S. Cathead, Immunology, 37:443, 1976); highly susceptible to measlesvirus (P. A. Neighbour ef al.. Infect. Immun.,21:764,1978); resistant to rabies virus (D.L. Lodmell, Fed. Proc., 41: 566,1982); deficient in a kidney metalloendoproteinase[R. J. Beynon and J. S. Bond, Science(Wash. DC) 279: 1351, 1983]. Maintainedby: Han, Hok, Ico, J, Odn, Ola, Ori, Ph, Wn,Y, Yok.

Origin: from CBA/H. Charac: carries a recessive gene for a B-cell defect, xld, which

prevents the mice from making antibodyresponse to thymic-independent antigens.They do, however, make good plaque-forming cell responses to the same haptenscoupled to hemocyanin (A. Berning ef al.,Fed. Proc., 37:1396,1978; B. Merchant efal., J. Immunol., 720: 1362, 1978). Main-


949




CBA/St

CC57BR

CC57W

CE

CFCW

CFW/Jic

tained by: Ao, Cr, Dub, Dv, Hsd, 1er,N, Nil,Rij, Scr.

Inbr (Man): 173. Genet: +. Origin: see C3H/St. Strong to Mann 1962. Charac: mammary tumor incidence high in both virginand breeding $$; long lived. Ki has 2 sub- CHI

lines, one with less than 1% mammary tumors and carrying rd, the other with 40%mammary tumors and normal eyes; skingrafts between them not accepted. Main- CL/Fr

tained by: Ao, Ki, Man, Ok.

Inbr (Y): 115. Genet: a b. Origin: Medvedev,1943, BALB/cN ? x C57BL/N a. Charac:no spontaneous mammary tumors butabout 60% when milk agent is introduced;primary lung tumors 22%. Incidence of allother tumors less than 1%. Maintained by:Igg, Novosibirsk, Sto, Y.

Inbr (Y): 107. Genet: abc. Origin and CSCharac: see CC57BR. Relatively resistantto Opisthorchis felineus (A. G. Zelentsov,Med. Parazitol. Parazitarnyes Bolezni., 43:95,1974). Maintained by: Sto, Y.

Inbr (J): 97. Genet: A c" rd*. Origin: wild

mutant trapped in Illinois by J. E. Knight. CWDColor genetics studied by Detlefsen. Inbredby Eaton at least 15 gen., some sent toWoolley. Speirs (2 gen. from Woolley) toWy and Jax in 1948. Charac: mammarytumors 3% in breeding ?$, ovarian tumorsless than 10%, reticular tissue neoplasmsless than 4% (Ki); high incidence of hepa- CXBD

tomas (M. Festing and D. K. Blackmore,Lab. Anim., 5: 179, 1971); high adrenocor-

tical carcinoma incidence in both sexes afterneonatal gonadectomy (J). Large amount oflipid in adrenals (BLM-2); hematocrit 54.8%,

systolic blood pressure 86 mm Hg (G.Schlager and R. S. Weibust, J. Hered., 67:295, 1976); serum Â«t-antitrypsin second

lowest of 34 strains tested (S. K. Chan,Arch. Environ. Health, 27: 272,1973); susceptible to Leishmania infection (D. J. Bradley, Clin. Exp. Immunol., 30: 130, 1977);highest activity level of liver arylsulfatase Cof 24 Jax strains tested [K. Nelson andW. L. Daniel, Experientia (Basel) 35:309,1979]. Maintained by: A, J, Univ. Coll. London, Univ. Helsinki (O. MÃ¤kelÃ¤). C3H/BI

Inbr (Rl): 100+. Genet: c Ca. Origin: Car-worth Farms 1/3/48 to Rl, b x s inbreedingby Rl. Maintained by: Rl.

Inbr (Jic): 58. Genet: c. Origin: from non-

inbred Carworth Farms mice, inbreeding

started in 1964. Maintained by: Jic. NOTE:There are several other inbred CFW lines.They should not be assumed to be identicalbecause of heterozygosity of the originalstock.

Inbr (Man): 160. Genet: +. Origin: see C3H/St. Charac: similar to C3H. Maintained by:Man.

Inbr (Fr): 70. Genet: b c. Origin: stock fromMorgan carrying "msl" (migratory spot le

sion, a variable white spot on the retina),crossed with A/J and inbred b x s withselection for high spontaneous deft lip frequency. Msl now has low penetrance.Charac: cleft lip in 25% of viable 17-day

fetuses (D. M. Juriloff, Prog. Clin. Biol. Res.,46: 39, 1980). Maintained by: Fr, Ksb, M.C. Johnston (Univ. North Carolina), Nem.

Inbr (Nga): 94. Genet: a b c D s. Origin:established in 1956 from hybrids betweenNBC and SII, both now extinct. Unrelatedto IVCS. Charac: good reproductive performance; quick moving; Japanese crookedtail 16%. Maintained by: Nga.

Inbr (Agi): 37. Genet: a b cw. Origin: CBA/CtH-sw (from Cbi) x B6C3Fi. Offspring

crossed to DBA/2 J, then inbred. Charac:strongly curled whiskers in cw/cw. Highincidence of spontaneous B-cell lympho-

mas. Maintained by: Agi.

Inbr (By): 91. Genet: +. Origin: D. W. Bailey,cross of BALB/cAnN $ x C57BL/6J a, thenb x s inbred. Charac: carries histocompati-

bility mutation which has arisen and becomefixed since F10. Maintained by: By. Therecombinant inbred strains CXBD, CXBE,CXBG, CXBH, CXBI, CXBJ, and CXBKwere each derived from the above crossand thereafter independently sib-mated for

54 gen. or more. For each strain it has beendetermined whether the BALB/c or theC57BL/6 alÃelehas been fixed at each of47 loci. These strains are useful in linkageand pleiotropism studies [D. W. Bailey,Transplantation (Baltimore) 11: 325,1971].Maintained by: By, Pt, Ty.

Inbr (Ki): 160. Genet: +. Origin: see C3H/St. Strong to Bittner 1931, Bi to Kirschbaum1952. Charac: mammary cancer more than99% in breeders and virgins (V. Likhite,personal communication, 1981); high incidence of hyperplastic alveolar nodules. Leukemia less than 0.5% in breeders, 14% in66. Hepatomas 0% in ?$, 10% in dd (Ki).


950




CSH/He

C3H/HeJ

C3H/St

Very susceptible to hepatic carcinogens;98% neonatally thymectomized developrunting syndrome (Urne). Maintained by: Ao,Icrf, Ki, Urne. NOTE: There are major differences between sublines of C3H mice (L. M.Glode and D. L. Rosenstreich, J. Immunol.,117:2061,1976; H-H. Krog and R. Moutier,J. Hered., 69: 66,1978). ~ C3Hf

Inbr (N): 160. Genet: rd. Origin: see C3H/St; Strong to Andervont 1930, An to Heston1941 after 35 b x s gen. Charac: 85%hepatomas at 14 mo, 97% mammary tumors in breeders at av. age 7.8 mo (Lac);100% in virgins at 10.6 mo (He); 90% inboth breeders and virgins (Crgl); 84% inbreeders at 272 days (Y). C3H/HeN have41 % primary hepatocellular carcinomas (F.F. Becker, Cancer Res., 41: 3320, 1981);high complement activity (S. Goto ef al., C3HAJpn. J. Exp. Med., 41: 311, 1971). Highlysusceptible to cardiac calcinosis (89%) inmated ?$ (G. L. Eaton ef al., Am. J. Pathol.,790: 173, 1978); resistant to Leishmaniainfection (D. J. Bradley, Clin. Exp. Immunol.,30: 130, 1977); the B6C3F, hybrid is thedesignated Nati. Toxico!. Program strain (M.F. Reilly ef al.. Infect. Immun., 42: 645, C3HeB/De1983). Maintained by: A, Ao, Bkl, Bog, Cox,Cr, Crgl, Cri, Cv, Dp, Dub, Dy, Ei, El, Gy, H,Han, Hsd, 1er,Imr, N, Nctr, Nii, Novosibirsk,Odn, Ok, Ola, Ph, Pt, Rl, Scr, Sim, Sy, Tac,Tru, Uct, W, Wn, Wrm, Y.

Inbr (J): 180. Genet: rd. Origin: see CSH/St.Heston to Jax 1947. Charac: some mammary tumors in breeding 9$, fewer in virgins;high mortality in <Ã®<Ã®exposed to chloroform C3HeB/FeJor turpentine fumes; hepatomas in <Jd(J).Mice protected from stress had 7% mammary tumors compared with 80-100% un

der conventional conditions [V. Reilly, Science (Wash. DC) 789: 465, 1975]. Hema-

tocrit 46.4%, systolic blood pressure 71 mmHg, both second lowest of 21 Jax strainstested (G. Schlager and R. S. Weibust, J.Hered., 67: 295,1976); relatively susceptible to isoniazid-induced seizures (B. A. Taylor, Genetics, 83: 373, 1976); defective li-

popolysaccharide response (K. Kelly and J.Watson, Immunogenetics, 5: 75, 1977); resistant to S. typhimurium C5 (C. E. HÃ¶r- C57BL

maeche, Immunology, 37: 311, 1979);highly susceptible to measles virus (P. A.Neighbour ef a/., Infect. Immun., 27: 764,1978). Maintained by: Bts, Cr, Cri, Dn, Dv,Dy, Fib, Han, Ico, J, Kt, N, Ori, Scr, Sf, Sg,Sid, Sx, Tu, Uct, Wn, Wrm, Yok.

Inbr (Man): 190. Genet: rd. Origin: Strong,

1920, from cross of Bagg albino $ x DBA<3.Strains C, CBA, CHI, and C12I also originated from this cross. Charac: high mammary tumor incidence in both breeders andvirgins. Maintained by: Ao, Hf, Kun, Man,N, Nmg, Ros, Scr.

Inbr (N): 141. Origin: Heston, 1945, from alitter of C3H bom by cesarean section andfoster nursed on C57BL/6. There are several other fostered C3H lines, not all fostered on C57BL/6 and not all from the sameC3H subline. All C3Hf lines lack the mammary tumor milk factor and hence are lowtumor but highly susceptible to its introduction. Maintained by: Bd, Cr, Cum, Dp, Ga,Gh, Hf, 1er, Imr, Kam, Kun, Nctr, Lac, N,Ok, Rl, Ros, Sed.

Inbr (Y). 102. Genet: +. Origin: Pogosianz,C3H 9 x A a, subsquent inbreeding.Charac: originally 30% mammary tumors,gradually decreased [V. I. Gelshtein, Probi.Oncol. (Engl. TransÃ.Vapr. Onkol.), 7(10):45, 1961]; susceptible to hepatic carcinogens. Maintained by: Y.

Inbr (Dt): 125. Origin: Deringer, fertilized ovaof C3H transferred to C57BL. Charac: lacksmilk agent; hepatomas 58% in virgin 99 after24 mo, 30% in breeders, 38% in force-bred,

90% in breeding dd; mammary tumor 4% invirgins, 55% in breeders, 74% in force-bred;

many ovarian tumors (M. K. Deringer, J.Nati. Cancer Inst, 77: 533, 1956). Maintained by: Dt.

Inbr (J): 123. Genet: rd. Origin: Fekete,1948, C3H/HeJ ova transferred to C57BL/6; original transplant animals to Hummel,F3 to Jax in 1950. Charac: low mammarytumor incidence, high susceptibility toagent; 64% ovarian tumors in breeders after19 mo (Hu); hematocrit 46.6%, systolicblood pressure 109 mm Hg (G. Schlagerand R. S. Weibust, J. Hered., 67: 295,1976). Midrange of radiation resistance(BLM-2); calcareous heart deposits in almost all retired breeders (BLM-2). Main

tained by: Dv, Hb, J, Ori, Scr, Sid.

Inbr (A): 7 + 142. Genet: a B. Origin: Little,1921, from mating of 9 57 x Ã¨52 from MissAbbie Lathrop's stock, d 52 mated to ? 58

gave rise to C58. Charac: sensitive to Graffileukemia agent; no spontaneous mammarycancer, low susceptibility to induction bychemical carcinogens (Ber); 6 lumbar vertebrae (Mel); no mammary cancer in breeding 9$, reticular tissue tumors less than 10%

CANCER RESEARCH VOL.45 MARCH 1985

951




C57BL/KS

C57BL/6

in 9?, 4% in <Sa(Ki); nonterritorial, no sensitive aggresion-flight balance, adapted tohole-living (GrÃ²);many skeletal variants (Gr);

sublines He and An have high liver catalasein comparison to other C57BL and otherC57 strains and C58; mammary tumor incidence less than 1%, adenomas of thehypophysis in older animals (He); 7% reti-culosarcomas at 14 mo, senile nephrosde-rosis frequent (Rd); 90-100% lymphomaincidence after whole-body irradiation (Ka);

Haag subline is susceptible to the milk factor in contrast to other sublines; some hy-

drocephalus; type B reticular cell neoplasms74.5% in HeDe subline breeders (T. B. Dunnand M. K. Geringer, J. Nati. Cancer lost.,40: 771, 1968); intermediate susceptibilityto measles virus (B. Rager-Zisman, Fed.

Proc., 35:391,1976). Maintained by: A, Ao,Cnb, Crgl, Cri, Cum, Cv, Dp, H, Icrf, Imr, Ki,Kw, Kun, N, Ok, Rij, Rl, Sy, Univ. Coll.London, Univ. Helsinki (0. MÃ¤kelÃ¤),Wq,zgr.

Inbr (J): 125. Genet: a B. Origin: C57BL/6Jto Biesele in 1947, then pen-bred, to Kaliss

in 1948. Ks resumed inbreeding, returnedthem to Jax 1948. Tumor EO771 originallykilled all animals, but as inbreeding progressed, all animals regressed the tumor.Charac: high incidence of toe malformations, microphthalmia, uniform high fertility(C. P. Dagg, Am. Zool., 3: 223, 1963); thedb mutation arose in this strain; this strainbackground causes severe diabetes in db/db and ob/ob mice; 77% neonatally thym-

ectomized develop runting syndrome(Umc). This strain differs from C57BL/6 at4 known histocompatibility loci and probably more; carries H-2" unlike other C57BL

strains. Maintained by: J.

Inbr (J): 150. Genet: a B. Origin: see C57BL.Sublines 6 and 10 were separated prior to1937. Charac: various tumor types in lowincidence after 18 mo (J); leukemia 7-16%

in 99 (D. D. Myers ef al. Life Sci., 9 (II); 1071,1970); high incidence of hepatomas afterirradiation (D. J. Mewissen and H. J. Rust,C. R. Soc. Biol., 157: 680,1963); incidenceof macroscopic pituitary tumors rises from6 to 61% between 14 and 30 mo (L. S.Felicioer a/., Exp. Gerontol., 15:139,1980).About 12% eye defects, 1% hydrocephalus,and 3% malocclusion in 3000 mice 6 weeksold (J); resistant to Listeria monocytogenes[E. Skamene and P. A. L. Kongshaven, J.Reticuloendothel. Soc., 24 (Suppl.y 32a,1978]; least susceptible to ectromeiia virus

of 8 strains tested [S. N. Ermolaeva et al.Sov. Genet., (Engl. TransÃ. Genetika), 8;681, 1972]; most susceptible to Eimeria of8 strains tested (P. H. Klesius and S. E.Hinds, Infect. Immun., 26: 1111, 1979; M.E. Rose, Parasitotogy, 88:45,1984); mostresistant to Opisthorchis felineus of 6strains tested (A. G. Zelentsov, Med. Para-

zitol. Parazitamye Bolezni, 43: 95, 1974);intermediate susceptibility to rabies virus(D. L. Lodmell, Fed. Proc., 41: 566, 1982);susceptible to Bacillus Calmette-Guerin F

(A. Forget ef a/., Fed. Proc., 41:730,1982);resistant to Plasmodium chabaudÃ¬(M. M.Stevenson et al.. Infect. Immun., 38: 80,1982); relatively resistant to Candida albi-

cans (R. F. Hector, Infect. Immun., 38:1020,1982); relatively resistant to Schistosoma mansoni [M. M. Fanning, ParasiteImmunol. (Oxf.), 6: 95, 1984]; resistant toencephalomyocarditis virus (P. C. Hartig efa/., J. Med. Virol.. 11: 23, 1983); for othersusceptibilities, see M. N. Nesbitt and E.Skamene (J. Leuk. Biol., 36: 357, 1984).Zero incidence of cardiac calcinosis in eithersex (G. J. Eaton ef al., Am. J. Pathol., 90:173, 1978); audiogenic seizure resistant,but can be primed early in life for laterseizure susceptibility (R. A. Schreiber, Exp.Neural., 56: 518,1977); nematocrit 49.4%,systolic blood pressure 117 mm Hg (G.Schlager and R. S. Weibust, J. Hered., 67:295, 1976). High alcohol preference (C. LGoodrick, J. Stud. Alcohol, 39: 19, 1978);more marked in younger animals (E. L. Abel,Phystol. Psychol., 6: 366, 1978); highestliver alcohol dehydrogenase activity of 10strains tested (K. J. Balak ef al., J. Biol.Chem., 257: 15000, 1982); high morphinepreference (G. P. Horowitz, Psychophar-

macology, 52: 119, 1977); more sensitiveto diethylstilbestrol than BALB/c (D. LGreenman ef al., J. Toxico). Environ. Health,3:589,1977); tow concentration of lipids inadrenals, midrange of radiation resistance(BLM-2); high complement activity (S. Goto

ef al., Jpn. J. Exp. Med., 41: 311, 1971;early-onset hearing loss (K. R. Henry, Dev.

Psychobtol., 17: 493, 1984); the B6C3F,hybrid is the designated Nati. Toxicol. Program strain (M. F. Reilly ef al., Infect. Immun., 42:645,1983). Maintained by: A, Ani,Ao, Bg, Bkl, Bog, By, Cox, Cr, Crc, Cri, Cri,Cum, Cv, Dn, Dp, Dt, Dv, Dy, Ei, Ess, Fhc,Fnn, Fre, Gh. H, Han, Hb, HI, Hok, Hsd, Ibg,Ico, 1er,J, Jena, Kun, Lil, Man, Mel, N, Nctr,Nii, Nmg, Novosibirsk, Ola, Ori, Ph, Pp, R,Ra, Ros, Saf, Scr, Sg, Sid, Sim, Ss, Tac,Tru, Tu, Ucsd, Uct, Umc, We, Wn, Wrm, Y,Yok, Zal.


952




C57BL/1OJ Inbr (J): 158. Origin: see C57BL/6J. Charac: C57Lincidence of eye defects 20% in $9, 3% inÂ¿Â¿,malocclusions and hydrocepnalus rarerthan in C57BL/6J (J); occasional vaginalsepta, some fusion of bones in feet (Fo).Hematocrit 50.7%, systolic blood pressure68 mm Hg, second lowest of 21 Jax strainstested (G. Schlager and R. S. Weibust, J.Hered., 67: 295, 1976); susceptible to S.typhimurium C5 (J. Plant and A. A. Glynn,J. Infect. Dis., 733: ;72, 1976); androgendeficient (A. Bartke et al., J. Endocrino!.,75:441,1977); 30% lymphomas in both sexes(G. S. Smith ef al., J. Nati. Cancer Inst., 50;1195,1973). Maintained by: Bg, J, Mod, Nii,on, RI.

C57BL/10ScSn Inbr (J): 7 + 136. Origin: see C57BL; Littleto W. L. Russell, to J. P. Scott at F26 as aseparate subline, to Snell at F35-36.Charac: behavior traits differ from C7BL/10J [V. H. Denenberg, Science (Wash. DC),730:451,1959]; susceptible to Lelshmaniainfection (D.J. Bradley, Clin. Exp. Immunol.,30: 130, 1977); intermediate susceptibility C57P/Ato rabies virus (D. L. Lodmell, Fed. Proc.,41: 566, 1982); susceptible to S. typhimurium C5 (C. E. Hormaeche, Immunology,37: 311, 1979); resistant to Cryptococcusneoformans due to the He1 Ã¡ltete(J. C. C58

Rhodes et al., Infect. Immun., 29: 494,1980). Has been used for the production ofcongenie resistant lines differing fromC57BL/10ScSn by single histocompatibilityloci (G. D. Snell and L. C. Stevens, Immunology, 4:366,1961 ). Maintainedby: A, Ao,Cr, Crc, Dv, Dy, Eg, Fre, Grf, Gy, Hsd, 1er,Icrf, J, Kun, Lac, Ul, Mob, N, Ola, Ph, Pp,Rl, Scr, Sf, Sg, Sx, Tu, W, Y.

C57BR/cd Inbr (J): 178. Genet: a b. Origin: Ã¼ttte,fromcross that gave rise to C57BL, C57BR/a,and C57L. Black and brown lineswere separated in the first generation. Subline cdwas established in gen. 13 from a cross of2 brown lines, one of which had previouslygiven rise to C57BR/a. To Heston 1938, to DA/HuJax 1947 at F66. Charac: low mammarytumor, some hepatomas in &o (J); very resistant to X-irradiation but sensitive to insulin (Lac); resistant to Leishmania infection(D. J. Bradley, Clin. Exp. Immunol.,30:130,1977); resistant to Cryptococcus neofor- DBAmans due to the He1Ã¡ltele(J. C. Rhodes ef

al. Infect. Immun., 29: 494, 1980). Hematocrit 55.1%, systolic blood pressure 73 mmHg (G. Schlager and R. E. Weibust, J. He-red., 67:295,1976). Maintained by: Han, J,Rl.

Inbr (J): 162. Genet:a o In. Origin: J. Murray,1933, mutation to In in F20 of a C57BRsubline which is now extinct. Maintained byCloudman, to Heston 1938, to Jax 1947 atF45. Charac: low mammary tumor incidence; some pulmonary tumors in old animals, congenital cystic ovaries frequent (J);type B reticular cell tumors 54.5% in breeders (T. B. Dunn and M. K. Deringer, J. Nati.Cancer Inst., 40:771,1968); uniformly susceptible to Plasmodiumberghei infection (H.Most ef al., Mil. Med., 737: 915, 1966);resistant to Leishmania infection (D. J.Bradley, Clin. Exp. Immunol., 30: 130,1977); hypersusceptible to infection withEchinococcus multilocularis (Z. Ali-Khan, J.ParÃ¡sito!.,60:231,1974); resistant to Plasmodium chabaudi (M. M. Stevenson ef al.,Infect. Immun., 38: 80, 1982); hematocrit54.1%, systolic Wood pressure 97 mm Hg(G. Schlager and R. S. Weibust, J. Hered.,67: 295,1976). Maintained by: J, N, Pt, Rl,Scr.Y.

Inbr (A): 115+. Origin: R. Korteweg, 1934;DBA 9 X C57BL a, then N20 to C57BL,then b x s inbred. Maintained by: A (formerly listed as P/A).

Inbr (J): 198. Genet: a. Origin: MacDowell,1921, from mating of littermates 9 58 and Â¿52 of Miss Lathrop's stock; d 52 mated to

9 57 gave rise to C57 strains. Charac: highincidence of leukemia before 1 year; frequent polyovular follicles; aplasia of kidneyabout 10% (J); 95% lymphatic leukemia inboth sexes (Urne);relatively resistant to P.berghei infection (H. Most, Mil. Med., 737:915,1966); resistant to Cryptococcus neoformans due to the We1alÃele(J. C. Rhodes

ef al., Infect. Immun., 29: 494, 1980); sexratio 0.552 Â¿Â¿,highest of 30 Jax strains (J.A. Weir, Genetics, 84: 755, 1976). Maintained by: A, Dv, J, N, Ok, Ola, Ori, Scr,Wm, Y.

Inbr (Mob): 125. Gent: c rd. Origin: Hummel,brother and sister bom 12/48 to a non-inbred "Swiss" with a mammary gland tu

mor. Charac: low mammary tumor; partitioned vaginas. Maintained by: Mob.

Inbr (A): 7 + 126. Origin: Little, 1909, fromcolor stocks. The oldest inbred strain. In1929-1930 crosses were made betweensublines and several new sublines wereestablished. Two of these were 12 (nowcalled 1) and 212 (now called 2). Maintainedby A, Cv, Rl.


953




DBA/1

DBA/2

Inbr (J): 7 + 117. Genet: a b d. Origin: seeDBA. Charac: resistant to most DBA/2 tumors; P1534 grows in 50% of DBA/1; S91grows in both strains; mammary tumors inabout % of breeders over 1 year and insome virgins after 18 mo, susceptible toinoculated TB (J); high RBC count, calcareous heart deposits in almost all retiredbreeders (BLM-2); 61.5% mammary tumors

in breeders at 460 days, 8.4% leukemias,3.8% primary lung tumors in 99 (Y). Uniformly resistant to Plasmodium berghei infection (H. Most, Mil. Med., 131:915,1966);susceptible to Lelshmania infection (D. J. DBAfBradley, Clin. Exp. Immunol., 30: 130,1977); highly susceptible to Schistosomamansoni [M. M. Fanning, Parasite Immun.(Oxf.), 6: 95,1984]; resistant to Cryptococ-cus neoformans due to the He' alÃele(J. C. DC/Le

Rhodes ef al., Infect. Immun., 29: 494,1980); susceptible toS. typhimurium C5 (C.E. Hormaeche, Immunology, 37: 311,1979); susceptible to Coxiella bumetil infection (G. H. Scott ef al., Lab. Anim. Sci., 28:673,1978). Maintained by: Bg, Glw, J, Lac,N, Novosibirsk, Ola, OrÃ,Ph, Ros, Ser, Tu,Y.

Inbr (J): 150. Genet: a b d rd+. Origin: see

DBA. Charac: tumor incidence varies be- DDtween colonies (SNISM-7); blood pressure

relatively low [G. Schlager, Nature (Lond.),272: 519, 1966]; audiogenic seizures in100% at 35 days, 5% after 55 days; highmortality in Ã´Ãexposed to chloroform andoxidation products of ethylene oxide, andto vitamin K deficiency (J); relatively resistant to Plasmodium berghei infection (H. DDDMost et al., Mil. Med., 737: 915, 1966);resistant to Leishmania infection (D. J.Bradley, Clin. Exp. Immunol., 30: 130,1977); susceptible toS. typhimurium C5 (C.E. Hormaeche, Immunology, 37: 311,1979); most susceptible to Opisthorchis fel-

ineus of 6 strains tested (A. G. Zelentsov,Med. Parazitol. Parazitarnye Bolezni, 43:95, 1974); resistant to Plasmodium cha-

baudi (M. M. Stevenson ef al.. Infect. Immun., 38:80,1982); susceptible to Candida DDIalbicans (R. F. Hector ef al., Infect. Immun.,38:1020,1982); intermediate susceptibilityto Schistosoma mansoni [M. M. Fanning,Parasite Immunol. (Oxf.), 6: 95,1984]; susceptible to Cryptococcus neoformans dueto He" alÃele(J. C. Rhodes ef al., Infect.

Immun., 29: 494, 1980). Low alcohol preference (C. W. Schneider ef a/., J. Comp.Physiol. Psychol., 82: 466, 1973); low morphine preference (G. P. Horowitz, Psycho-

pharmacology, 52: 119, 1977). About half

the animals develop liver granulomas thatconsist mainly of macrophages accumulating ceroid-like lipopigment (Jena). High RBC

count, low concentration of lipid in adrenals,calcareous heart deposits (BLM-2). Main

tained by: Ao, Bg, Bkl, Bog, Cox, Cr, Cri,Cum, Dub, El, Fhc, Fib, Fnn, H, Han, Hsd,Ibg, Ico, 1er, Icrf, Imr, J, Jena, Ki, Lac, N,Nii, Nmg, Novosibirsk, Ola, Ori, Pp, R, Rij,Ros, Saf, Ser, Sg, Sid, Sim, Smn, Sx, Sy,Tac, Tru, Tu, Uct, Urne, Univ. Coll. London,We, Wn, Y, Yok.

Several lines. Not all are the same DBAsubline or fostered on the same strain.Charac: low tumor incidence, no mammarytumor agent.

Inbr (Le): 100. Genet: Dc/+. Origin: mutation to dancer arose in an obese stockoutcrossed to a BALB/cHu x C3H/HeDihybrid in 1956. One cross to C3H/HeJ, theninbred. Charac: semidominant mutation located on chromosome 19. HÃ©tÃ©rozygotesexhibit circling and head tossing behaviorand are not deaf. Homozygotes die at birthwith cleft lip and cleft palate. Penetrance isincomplete. Maintained by: Le.

Inbr (A): 91. Genet: A B c S. Origin: fromnoninbred ddN of Central Lab. Exp. Anim.to Osaka Univ., 1956, to Heston 1957, toNara 1959. Charac: mammary tumors 77%in breeders; both sexes transmit mammarytumor virus (Tbr). Maintained by: A, Novosibirsk, Tbr.

Inbr (Hok): 81. Genet: A B c D S. Origin: dd-stock mice taken by Dr. S. Hata from Germany to Kitasato Inst. before 1920 (dd =Deutschland-Densenbyo Kenkyosho). To

Manchuria (K. Ando) and back to Japan;inbreeding begun by Suzuki in 1962 at Univ.Tokyo (A. Matsuzawa ef al., Jpn. J. Exp.Med., 40:159,1970). Charac: carries mammary tumor virus; tumor incidence has declined. Maintained by: Hok.

Inbr: 83. Genet: a B c D S Hbb'. Origin:

animals from Lab. Infect. Dis., Tohoku Univ.in 1948 and 1953. Maintained by D. Taka-suka (1948-1963), by H. Nikaido (1960-

1965), and by Sadao Ishigaki since 1965. bx s inbreeding started April 1960 by Nikaido; F20 achieved March 1968. Selectedonly for good growth and reproductive performance. Charac: pregnancy rate 82.7%,av. litter size 8.2; survival rate at 20 days97.8%; av. body wt. at 20 days 9.7 g(JEARA, 1973); induced the highest inter-


954




DDK

DHS

DKI

DKI-R

DL

DLS

DRC/Hok

DW/J

feron titer as compared with ddy, ICR, C3H/ EBT/HaHe, C57BL/6J, BALB/c, and DBA/2 (S.Matsubara ef a/., Cell. Immuno!., 43: 214,1979. Maintained by: Tohi.

Inbr: 105. Genet: A B c D S. Origin: K. ELKondo, from so-called German mice (dd

stock) from Inst. Infect. Dis., Tokyo, in1944. Charac: fertility is reduced when Ã‡Ã‡are outcrossed, caused by embryonic deathat the morula-blastocyst stage (N. Waka-

sugi, J. Reprod. FÃ©rtil.,33:283,1973). Skeletal characters: fusion of frontal and perietalbones 94%, predominantly 26 presacraivertebrae. RBC 8.5 Â± 0.22/10" cu mm, F/St

hematocrit 48.9 Â±0.9%; WBC 5.81 Â±1.05/103 cu mm. Maintained by: Lac, Nga.

Inbr (Hok) 98. Genet: c. Origin: Germany toInst. Kitasato Med. Res. in 1910 to 1920,to Inst. Infect. Dis. (Univ. Tokyo) in 1944, toHok July 1957; b x s inbreeding started in1957. Charac: high incidence of polydactyly(R. Shoji and E. Ohzu, Zool. Mag. (Tokyo), FB/Ki74:115,1965). Maintained by: Hok.

Inbr: 92. Genet: a Be S. Origin: noninbredddN of Central Lab. Exp. Anim.; inbreedingstarted by B. Kitasato, 1953. Charac: uniform sensitivity to Salmonella enteritidis (D. FL/1 ReUshiba et al., Jpn. J. Exp. Med., 32: 519,1962). Maintained by: Jko.

Inbr (Jko): N11 F36. Genet and Origin: seeDKI. Offspring of DKI/Jko x C3H/He werebackcrossed to DKI. Gene for relative resistance to S. enteritidis was introducedfrom C3H (D. Ushiba, Med. Biol., 83: 341,1971). Charac: congenie with DKI but resistant to S. enteritidis. Maintained by: Jko.

Inbr (Ra): 105. Genet: a se +/+ d1. Origin:balanced se +/+ d1 from Truslove to E. S.

Russell, to Kelton 1958. Inbred by Kelton.Maintained by: Ra.

Inbr (Le): 85. Genet: a se +/+ d1. Origin:mutation to d1 occurred in C57BL/Gr in FL/4Re

1950. Truslove to E. S. Russell 1957 asbalanced stock. To Le 1968 at F32. Charac:d'/d' die before weaning. Maintained by: Le.

Inbr (Hok): ? + 48. Origin: DDD mated toC57BL/6; Fi offspring backcrossed 8 times FRGto DDD, then b x s; to Hok in December1972 from Univ. Tokyo. Maintained by: Hok.

Inbr (J): 110. Genet: dw/+ In. Origin: Le toJ 1966. Charac: dwarf, useful for endocrine FSstudies. Maintained by: Dt, J.

Inbr (Cv): 63. Genet: a of e Gusa. Origin:

cross of noninbred bt/bt x C57BL/Ha-e/e.

To Chapman 1974. Charac: of/of. Maintained by: Cv.

Inbr (Yok): 84. Genet: El/El. Origin: K. Imai-

zumi, mutation in noninbred albino mice in1954. Charac: epilepsy-like behavior; brief,

violent convulsion after being tossed upgently 10-15 cm several times; susceptibil

ity begins at about 7 weeks (K. Imaizumi efal., Bull. Exp. Anim., 8:6,1959). Maintainedby: Yok.

Inbr: 140 +. Genet: a b c01 d s. Origin:Strong, from a group of unpedigreed Bus-

sey Inst. mice. Charac: high leukemia inolder animals regardless of breeding conditions; white head markings; resistant toLeishmania infection (D. J. Bradley, Clin.Exp. Immunol., 30: 130, 1977). Maintainedby: Hm, Lac, N, Pt.

Inbr (Ki): 58. Origin: Kirschbaum, 1942-

1952. Multiple crosses between A, F, andNH. Charac: reticular tissue neoplasmsabout 50%; some myeloid leukemia. Maintained by: Ki.

Inbr (Brk): 93 since establishment of f/f line,1956. Genet: afrd Lv". Origin: flexed gene

originally obtained from George Jay fromSnell's WA linkage testing stock; 7 rounds

of cross-intercross to C3H by Jay and E. S.

Russell; outcross to WB/Re by Re; b x smatings of f/f progeny started 1956.Charac: homozygous W+/W+ f/f stock, with

diffuse hemoglobin, both Â«-chain and fi-

chain hemoglobins characterized. FL/4, aline congenie to FL/1, is maintained, segregating for W/+ and f/+. Fetuses and new-

bom of FL/1 show microcytic siderocyticanemia, completely cured by 14 days. Variable belly spotting and tail flexure. Goodbreeding when young, later impaired byobesity. Maintained by: Brk, Mob.

Inbr (Mob): N30 F46. Origin: separated fromFL/1Re-f/+ W/+ at N30 in 1968; in 1980 to

barrier facility by hysterectomy derivationand fostering on C57BI/6J at N30 F28.Maintained by: Mob.

Inbr (Tbr): 35. Origin: non-inbred dd mice;

Chugai Lab. to Tbr 1981 at F26. Charac:resistant to Friend leukemia virus. Maintained by: Tbr.

Inbr (Dn): 77. Genet: b c01 frpsh-1. Origin:

Snell, linkage testing stock, to M. C. Green,


955




FSB

GL/Le

GLF

GRS/A

HLC/Ckc

HRS/J

to Eicher 1971, to Davisson 1983. Maintained by: Dn.

Inbr (Dn): 98. Genet: a fr/+. Origin: furtessmutation arose in unpedigreed stock atOhio State Univ. in 1951; mutant $$ matedwith C57BL/10<Ã•Â¿.Charac: low fecundityand viability; fs/fs have periodic partial hair-

lessness; all types of hairs are shorter thannormal (E. L. Green, J. Hered., 45: 115,1954). Maintained by: Dn.

Inbr (Le): 50. Genet: gl +/+ dlj. Origin:

mutation to gray-lethal discovered in astock segregating for c* by H. GrÃ¼neberg

in 1935. From G. Jay to M. Dickie to P.Lane. Inbred to F25. One outcross to dljÂ¡dlj from heterogeneous stock and main

tained b x s as balanced stock. Charac:recessive lethal mutation on chromosome10. Homozygotes die at about 20 days ofage. They lack the power of secondarybone rÃ©sorption.Coat lacks yellow pigment.Maintained by: Le.

Inbr (Y): 65. Genet: +. Origin: from Jax asbearers of gray-lethal mutation; selected forthe normal genotype by progeny testing.Maintained by: Y.

Inbr (A): 101. Genet: a c. Origin: MÃ¼hlbockobtained breeding pairs of "Grunder" mice

from A. Grumbach, Zurich, in 1955 andinbred (0. MÃ¼hlbock,Eur. J. Cancer, 1:123,1965). Charac: breeding ?$ have nearly100% mammary tumors, latent period 3 mo(R. van Nie and J. Hilgers, J. Nati. CancerInst., 56:27,1976), highly hormone responsive, carries a mammary tumor agent different from MTI, transmitted both by milk andgametes (G. Vlahakis, J. Nati. Cancer Inst.,59: 447, 1977). This strain was never selected for high mammary tumor incidencein contrast to many others. The host rangeof GRS mammary tumor virus is differentfrom that of C3H mammary tumor virus.Very similar genetically to MAS/A: bothcarry Hbb3 and Â»-2a*.15% leukemia in 63,

38% lung tumor in <5<3.Maintained by: ABom, Fib, Imr, Js, N, Rij, Tbr.

Inbr: 47. Origin: see LLC. Selected for highleukocyte count. Charac: mean total leukocyte count 36,000 (<Ã®<Ã®)to 38,000 (??).Thymus and spleen weights much higherthan in strain LLC (Ckc). Maintained by:Harrison (JaxLab).

Inbr (J): 79. Genet: bed hr/+. Origin: hrstock originally from Crew to Camochan, to

HTG

HTH

HTI

HYIII

IC/Le

Heston, to Chase, to E. L Green 1952, toLes 1956, to M. C. Green 1959, to Jax1964. Mating pattern +/hr ? x hr/hr S.Charac: permanent near-hairlessness after

first moult; tylotrichs may persist up to 1.5years (S. J. Mann, Anat. Ree., 770: 485,1971). Some +//v tose most of their furafter 4 mo. Leukemia in hr/hr 45% at 8-10

mo, 71% at 18 mo (H. Meier ef a/., Proc.Nati. Acad. Sci. USA, 63:759,1969). Hem-

atocrit 50%, systolic blood pressure 63 mmHg, lowest of 21 Jax strains tested (G.Schlager and R. S. Weibust, J. Hered, 67:195,1976); show premature decline in immune competence (H-J. Heiniger et al., Can

cer Res., 34: 201,1974); absolute and relative kidney weight greatest of 21 strainssurveyed [G. Schlager, Nature (Lond.), 272:519,1968]). The Charles River "hairless" is

not the same gene (S. J. Mann, J. Invest.Dermatol., 56: 170, 1971). Maintained by:J, Kun, Y.

Inbr (Mob): 51. Formerly called H-2G. Main

tained by: Ao, Mob.

Inbr (Ao): ? + 53. Formerly called H-2H.

Maintained by Ao.

Inbr (Ao) ? + 54. Formerly called H-2I. Main

tained by: Ao, Fre.

Inbr (Le): 83. Genet: hy-3/+. Origin: mutation to hydrocephalus-3 discovered in a het

erogeneous stock by H. GrÃ¼neberg.To M.C. Green in 1963 and b x s inbred. To Lane1975. Charac: recessive lethal mutation onchromosome 8. Homozygotes die withfrank hydrocephalus by 4-5 weeks. Main

tained by: Le.

Inbr (N): 143. Genet: a b d p s; some linescarry In and/or e0" and some do not. Origin:

Strong, 1926, from a group of unpedigreedmice. Charac: resistant to chemical induction of tumors; complement is not detectable (Urne); sex-linked phosphorylase kinase

deficiency (J. B. Lyon, Jr., Biochem. Genet.,4: 169, 1970). Maintained by: Crgl, Cv, J,N, Ph, Y.

Inbr (Le): 59. Genet: /c/+. Origin: Carter toSnell 1950, to M. C. Green 1970, to Lane1975. Ic/ic from heterogeneous stockcrossed to CBA and nonsib followed bysibmatings. A +/+ line was derived at F22.Charac: homozygous ic/ic show abnormalclumping of chromatin in nuclei, most severely in leukocytes. Useful as cell marker.Maintained by: Le.


956




IF

IITES

IS/Cam

ITES

IVCE

IVCS

J/Glw

JBT

Inbr (A): 70. Genet: a'. Origin: G. Bonser

(Leeds) in 1932-1936; selection for early

papilloma development after treatment withcarcinogens. Charac: no mammary tumoragent or spontaneous mammary tumors,but highly susceptible to induction by chemicals or the agent; susceptible to chemicalovarian tumor development; high incidence jE/Leof pseudopregnancy. Maintained by: A.

Inbr (Nga): 76 [ll-tester]. Genet: a b d s.

Origin: crossbred among CS, DBA/2, NBC,and ITES. Charac: useful for testing forcolor genes. Maintained by: Nga. JGBF

Inbr (Dn): 42+46. Genet: +. Origin: Musmusculus praetextus caught in Israeli portx M. m. musculus composite stock carryingbf/bf, m/m, b/b, and a/a. Inbred by M. Wallace; to Roderick and Eicher 1971 at F42,to Dn 1983. Maintained by: Dn, H, Univ.Coll. London.

Inbr (Nga); 87 [l-tester]. Genet: a b d/+ s. ju

Origin: Crossbred among CS, DBA/2, andSII in 1962. Charac: useful for testing forcolor genes; radiation resistant, LD50/3ois790 R. Maintained by: Nga.

Inbr (Csk): 73. Origin: separated during inbreeding and selection of IVCS. Charac:docile; regular 4-day estrus cycle; littler size

9; mean body wt. at 70 days, 99 25.1 g, 6629.9 g (T. Nobunaga, Lab. Anim. Sci., 23:803,1973). Maintained by: Csk.

KEInbr (Csk): 73. Genet: a B c S. Origin: fromddN stock of Central Lab. Exp. Anim., selected for regular estrus cycling 1960.Named 4CS for "4-day cycle of vaginalsmear"; designation changed to conform

with nomenclature rules. Charac: docile;regular 4-day estrus cycle established byvaginal smear; appearance of 3-day estrus

cycle by the proximity of males or by estradici injection (K. Takahashi, Bull. NipponVet. Zootech. Coll., 26: 109, 1977). Highly Â«Fsusceptible to toxoplasma (K. Kamei et al.,J. Parasitol., 62:714,1976). Maintained by:Csk, Jic.

Inbr (Glw): 92. Genet: A b. Origin: Falconer. KlCharac: high frequency of cleft palate (M.Vekemans and F. C. Fraser, Teratology, 75:18A, 1977). Maintained by: Glw.

Inbr (Jd): 86. Genet: a b bt. Origin: fromFalconer's outbred JC stock [D. S. Fai- KK

coner, J. Cell. Comp. Physiol., 56(SupplV153, 1960]. Charac: very low incidence of

congenital malformations, except for frequent tail kinks; suffers from minor inbreeding depression: about 15% mortality ofnewboms up to 3rd postnatal week (Jd).Used for testing teratogenic effects of psy-

chotropic drugs (Jd). Maintained by: Cv, Jd.

Inbr (Le): 47. Genet: a f ru Â¡e/ru+. Origin:Fisher to Snell 1948, to Lane 1969, b x ssince 1972. Charac: female/e/y'e are poor

mothers. Useful for linkage testing. Maintained by: Le.

Inbr (Ty): 55. Genet: a jg +/+ bf. Origin:mutation to jagged tail occurred in C3H/HeJin 1960. Crossed once to C57BL/10 and bx s; crossed once to C57BL/6J-te and b xs to F5; crossed once to C57BL/6J-bf andinbred as balanced stock. Charac: homo-

zygous jg/jg usually bom dead in inbredstrain; if they survive 66 are sterile and 9$are poor breeders. Maintained by: Le, Ty.

Inbr (Ct): 99. Genet: a c. Origin: Falconer,1952, from crosses involving Goodale's andMacArthur's large strains, Bateman's high-

lactation strain, and various mutant stockswith about 50% of C57BL/Fa ancestry (D.S. Falconer, Mouse News Lett., 18: 5,1958). Charac: av. first litter size 9 (Cam);high prenatal mortality (50%) in second litters when gestation is concurrent withsuckling first littler (Fa); low penetrarle ofNil (Cam). Maintained by: Ct, Fa.

Inbr (Kw): 94. Genet: abc P. Origin: Krza-

nowska, 1952, from mice of unknown origin; cross also produced KP (H. Krza-

nowska, Mouse News Lett., 32: 54,1965).Charac: mean litter size 6.1 ; tow percentageof fertilized ova (H. Krzanowska, Folia Biol.,8: 269,1960); 17.6% of spermatozoa haveabnormal heads, the inheritance of thischaracteristic being associated with the Ychromosome. Maintained by: Kw.

Inbr (Tbr): 48. Genet: a Be S. Origin: non-

inbred ddN stock of Central Lab. Exp. Anim.to Nara in 1964. Charac: recipient for Leydigcell tumor. Maintained by: Tbr.

Inbr (Glw): 141. Genet: c FuM/+. Origin:

Dunn and Gluecksohn-Waelsch. Charac:

kinky incomplete dominant; hÃ©tÃ©rozygotesshow tail abnormalities; homozygotes diebefore birth. Maintained by: Glw.

Inbr: 90 +. Genet: a B c D S. Origin: K.Kondo, 1944, from Japanese dealer stock(Kasukabe group). Charac: small litters, 5.6.


957




KP

KR

KSB

LG

LIS/A

LLC/Ckc

LP/J

Frequent diabetes mellitus, occasional obesity in old animals (H. Iwatsuka et al., Endocrino!. Jpn., 17: 23,1970); skeletal characters: cervical rib 66%, predominantly 25presacrai vertebrae; liver and kidney esterase different from C57BL/6J and DBA/2;erythrocyte count 9.35 x 106, hematocrit

51.6%, hemoglobin 18.62, leukocyte count5.23 x 103. Maintained by: Jic, NY Med.

Coll., Univ. Toronto. LPT/Le

Inbr (Kw): 91. Genet: ab p. Origin: see KE.Charac: mean litter size 5.0; high embryonaland postembryonal mortality; frequent sterile matings; low sperm production and lowlibido of d<5;testis abnormalities; degeneration of some tubules and cells, large amountof interstitial tissue (B. Godowicz, FoliaBiol., 73:297,1965). Maintained by: Kw.

Inbr (Nga): 102. Genet: A B c D S. Origin: LS/Leas KK, 1952. Charac: good reproductiveperformance; liver and kidney esterase likeDBA/2; imperforate vagina 2%. Maintainedby: Nga.

Inbr (Nga): 80. Genet: a B D s. Origin: asKK, 1944-1948. Charac: resembles KK. LT

Maintained by: Nem, Nga.

Inbr (J): 104. Genet: a c. Origin: developedby Goodale through selection for large size,beginning in 1931; inbred by Runner.Charac: birth wt. 1.8 g, 28-day wt. 20.1 g,60-day wt. 47.4 g. Av. litter size 6, sex ratio

56% dd, mean life span 491 days; docile,thyroid activity low. Maintained by: J.

LTS/AInbr (A): 101. Genet: c. Origin: MÃ¼hlbock,from Hyg. Inst. ZÃ¼richin 1955; closely related to STS/A and LTS/A (J. Hilgers, personal communication). Charac: low mammary tumor incidence in 99, lung tumors inboth sexes. Maintained by: A.

Inbr: 46. Origin: from a hybrid stock derived MAby cross-breeding C57BL/6J, C57BR/cdJ,

A/J, BALB/cJ, LG/Ckc, and SM/Ckc. Selected for low and high leukocyte count (seealso HLC). Charac: mean total leukocytecount 4000-5000/cu mm. All mice 10-18

mo old have amyloid deposition in spleenand kidney; most exhibit reticular cell hy-perplasia (C. K. Chai, Am. J. Patriot., 85:49, 1976). Thymus and spleen weightsmuch lower than in strain HLC. Maintainedby: Gorevic (SUNY Stony Brook), D. Harrison (JaxLab).

Inbr (J): 125. Genet: A" s. Origin: Dunn.

Charac: 55% late-occurring tumors of var

ious types in 99,19% in dd (J. B. Storer, J.Gerontol., 21: 404, 1966); hematocrit52.4%, systolic blood pressure 109 mm Hg(G. Schlager and R. S. Weibust, J. Hered.,67: 295, 1976); large amount of lipid inadrenal glands in both sexes (BLM-2). Main

tained by: J, Univ. Helsinki (O. MakelÃ¤).

Inbr (Le): 89. Genet: Lp/+. Origin: mutationto loop-tail arose in A strain in 1949. From

W. Hollander to G. Snell 1950. Crossed 7times to C57BL/6J, once to C3H/He, thenb x s. To Lane 1969. Charac: semidominanton chromsome 1. HÃ©tÃ©rozygoteshavelooped or crooked tails and often showhead wobbling. 99 have high incidence ofimperforate vagina. Homozygotes die atbirth. Maintained by: Le.

Inbr (Le): 80. Genet: a* /s/++. Origin: mutation to Is occurred in C57BL-a'at Harwell.

Phillips to Lane as balanced stock 1961.Charac: homozygous /s//s develop mega-

colon but some live and breed. Maintainedby: Le.

Inbr (Sv): 121. Genet: a fl*. Origin: Mac-

Dowell, 1950, mutation at the brown locusin strain C58, outcrossed to BALB/c. ToChase, to Re in 1957 at F28. Charac: hairalmost white except for blackish tip. Spontaneous ovarian teratomas in about one-

half of females (L. C. Stevens and D.Vamum, Dev. Biol., 37: 369, 1974). Maintained by: Cv, Hok, Lac, Ph, Sv.

Inbr (A): 98. Genet: c. Origin: MÃ¼hlbock,from P. Loustalot, Ciba, Basel, in 1954.Charac: high mammary tumor incidence inboth virgins and breeders; closely relatedto LIS/A and STS/A, as deduced from iso-

zyme pattern. A fostered low tumor line,LTSv/A, is also kept. Maintained by: A.

Inbr (J): 132. Genet: c. Origin: Marsh's

strain 3; started from a pair of mice fromthe Lathrop-Loeb colony; 32 gen. of cousin

matings by Marsh, to W. S. Murray whoinbred b x s. Charac: 5% gross tumor incidence in virgin 99, 0% in dd; polydipsia-

polyuria 79% in virgin 99, 12% in dd; 25%gross kidney disease in dd (J. B. Storer, J.Gerontol., 21: 404, 1966). High resistanceto chronic whole-body X-irradiation; pitui

tary cysts in over 50% (J); reduction in sizeof lateral septal nucleus (R. E. Wimer). Hematocrit 49%, systolic blood pressure 128mm Hg, highest of 21 Jax strains tested (G.Schlager and R. S. Weibust, J. Hered., 67:


958




MAS/A

MK/Re

MOR/Cv

MRL

MS/Ae

295, 1976). Serum ai-antitrypsin at midpoint of 34 strains tested (S. K. Chan, ArchEnviron. Health, 27:272,1973). Maintainedby: J, Wim.

Inbr (A): 98. Genet: c. Origin: MÃ¼hlbock,as MWTGRS/A. Charac: low mammary tumor incidence in 99, high lung tumor in both sexes.As in BALB/c, this strain is susceptible toboth C3H mammary tumor virus and GRSmammary tumor virus. Very similar to GRS/A; of over 50 genetic markers, only 2 are MYD/Le anddifferent. Maintained by: A. MYD/Le-+/+

Inbr (Ty): 78. Genet: mk/+. Origin: Jax mutant 63-36, B6D2F,-mfr from M. M. Dickieto Re, 1963. Charac: segregates for compensating microcytic anemia. All mk/mk arebom alive; Vs to Vz die before 3 weeks,developing skin lesions and tail amputation,but surviving mk/mk are fertile and appearnormal except for supernormal numbers ofvery small erythrocytes. Hematology well N/Stcharacterized (BLM-2). Maintained by: Bn,Ty.

Inbr (Cv): 44. Genet: a Mor-1". Origin: wild

trapped in Ohio by Bruell; to T. Shows, YaleUniv., to Chapman, 1972. Charac: mitochondria! malate dehydrogenase varient NBRMOR-1B (T. B. Shows ef al., Biochem. Genet., 4: 707,1970). Maintained by: Cv.

Inbr (J): 65. Genet: a c lpr/+. Oirgin: E. D.Murphy, from a series of crosses involvingC57BL/6J, C3H/DÃŒ,AKR/J, and LG/J followed by b x s inbreeding; matings aremade to produce /pr//pr, /pr/+, and +/+. NCCharac: Ipr/lpr mice have massive generalized lymph node enlargement beginning by8 weeks of age and progressing to over100 times control lymph node weight by 16weeks. $9 die at approx. 17 weeks and <Jdat 22 weeks with advanced immune complex glomerulonephritis. Juvenile thymec-tomy suppresses the syndrome; +/+ micedo not develop it (H. C. Morse ef a/., J. NFR/NImmunol., 129:2612,1982). Maintained by:Dv, Hsd, J, Ori, Ser, Umm.

Inbr (Ae): 30. Genet: c. Origin: A. U. Aesch-bacher selected 4 66 from a group of 300Swiss CD-1 mice having received p.o. 300mg of methylurea and 17 mg of sodiumnitrite per kg of body weight per day for 5 NFS/Ndays. These males had induced an exceptionally high fetal death rate in their offspring. Based on good reproduction data,the offspring from one male were selectedafter the 3rd generation for further inbreed

ing (H. U. Aeschbacher ef a/., MutÃ¢t.Res.,59: 301, 1973). Charac: more susceptiblethan other strains to several mutagens/car-cinogens. Maintained by: Ae.

Inbr (Le): 59. Genet: a'Mf" W T. Origin: M.

C. Green, from heterogeneous background,about 1959. Charac: has been characterized for many polymorphic loci. Useful forlinkage testing. Maintained by: Le.

Inbr (Le): MYD N7 F11, MYD-+/+ 65. Genet: Os +/+ myd. Origin: mutation to mydoccurred in 1963 in te stock received fromR. Phillips in 1961. Crossed to C57BL/6J-A^/A^and sib-mated; a +/+ line was de

rived at F35. Charac: homozygous myd/myd show a progressive and diffuse my-opathy in all skeletal muscles and die between 5 weeks and 5 mo. Maintained by:Le.

Inbr (Ao): 119. Genet: a b d s. Origin:Strong, about 1926, from a group of un-pedigreed mice; ancestral to PBR strain.Charac: low tumor incidence, resistant tochemical carcinogenesis. Maintained by:Ao.

Inbr (Nga): 90. Genet: a b. Origin: frommongrels of Japanese fancy mice (Nishiki-Nezumi group) between 1944 and 1949 (K.Kondo ef a/., Bull. Exp. Anim., 6:107,1957).Charac: poor reproductive performance;liver and kidney esterase like DBA/2. Maintained by: Nga.

Inbr (Nga): 112. Genet: A b. Origin: K.Kondo, from Japanese fancy mice (Nishiki-Nezumi). Charac: leukocyte count 2.95 x103/ml, erythrocyte count 9.06 x 106/rnl,

hematocrit 50, hemoglobin 19 g/100 ml.Liver and kidney esterase like DBA/2. Susceptible to X-irradiation; LDso/aois 547 R.Maintained by: Nem, Nga.

Inbr (N): 59. Genet: Car-^, Ce-2', Es-1",Es-y, ES-1&, Gpd-1", Hbb', ldh-1', Mod-1", Mup-r, Pep-y, Pgm-1", Trf", Hc\ Lyt-1", Thy-1". Origin: derived from NIH outbred

stock; selectively bred for resistance to theaction of histamineafter treatment with Bor-detella pertussis. Maintained by: N, Umm.

Inbr (N): 57. Genet: a, c, Car-2", Ce-2', Es-1",Es-y, Es-10", Gpd-1", Gpi-1", Hbb", Idg-r, Mod-r, Mup-r, Pep-y, Pgm-1', Trf",Hc\Lyt-1Ã¶,Thy-1". Origin: derived from NIH

outbred stock; selectively bred for sensitivity to the action of histamine after treatment


959




NGP/N

NH

NIH/Ola

NMRI

NRH

NYLR

with BÃ³rdeteIla pertussis. Charac: no eco-

tropic murine leukemia virus inducibility [C.A. Kozak and W. P. Rowe, Science (Wash.DC), 204:69,1979]. Maintained by: Cr, Fib,Ul, N.

Inbr (N): 69. Genet: a c. Origin: a randomlyselected litter from the NIH General Purposeoutbred stock N:GP(S). Maintained by: N.

Inbr (Ao): 109. Genet: a d p s. Origin:Strong, from crosses involving CBA, N, andJK. Charac: low tumor incidence; nodularhyperplasia and adrenal adenomas in atleast 10% of old mice; gonadectomy at 6weeks enhances adenomas; some obesity;breeding ceases at approx. 9 mo. Maintained by: Ao, Ki, N, Pt.

NZB

Inbr (Mrs): 71. Genet: abc Es-2", Hbbf,

Thy-r. Origin: CF-1 (Carworth Farms) to

Takeda Chem. Industries, Ltd., to Jmo toNrs. Inbreeding started Sept. 1960 withoutselection. Foster-nursed on germ-free ND-II in 1972. Charac: litter size 5.5-6, weaning

rate about 96%. Body wt. at 60 days, 2?24 g, 66 33 g. More sensitive to X-irradiation

than C57BL/6JNrs and C3H/HeMsNrs;glomerulosclerosis and hyaline degeneration of small and medium-sized arteries frequent in year-old 99 (JEARA, Exp. Anirn.,

22: 271,1973). Maintained by: Nrs.

Inbr (Nya): 89. Genet: c. Origin: from non-

inbred colony originated from a single pairof unknown origin obtained from a breederin Albany, NY, in 1930. b x s matings startedin 1942. Charac: intrastrain skin grafts arenot rejected (L. M. Benson and M. K. Abel-

seth, Lab. Anim. Sci., 27:333,1977). Maintained by: Nya.

Inbr (J): 121. Genet: a B. Origin: see NZO;from a black pair of segregants in the F3 of

NZBR

Inbr (Ola): ? + 27. Genet: a herd. Origin:Pitman at NIH, from N:NIH(S) stock, to Nati.Inst. Biol. Standards, Hampstead, Englandin 1968. To Burroughs Welcome 1970, andOla in 1975. Charac: vigorous and productive general-purpose strain. Maintained by:

Ola. NZC

Inbr (Lac): 50. Genet: c. Origin: noninbredSwiss mice from Lynch to S. Poiley at NIHin 1937. Inbred by PI, known as NIH/PI. ToU. S. Naval Med. Res. Inst. at F51, knownas NMRI. Maintained by: Lac, Nev. NOTE:most colonies called NMRI, particularly European, are random- or pen-bred.

NZO

NZW

NZO. Charac: autoimmune hemolytic anemia; extramedullary erythropoiesis (Ori); lupus-like nephritis (Scr); high incidence of

chronic gastroduodenal ulcÃ©ration (J. B.Howie, Proc. Univ. Otago Med. Sch., 62: 7,1984); spontaneous hypertension and hypertensive vascular disease (U. G. Svend-son, Acta Pathol. Microbio!. Scand., 85A-

548, 1977); susceptible to Cryptococcusneoformans due to the He" alÃele(J. C.

Rhodes ef al., Infect. Immun., 29: 494,1980); resistant to Leishmania infection (D.J. Bradley, Clin. Exp. Immunol., 30: 130,1977). Maintained by: A, Cr, Hok, Hsd, J,Lac, N, Ola, Ori, Scr, Urne, A. Gabrielson(Albany).

Genet: a b. Origin: from NZB/BI at F73,brother-sister pairs with brown coat color.

Charac: spontaneous autoimmune hemolytic anemia, like NZB. About 20% of <JÂ¿have deformed tibiofibula [C. P. Geary andM. Bielschowsky, Proc. Univ. Otago Med.Sch. 56(2); 46,1978]. Maintained by: Wehi.

Inbr (Wehi): 137. Genet: a b. Origin: seeNZO. Charac: low mammary cancer, congenital cystic kidney, increasing incidenceof adenoacanthoma (Bl). Maintained by:Wehi.

Inbr (Wehi): 128. Genet: +. Origin: Bielschowsky, 1948, from the mixed mousecolony at Univ. Otago Med. Sch.; this colonyhad been brought from Imp. Cancer Res.Fund London, in 1930. Several pairs, selected for similar coat color but having nosystematic relationship, were obtained fromthe Med. Sch. colony and maintained in theHugh Adam Dept. Cancer Res.; no otherintroductions have been made. NZC, NZB,NZX, and NZY strains also descended fromthis colony (M. Bielschowsky and C. M.Goodall, Cancer Res., 30: 834, 1970).Charac: tumors: lung 9 34%, Ã´27%; duodenal 9 20%, a 15%; lymphoma, many ofPeyer's patches, 9 10%, <J5%; granulosa

cell ovarian tumor 5.5%; other tumors lessthan 5% (C. M. Goodall et al., Lab. Anim.,7:65,1973); impaired glucose tolerance by2 mo, diffuse and nodular glomerulosclerosis by 7 mo (C. P. Geary and J. G. T.Sneyd, Proc. Univ. Otago Med. Sch., 62:27,1984). Obese, life span up to 800 days,slightly shorter in <&. Maintained by: L. Harrison (NIH), HI, L, Wehi.

Inbr: 100+. Genet: b c. Origin: W. H. Hall,Animal Breeding Station, Otago Univ., froma pair of pink-eyed white mice of the Sta-


960




NZX

NZY

O20

P/J

tion's foundation stock. Charac: glomeru- PAA

lonephritis beginning at 13 mo (J); hybridsbetween NZB and NZW develop lupus nephritis with positive LE cell tests (Lac) andantinuclear antibodies (Umc); susceptible toLeishmania infection (D. J. FVadley, Clin.Exp. Immunol., 30:130,1977). Maintainedby: Cr, Hsd, J, Mcd, N, Ola, Ser, Umc, Y, PABA. Gabrielsen (Albany). The subline maintained by Univ. Otago has been designatedOUW.

Inbr (Wehi): 90. Origin: see NZO. From anNZC 9 (F33) and an NZY 6 (F27), offspringb x s mated. Charac: from F13, some 99have shown imperforate vagina, and bothsexes have a low incidence of megacolon.Maintained by: Wehi.

PAC

PADInbr (Wehi): 120. Genet: b s. Origin: seeNZO; a piebald a which appeared at F2 wasmated with a tan sister; at F4 a piebaldbrother-sister appeared; b x s mating with

selection for s led to fixation of the coatpattern at F7. Charac: high mammary can- PE

cer incidence associated with pituitary enlargement in breeders; heritable megacolon(Bl); highly susceptible to ovarian tumor induction by chemicals (Ber). Maintained by: PETWehi.

Inbr (A): 194. Genet: a c. Origin: R. Kor-

teweg, 1931, from an Amsterdam petshop(P. I. Van Gulik and R. Korteweg, Am. J.Cancer, 38: 506,1940). Charac: Mammarytumor 0% in virgins, 5% in breeders, 13% PFin force-bred; believed not to carry the milk

agent, but susceptible to it and can transmitit to offspring (0. MÃ¼hlbockand T. G. vanRijssel, J. Nati. Cancer Inst., 15: 73,1954).Maintained by: A, Cv, Sid.

Inbr (J): 153. Genet: a b d se p rd. Origin:Snell, extracted following outcross of similar PHHstock (BDP) developed by W. Gates.Charac: high resistance to chronic whole-

body irradiation. Tumor incidence: 23% various kinds in virgin 99, 6% in 66; somepolycystic or granular kidneys, both sexes;mean life span 510 days in virgin 99, 384days in 66 (J. B. Storer, J. Gerontol., 21:404,1966). Sex ratio 47% 66, lowest of 30Jax strains (J. A. Weir, Genetics, 84: 755,1976). Hematocrit 54.5%, systolic Wood PHLpressure 94 mm Hg (G. Schlager and R. S.Weibust, J. Hered., 67: 295,1976). Serumai-antitrypsin highest of 34 strains tested

(S. K. Chan, Arch. Environ. Health, 27:272,1973). Maintained by: Cr, Glw, J, N, Univ.Coll. London.

Inbr: 45. Origin: live-trapped pair from a

Philadelphia factory (J. L. Connor, J. Comp.Physiol. Psychol., 89:118; 1975). See alsonext 4 strains. Charac: reasonably fertile,no obvious abnormalities. Maintained by: N.Henderson (Oberlin Coll.).

Inbr: 42. Origin: see PAA. Charac: smalllitters, otherwise fertile; white spot on forehead of 91% of breeders. Maintained by: asPAA.

Inbr: 42. Origin: see PAA. Charac: relativelyinfertile unless maintained on vitamin A andD supplements. Deterioration of skin andepithelium starts at about 3 days, producingeventual baldness and skin lesions. Maintained by: Cv, N. Henderson (Oberlin Coll.).

Inbr: 45. Origin: see PAA. Charac: relativelyinfertile even with vitamin A and D supplements; slow breeder. Maintained by: asPAA.

Inbr (RI): 90+. Genet: pe/+. Origin: Themutation pe arose in C3H/HeRI. b x s mated(pe/+ x pe/pe). Maintained by: Rl.

Inbr (Wmr): 91. Origin: mixed stock of C3Hand black pet shop mice, Med. Coll. Va.1956, to Wmr 1958. Charac: PigmentedExtraepidermal Tissues; occasional mammary tumors in older 99. Maintained by:Wmr.

Inbr (Fo): 35. Genet: a s tef/+. Origin: selection for high expression of hindfoot polydac-tyly. Charac: high expression of forefootand hindfoot polydactyly and occasionalmoderate tibial hemimelia in hÃ©tÃ©rozygotes,great reduction of radius and tibia in homozygotes. Maintained by: Fo.

Inbr (We): 95. Genet: a In. Origin: Weir, fromMacArthur outbred stock obtained fromButler 1949; b x s inbreeding with selectionfor high blood pH. Charac: blood pH 7.48Â±0.004, blood lactic acid 3.6 Â±0.2 mol/ml.CO2 output 5.90 Â± 0.01 mg/hr/g bodyweight, sex ratio 0.535 66 (J. A. Weir. Genetics, 84: 755, 1976). Overall fertility low.Maintained by: We.

Inbr (We): 97. Genet: a* b In. Origin: same

as PHH, selected for low blood pH. Charac:Wood pH 7.43 Â±0.004, blood lactic acid5.4 Â±0.3 mol/ml, CO2 output 5.90 Â±0.03mg/hr/g body weight, sex ratio 0.435 66 (J.A. Weir, Genetics, 84: 755, 1976). Overallfertility high. Maintained by: We.


961




PL

PUH/Cam

PM/Se

PN

PRO

RBA/Dn

Inbr (J): 130. Genet: c. Origin: from non-inbred "Princeton" mice started in 1922

from 200 mice purchased from a dealer (J.B. Nelson, J. Infect. Dis., 82: 169, 1948).Inbred by Lynch, giving rise to a high leukemia line B (PL) and a second line (PLA)with lower incidence. Maintained by: J, Pt.Sf.

Inbr: 80. Origin: C. Biancifiori, Perugia;C3Hb ? x BALB/cfC3H a, descendants sib-

mated with selection for high incidence ofmammary tumors. Charac: high mammarytumor incidence; polycystic kidney traitarose in the 49th inbred generation, transmitted as an autosomal recessive characteristic (R. Ribacchi, Lav. Ist. Anat. Istol.Patol. Univ. Studi Perugia, 37: 27, 1977):Maintained by: Perugia.

RBB/DnInbr: 52. Genet: c. Origin: albino mice froma pet shop in New Zealand in 1948. Offspring were named "TW outbred" and

raised at Palmerston North Hosp. Somewere taken to Massey Univ. where theywere renamed "NOS outbred." NOS were

sent to Glaxo Labs of New Zealand andnamed "GW ourbred." Breeding pairs were

returned to Palmerston North Hosp. wherethey were renamed "PN mice" and main

tained in the Med. Res. Dept. under Dr.Wigley. Inbreeding started 1964, with selec- RBC/Dn

tion for positive ANA tests in the first 3generations. The primary breeding line wasnamed PN/nA. At F9, a subline (PN/nB) wasstarted by cousin-cousin mating and contin

ued with b x s. Subline A mice were discarded in 1975. Cesarean-derived micewere raised on pathogen-free CD-1 fe

males. Charac: animal model of systemiclupus erythematosus; positive tests for an-

tinuclear antibodies appear at 5 mo; 80%are ANA positive by 10 mo. Glomerulardeposits of IgG, IgM, IgA, and complementappear at 2-4 weeks. Neoplasms in 14%

(S. E. Walker ef al., J. Lab. Clin. Med., 97:932,1978). Maintained by: Hm, Mac.

Inbr (Brk): 61. Genet: ac0" p Pro-f. Origin:

E. S. Russell, 129/ReJ x C57BL/6J, progeny tested for a, e0", and p; b x s inbred.

Charac: hyperprolinemia and prolinuria, increased taurine excretion (R. L. Blake ef a/.,Life Sci., 14:1285,1974); altered polyaminemetabolism (C-A. Manen ef a/., Biochem.J., 758: 529, 1976); aminonucleoside ne-

phrosis (Y. S. Kanwaref al., Proc. Soc. Exp.Bid. Med., 755:339,1977); sluggish movements, 50% generalized hair loss [Y. S.

Kanwar ef al., Biomedicine (Paris), 22:209,1975]. Maintained by: Brk.

Inbr (Cam): 50. Origin: wild Peru-Harland x

CBA. Wild mouse from Rimach Valley inPeru (Mouse News Lett., 67: 28, 1979).Charac: many mutations in this strain. Maintained by: Cam.

Inbr (Dn): ? + 25. Genet: A. Origin: derivedfrom wild mice captured near Mutten, AlbulaValley, Grisons, S. E. Switzerland [A. Groppand H. Winking, Chromosoma (Beri.), 39:265,1972]. Gropp to Davisson and Roderick 1977, to Davisson 1981. Charac: homo-

zygous for Robertsonian translocationRb(4.12)9Bnr; males are aggressive; hasnever been outcrossed to a laboratorystrain. Maintained by: Dn.

Inbr (Dn): ? + 35. Genet: A. Origin: derivedfrom wild mice captured near Bondo, ValBregaglia, Grisons, S. E. Switzerland [A.Gropp and H. Winking, Chromosoma(Beri.), 39: 265, 1972]. Gropp to Davissonand Roderick 1977, to Davisson 1981.Charac: homozygous for Robertsoniantranslocation Rb(1.10)1 OBnr; probably havenever been outcrossed to a laboratorystrain, but not as wild as RbOBnr. Maintained by: Dn.

Inbr (Dn): ? + 33. Genet: c. Origin: theRobertsonian translocation Rb(8.17)1lemarose in "a colony of nonlinear white mice"

at the Inst. Exp. Med. In Leningrad (V. S.Baranov and A. P. Dyban, Ontogenez, 2:164,1971 ), originally from Rappolovo Nursery of the Academy of Medical Sciences ofthe USSR; to Gropp, to Davisson and Roderick 1977, to Davisson 1981. Maintainedby: Dn.

Inbr (Dn): 60. Genet: c F*. Origin: derived

from crosses of Swiss mice (probablyNMRI/Han; Gropp, personal comunicationto Dn) to wild mice captured in the Valle diPoschiavo in S. E. Switzerland. The wildpopulation was originally published as the"tobacco" mouse because of their coat

color. They also appear in the literature asMus poschiavinus Patio and more recentlyMus musculus poschiavinus [A. Gropp efa/., Cytogenetics (Basel), 9: 9, 1970]. F1's

from Alfred Gropp (probably via F. Ruddle)to Roderick in 1970, b x s ever since; toDavisson 1981. Charac: homozygous forRobertsonian translocations Rb(1.3)1Bnr,Rb(8.12)5Bnr, and Rb(9.14)6Bnr. Maintained by: Dn.


962




RF

RFM/Un

RHJ/Le

RNC

ROP

RSV

Inbr (J): 113. Genet: a c. Origin: Furth, 1928, Rillfrom Rockefeller Inst. General-purpose

stock of domestic origin, transferred to OakRidge. History somewhat questionable.Charac: up to 50% leukemia (Ms); skinpainting with methylcholanthrene markedlyenhances leukemia incidence (M. L. Duran-

Reynals ef al., J. Exp. Med., 147: 459,1978); glomerulosclerosis progressive withage (W. D. Gude and A. C. Upton, J. Ger-

ontol., 15:373,1960); midrange of radiationresistance (BLM-2); resistant to infection Rill/An

with Sendai virus (J. C. Parker ef a/., Infect.Immun., 19: 123, 1978). Maintained by: J,Ok, Univ. Helsinki (O. MÃ¤kelÃ¤).

Inbr: 120+. Genet: a c. Origin: Furth, to OakRidge 1949. Charac: 78% leukoses, 26%lung tumors (G. E. Cosgrove ef al., J. Ger-

ontol., 33:178,1978); ovarian tumors 3.8%(N. K. Clapp, RadiÃ¢t.Res., 74: 405,1978);leukemia higher after X-irradiation. Main

tained by: Cr, Bd, Rij.

Inbr (Le): 72. Genet: hr^l+a b c. Origin: RIIIS/J

mutation to rhino-J arose in a CarworthFarms stock received by E. P. Nagler. Na-

gler returned the mutation to C. F. and C.F. sent it to M. M. Dickie, 1951. To Lane1960. Crossed to BALB/cHu 6 times, b x sto F16. One outcross to c/c Hk/+ stockand b x s. Charac: mutation on chromosome 14. Homozygotes begin to lose hairat about 10 days; skin becomes thicker andmore wrinkled than in hr/hr. Females do notnurse young. Maintained by: Le.

Inbr: 50+. Genet: nu Re/++. Origin: 3 pairs SB/Leof mice from R. C. Roberts, Edinburgh, inOct. 1968. $9 were heterozygous nu andTr, So were heterozygous nu and Re. Trwas lost. Recombinant Re nu/+ + weremated and b x s continued for 16 gen. (B.A. Croy and D. Osoba, J. Immunol., 773:1626, 1974). Maintained by: B. A. Croy,Brock Univ. (St. Catherines, Ontario, Canada). SD

Inbr (Le): 67. Genet: Ra/+ Os/+ Pf/+. Origin: M. C. Green from very heterogeneousbackground in 1960; to Lane 1975. Charac:useful for linkage testing. Maintained by:Le, Ori. SEA

Inbr (Le): 66. Genet: Re/Re Sd/+ Va/+.Origin: Carter's Stock 1 (Edinburgh linkage

testing stock E1) to Woodworth 1950. Out-

crossed to C57BL/6, CBA, and C3H and SEC/RInon-sib-mated. To Lane 1967, b x s there

after. Maintained by: Le.

Inbr: 80+. Genet: c. Origin: Dobrovolskaia-

Zavadskaia, Inst, du Radium, Paris, 1928(N. Dobrovdaskaia-Zavadskaia, C. R. Soc.

Biol., 704: 1191, 1930). Charac: have milkagent; non-mammary tumors rare; urethan

causes hepatic angiomatosis; susceptibleto Graffi virus; resistant to gold thioglucoseobesity (Rd). Mammary tumor incidence65-95%. Maintained by: A, Imr, Rho, Sy,

Univ. Helsinki (O. MÃ¤kelÃ¤).

Inbr (N): 105. Genet: A c. Origin: see Rill.Charac: 45% mammary tumors in virgin $$,10% various tumors in dd; mammary tumorincidence in one line declined from 100% inbreeders and virgins in 1954 to less than3% in 1961 (H. B. Andervont and T. B.Dunn, J. Nati. Cancer Inst., 28:159,1962).Have audiogenic seizures at sufficientlyloud sounds (Up); hematocrit 50.1%, systolic blood pressure 79 mm Hg (G. Schlagerand R. S. Weibust, J. Hered., 67: 295,1976). Maintained by: Ki, N, Ok.

Inbr (J): 59 since reconstitution. Genet: crd. Origin: in 1967, both RIII/AnJ (at F66)and RIII/J (at F58) stopped producing viableyoung. The following crosses were made:RIII/AnJ x SEC/1 Re, 9 progeny mated to aRIII/AnJ. ? progeny of that cross-mated to

a RIII/J d- Charac: as Rill/An except thatRIIIS/J mice can be expected to have Vaoftheir genes derived from SEC/1 Re (L. E.Mobraaten, Mouse News Lett., 57: 20,1977, and Mouse News Lett., 60:49,1979).Maintained by: J.

Inbr (Le): 101. Genet: sa bg Aw rd. Origin:

mutations to sa and bg, possibly radiationinduced, occurred independently in stocksused for mutation rate studies at OakRidge; nonsib pair from Rl to Le 1961; sib-

mated since. Charac: high susceptibility tochronic respiratory disease. Maintained by:Le.

Inbr(Glw): 122. Genet: cSd/+. Origin: Dunnand Gleucksohn-Waelsch. Charac: Sd in

complete dominant affecting axial skeletonand urogenital systems; homozygote lethalafter birth. Maintained by: Glw.

Inbr (J): 142. Genet: b d +/d se. Origin: E.L. and M. C. Green, from BALB/c x P.Charac: host for transplantable rhabdomy-

osarcoma T811. Maintained by: J, Rl.

Inbr (RI): 100+. Genet: a b cc" of se/++.

Origin: from E. L. Green 5/19/48 at F20 andF21. Maintained by: Pp, Rl.


963




SEC/1 Gn

SEC/1 Re

SF/Cam

SH1/Le

SHN

SHR

SJL/J

Inbr (Le): 149. Genet: a b cch se/+. Origin:

Green, from cross of NB x BALB/c. Charac:multiple lung cysts, especially in se/se.Maintained by: Le.

Inbr (J): 138. Genet: a b e0". Origin: from

SEC/1 Gn, short-ear eliminated by E. S.

Russell. Charac: excellent breeder (Re);serum ai-antitrypsin second highest of 34

strains tested (S. K. Chan, Arch. Environ.Health, 27: 272, 1973). Maintained by: El,J.

Inbr (Dn): 42 + 32. Genet: +. Origin: wildmice trapped in a coal mine and sib-mated

to F10 by M. Bamawell (Berkeley, CA) as"Corte Madera," to Cambridge 1959.

Charac: adrenal X-zone relatively and ab

solutely large in 99; very poorly developedzona glomerulosa (M. E. Wallace, Environ.Pollut., 1: 175, 1971). Maintained by: Dn,Rk.

Inbr (Le): 78. Genet: c^ sh-1/tÃa<+.Origin:Snell's FS stock to M. C. Green. Out-

crossed to C57BL/1 OGn and b x s. To Lane SK/Cam1975. Charac: homozygotes show circling,head tossing, deafness, and hyperactivity.Maintained by: Le.

Inbr (Mei): 51. Genet: Abe. Origin: SWM/Ms from Nati. Inst. Genet., Misima, Dec.1963. Lines were selected for high early SL/Msmammary tumor incidence and for high lateincidence; SHN is early tumor line, see a/soSLN; b x s started April 1964; F20 attainedin June 1972. Charac: have mammary tumor incidence, tumor incidence 90-100% SLN

in breeders at 6.6 mo, slightly tower in virgins (H. Nagasawa, Exp. Anim., 28: 561,1979); litter size 7.6, weaning rate 89%.Maintained by: Mei, Tbr.

Inbr (Dn): 59. Genet: fÃe+/+ shm. Origin:E. L. Green, shm mutation arose in random- SM

bred stock in March 1960. Crossed on successive occasions to C57BL/6J, C3HeB/FeJ, and finally to rex linkage testing stock.Antecedent strains SHM and SHM/2 werediscontinued in 1970 and 1977. Charac:homozygotes have abnormal gait, smallbody size, phospholipidosis, sterility, lowviability (Gn). Maintained by: Dn.

Inbr (J): 104. Genet: c p rd. Origin: SwissWebster stock of 3 sources that werebrought to Jax between 1938 and 1943.Pen-bred until 1955 when b x s was started. SRH

Charac: multicellular reticulum cell sarcomas resembling Hodgkin's disease in 91%

of virgin 9$ at av. age 13.3 mo, 88% ofbreeders at 13.5 mo, 91% of Ã¢Ã¢at 12.5 mo;high resistance to chronic whole-body X-

irradiation; relatively large litter size. Fastestheart rate of 7 strains tested (D. A. Blizardand R. Welty, J. Comp. Physiol. Psychol.,77:337,1971); susceptible to experimentalautoimmune thyroiditis [A. O. Vladutiu andN. R. Rose, Science (Wash. DC), 174:1137,1971]; 71 and y2 paraproteinemia [H. J.Wanebo ef al., Science (Wash. DC), 754:901,1966]; plaque-forming cell response to

SHI begins to decline by age 42 weeks (A.M. Smith, J. Immunol.. 776:469,1976); <Ã®:9sex ratio at weaning 46:54; dd have lowerythrocyte count (C. G. Crispens, Lab.Anim. Sci., 23: 408, 1973); hepatosplenicamyloidosis after 6 mo (Rd); highly resistantto measles virus (P. A. Neighbour ef a/.,Infect. Immun., 27: 764, 1978); least susceptible to Sendai virus of 19 strains tested(J. C. Parker ef al.. Infect. Immun., 79:123,1978). Maintained by: A, Cr, Crc, Han, Hok,J, N, Ola, Ort, Pt, Scr, Wn, Y.

Inbr (Dn): ? + 38. Origin: from 3 mice trapped on Skokholm Island off Pembrokeshirein 1962 (R. J. Berry); inbred by M. Wallace.Charac: fairly large litters, the size of whichdropped little on inbreeding. Maintained by:Dn, Rk.

Inbr (A): ? + 90. Genet: A B c. Origin:derived from SMA as high-leukemia strain

by K. Tutikawa; in Misima, leukemia incidence is low. Maintained by: A, Ms, Wn.

Inbr (Mei): 45. Origin: see SHN; SLN is thehigh-late-tumor incidence line. Charac:mammary tumor incidence 50-60% inbreeders, 9-10% in virgins at 10 mo, litter

size 5.8, weaning rate 60%. Maintained by:Mei, Tbr.

Inbr (J): 112. Genet: Aw/a or a/a. Origin:

MacArthur, 1939, by crossing 7 stocks (including DBA) and selecting for small bodysize; to Runner in 1948, who began b x smating. Charac: small body size at birth andat weaning; relatively small size tends todisappear as the animals mature; very lowtumor incidence of any kind; both sexes livefor 570-600 days (J); amyloidosis at 1 year

or older (Ml). Maintained by: A, Cv, H, J,Sid, Univ. Coll. London, Univ. Helsinki (0.MÃ¤kelÃ¤).

Inbr (Nmg): 50. Origin: van Abeelen, C57BL/6J x DBA/2J, backcrossed to DBA/2 4gen., followed by b x s with selection for


964




SRL

ST/a

ST/b

STAR/N

STR

STR/1

STS/A

behavioral traits. Charac: high frequency of STUexploratory rearing responses and high lo-

comoter activity [J. H. F. van Abeelen, Nature (Lond.), 254: 239, 1975]. Maintainedby: Nmg.

Inbr., Genet., and Origin as SRH. Charac:low frequency of exploratory rearing andlow locomoter activity. Significant developmental age-dependent differences between STX/Le

SRH and SRL in behavioral components (J.H. F. van Abeelen and A. H. Schoones,Dev. Psychobiol., 10:17,1977). Maintainedby: Nmg.

Genet: H-2". Subline separated after con

siderably more than 8 gen., differs from ST/b at the H-2 locus. Maintained by: Fib, Si.

Swiss

SWR

Inbr (J): 143. Genet: abcrd H-2*. Origin: a

Mrs. Street started breeding Danish whitemice in 1932 as a closed colony; Engel-breth-Holm started b x s mating about

1940. Eh to Heston 1947 at F23, He to J1948 at F25. Charac: uniformly sensitive toPlasmodium berghei infection (H. Most etal., Mil. Med., 131: 915, 1966). 1-2% leu-

kemias including some plasma cell types;other tumors including pulmonary adenomas and mammary carcinomas, about 3%(J); hematocrit 47.2%, systolic Wood pressure 80 mm Hg (G. Schlager and R. S.Weibust, J. Hered., 67: 295, 1976). Maintained by: J, N, Univ. Helsinki (O. MÃ¤kelÃ¤).

Inbr (N): 83. Genet: c. Origin: from Brownat F46. Charac: homozygous for dominantcataract. Maintained by: N.

Inbr (N): 145. Genet: a b. Origin: Strong; SWVbetween F4 and F27, mice were given injections of methylcholanthrene. Charac:susceptible to periodontal disease (P. N.Baer ef al., J. Dent. Res., 40: 23, 1961).Maintained by: N.

Inbr (N): 138. Genet: a b s. Origin: piebaldbranch of STR/N, 1961. Charac: osteoar-

thropathy of the knee joints [M, Silberbergand R. Silberberg, Gerontologia (Basel), 6:91,1962]; obstructive uropathy in 66 before16 mo (L. Sokoloff and M. F. Barile, Am. J.Pathol., 41: 233, 1962). Maintained by: N,Ort.

Inbr (A): 100. Genet: c. Origin: MÃ¼hlbock,from Hyg. Inst. ZÃ¼richin 1955. Charac: nomammary tumors; lung tumors in bothsexes; closely related to LIS/A and LTS/A.Maintained by: A, Nii, Pt.

Inbr: 90. Origin: Swiss; GÃ¶nnert,Bayer-Leverkusen, to Max-Planck-lnst. FÃ¼rVirus

forsch. (TÃ¼bingen)in 1950. Charac: usedfor passage of Ehrlich asertes tumor andRous sarcoma virus-induced fibrosarco-

mas, and for transplantation experimentswith Rous sarcomas. Maintained by: Tu,Tumor Bid. Unit (Univ. Florida, Gainesville).

Inbr (Le): 59. Genet: E^/F0 Tw/+ Xfy/+.Origin: M. C. Green, from F" on C3H from

N. Bateman to M. Foster to M. C. Green1966; Tw from M. Lyon to M. C. Green in1967 and b x s inbred. Charac: has beencharacterized for many polymorphic loci;useful for linkage testing. Maintained by:Le.

Various lines from mainly commercialsources, inbred in different laboratories, asICR/Bc, SW/Fr, SWJ/Mk, SWM/Ms, etc.

Inbr (J): 148. Genet: c rd. Origin: 1926,"Swiss" mice from Albert de Coulon of Lau

sanne, inbred by C. Lynch (C. J. Lynch,Lab. Anim. Care, 79: 214, 1969). Charac:low incidence of mammary tumors in breeders and virgins; about half primary lungtumors; high mortality in 66 exposed toethylene oxide products and to vitamin Kdeficiency (J). Midrange of radiation resistance, arteriosclerosis common in bothsexes (BLM-2); hematocrit 52.9%, systolic

blood pressure 118 mm Hg (G. Schlagerand R. S. Weibust, J. Hered., 67: 295,1976). Maintained by: Bkl, Dt, Fnn, Fo, J,Ola, Pp, Scr, Y.

Inbr (Be): 73. Genet: A c and unknown coatcolor dilution gene. Origin: from Central Animal Depot, Univ. British Columbia, whichhad obtained stock from Defense Res. Bd.,Suffield, Alberta, Canada, in 1949 and maintained as a closed colony; inbreedingstarted in 1959. Charac: 9$ over 8 mo havea hereditary polydipsia-polyuria defect with

a severe increase in water turnover and withhypotonie urine that contains no glucose,blood, or protein; i.e., nephrogenic diabetesinsipidus. They are vasopressin resistant;$? also have a progressive kidney defectwhich, although it resembles nephronophth-

isis in some aspects and hypokalemia inothers, is unique. 66 have a milder form ofthe defect at an older age and show nosigns of histopathology (N. S. Virgo and J.R. Miller, Can. J. Genet. Cytol., 19: 667.1977). Maintained by: Be, Fnn, Fr, W. Lay-

ton (Dartmouth). Ucsd.


965




TA1

TA2

TF

TH

TL

Inbr: 90. Genet: abc Akp-1", Amy-1", Es- TMT, Es-20, Gdc-1", Got-r, Got-?, Gpd-1b,Gpi-T, Hbtf, Id-r, Ldr-1", Mod-1", Mup-1",Pep-3Â°,Pgm-r, Pgm-2", Sep-7a, Tam-1",Trt". Origin: noninbred strain obtained from

Tianjin in June 1956: inbred since then.Charac: mammary tumors about 1% inbreeders, 0 in virgins and males; ovariantumors 9.5%; pulmonary tumors 2.4%; lym- TPphocytic leukemia 1% [Y. Li and B. S. Un,Shanghai Bull. Anim. Vet. Sci., 3 (2V1983]. Sensitive to 20-methylcholanthrene,particularly /V-phenyl-0-napththylamine inmale kidney; susceptible to chronic pneumonia, extremely sensitive to radiation. Av. TPS/Ylife span: 99 673 days, 66 555 days; av. wt.at 43 days, 5$ 20 g, 66 21 g. Maintainedby: Lab. Exp. Oncol. of Tianjin Med. Coll. inChina (Y. U).

TRInbr: 66. Genet: a B c d Akp'1", Amy-1",Es-1", Es-26, Gdc-1", Gof-i", Gof-2", Gpd-1", Gpi-1", Hbb", Id-r, Ldr-r, Mod-1",Mup-1", Pgm-1", Pgm-2*, Pep-3", Sep-1",Tam-1", Trf". Origin: noninbred strain mating, Kun Ming mice, obtained from Bioprod-uct Institute in Peking in 1962; inbred sincethen. Charac: mammary tumors 81.4% inbreeders, 41.4% in virgins, 3.2% in males. TSIOvarian tumors 4.4%; pulmonary tumors2.7%; lymphocytic leukemia 1.3% [B. S.Lin, Shanghai Bull. Anim. Vet. Sci. 2 (iy1982]. Sensitive to radiation. Av. Life Span:9$ 416 days, 66 479 days; av. wt. at 56days 66 22 g, 99 21 g. Maintained by: Lab TSJExp. Oncol. of Tianjin Med. Coll. in China(Y. Li).

Inbr (Le): 77. Genet: T tf/+ tf. Origin: M. C.Green, from T tf/t6 stock received from M.

F. Lyon in 1961, outcrossed to C57BL/10Gn to obtain +tf chromosome in 1962,thereafter b x s. To Lane 1975. Charac:good chromosome 17 markers. Maintained TTR/I eby: Le.

Inbr (Wl): 93. Genet: a*. Origin: mass se

lected for high blood pH (H. G. Wolfe, Genetics, 46: 55, 1961). Charac: good reproductive performance; arterial heart blood pH7.34, sex ratio at birth 57.1% 66 (H. G.Wolfe and J. A. Weir, J. Hered., 63: 109, v/Le1972). Maintained by: Wl.

Inbr (Wl): 96. Genet: Awb. Origin: see TH.

Mass selected for low blood pH. Charac:good reproductive performance; arterialheart blood pH 7.30, sex ratio at birth50.6% 66. Maintained by: Wl.

Inbr: 90+. Origin: Casas, b x s inbred from2 unpedigreed Swiss albinos since 1948.Charac: no mammary tumors, some adren-ocortical tumors; unusually large postcas-trational accumulation of body fat; no livertumors. Maintained by: Szepsenwol (Univ.Puerto Rico).

Inbr (Rl): 68+. Genet: a fp/+. Origin: Jax;taupe mutation arose in C57BL/10J in Dec.1948; after 6 gen. of backcross-intercrossto C57BL/10, b x s inbred. Charac: tp/tpare poor mothers. Maintained by: Rl.

Inbr (Y): 34. Genet: a. Origin: from heterogeneous background through selection forhigh sensitivity to cytogenetic effect of thi-otepa. Maintained by: Y.

Inbr (Dn): 81. Genet: McfÂ°.Origin: Dickie;

tortoise mutation arose in noninbred obesestock in 1952. Charac: maintained by triomatings for 23 years, now by pair matingsMo'Â°/+9 x +/Y 6. Mo'Â°/+99 with much

white in coat usually do not mature; darkerones survive well. In this line no McfÂ°[ihave

appeared. Maintained by: Dn.

Inbr (A): ? + 72. Genet: a c. Origin: MÃ¼hlbock, from P. SchÃ¤fer(TÃ¼bingen)in 1958.Charac: no mammary tumors; high incidence of leukosis in both sexes; polyuric.Maintained by: A.

Inbr (Le): 64. Genet: b Ts/+. Origin: mutation to 7s arose at NCI in 1946 (W. C.Morgan, J. Hered., 41: 208, 1950). FromMorgan to G. D. Snell in 1950. Crossed toC57BL/6, C57BR/cd, and BALB/cSn, thensib-mated. Charac: 7s behavesas dominanton this background, with short kinky tail.Maintained by: Le.

Inbr (Le): 54. Genet: 7 tf/t6 + AÂ¡A.Origin:TR" stock of M. F. Lyon to M. C. Green in1961, to Le 1970. One cross to jittery-grizzled stock, b x s to F7, one cross toBÃ´CBAFr/r^/A in 1972, b x s thereafter.

Charac: small litters, some sterility, usefulfor testing 7 alÃeles.Maintained by: Le.

Inbr (Le): 49. Genet: a fz In/fz In s v/+.Origin: G. D. Snell, v, s, In from Ludwin1947. Crossed to C57BL/10, crossed to fz1960 and non-sib-mated.To Lane 1969 andsib-mated. Charac: original Japanesewaltzer mutation, v/v are poor mothers.Useful for linkage testing. Maintained by:Le.


966




VY

WB

WC

WHT

WLHR

WLL

WN

X/Gf

Inbr (Nctr): 74. Genet: A^/a. Origin: C57BL/6J-XÂ»""from M. M. Dickie, 1962. Charac:

prolific and vigorous; frequency of agouti-

colored /r/a offspring about 10%. 24%hepatoma in A"*/a Ã¡Ã¡at 12-16 mo; 13% in

a/a. Maintained by: Granholm (S. DakotaSt. Univ.), L, Nctr.

Inbr (J): 119. Genet: a W rd/+ rd. Origin: IVhÃ©tÃ©rozygotesfrom S. J. Holman and S. G.Waelsch; b x s inbreeding started in 1948.Charac: W/W homozygotes are anemic,sterile, lack pigmentation in coat; hÃ©tÃ©rozygotes have normal blood picture and fertility, but white ventral spotting; anÃ©miesdie YBRa approximately 11 days. Many other anemia-producing mutant alÃeles are main

tained congenie with this strain. Maintainedby: Bn, J, Pp.

Inbr (J): N58 F37. Genet and Origin: as WB.Charac: as WB, except that anÃ©miesdie atapproximately 14 days. Maintained by: 1er, YSJ.

Inbr (Gy) 125+. Genet: c. Origin: Hewitt,Westminster Hosp., London, 1958. Charac:hardy, breeds well; origin of several spon- YTtaneous squamous carcinomas (J. Dene-

kamp ef a/., Br. J. Cancer, 41:1,1980); 12transplantable nonimmunogenic tumors ofspontaneous origin maintained in this strain.Maintained by: Cbi, Gy, Uct. YX

Inbr (Le): 97. Genet: a b wl +/+ hr. Origin:mutation to wl occurred in pirouette stockin 1948. Crossed to hr from K. P. Hummelin 1949. Dickie to Lane in 1958 and inbred 101as balanced stock. Charac: homozygouswl/wl die before weaning. Maintained by:Le.

Inbr (A): 7 + 112. Genet: c. Origin: Krey-

berg, 1929, from a commercial dealer inOslo (L Kreyberg, Br. J. Cancer, 6: 140, 129/Re1952). In 1934 "White Label" mice were

sent to Leeds, becoming WLL, and somestayed in Oslo, becoming WLO (that strainnot recently reported). Maintained by: A.

Inbr (Nga): 60. Genet: a W/+. Origin: new 129/RrJmutant at W locus. W"IW die at 16-18 days

gestation with anemic syndrome, occasionally survive birth but die in a few days.HÃ©tÃ©rozygotehas normal blood and is viable and fertile. Amount of white spotting isgreater than in W/+. Maintained by: Nga.

Inbr (GÃ¬):89. Genet: a B/b c. Origin: unknown; inbred by Gf since 1953 (A. Gold

feder, Br. J. Cancer, 20: 361, 1966).Charac: no tumors of any kind; does notcarry milk agent but produces antibodiesagainst it; gives immune responses tosheep RBC and possesses high phagocyticactivity; newborn are moderately susceptible to Friend leukemia virus, adults are resistant; resistant to polyoma and FBJ viruses; resistant to liver carcinogenesis with2-acetylaminofluorene; partially resistant toleukemogenesis by dimethylbenzanthra-

cene; irradiation not carcinogenic. Maintained by: Gf.

Inbr (Ki): 132. Genet: A"/a b. Origin: Little toAndervont 1936, to Heston 1946 at An's

F30. Charac: amyloid at least 50% in bothsexes with A*/a or a/a; obesity in hybridsbetween A"Â¡aand other strains; low tumor;lacks microsomal /3-glucuronidase. Main

tained by: Ki.

Inbr (Nctr): 84. Genet: A*/a s. Origin: Chase,

1959. Charac: hepatoma incidence in ?$ at12-16 mo: 11% in A"/a, 4% in a/a. Main

tained by: Nctr.

Inbr (Y): 42. Genet: abcchpd goY In H-2".

Origin: from crosses of C57L, DBA/2,C57BL-go, 129/J. Charac: multiply reces

sive. Maintained by: Y.

Inbr: 50. Genet: A*/a*. Origin: /Â»"/a*from L.B. Russell crossed with AÂ»/a 6 in 1968.

Maintained by: Roger Pederson (San Francisco).

Inbr (El): 93. Genet: A". Origin: Dunn (L C.

Dunn, J. Genet., 33: 443, 1936). Charac:low mammary tumor incidence; slow tobreed, fertility moderate (H); high susceptibility to skin and lung tumor induction. Maintained by: Cum, El, H, Rl, Y.

Inbr (J): 89. Genet: A" cch p/cc/>p. Origin:

see 129/RrJ; b x s dystrophic-normal sub-line, descended from the 129/Re-dy sub-line, from tested dy+/dy+ offspring. Main

tained by: J, Y.

Inbr (J): 97. Genet: A" cc/1p/c p. Origin:

Dunn, a derivative of strain 101 (W. L. Russell and J. G. Hurst, Proc. Nati. Acad.Sci., 37: 267, 1945, and correspondence).Charac: 5% spontaneous testicular tera-

toma (Sv); not susceptible to mammary tumor agent; useful for ovary transplant andova transfer studies; highly sensitive to estrogen at all ages (J); very resistant to X-irradiation, high incidence of urinary calculi





129/terSv

201/R1

615

(BLM-2); slowest heart rate of 7 strains

tested (D. A. Blizard and R. Welty, J. Comp.Physiol. Psychol., 77:337,1971). Resistantto Leishmania infection (D. J. Bradley, Clin.Exp. Immunol., 30: 130, 1977); most susceptible to Sendai virus of 19 strains tested(J. C. Parker er a/., Infect. Immun., 19:123,1978). 129/J is this subline. Maintained by:Dt, J, Kun, Ola, Ori, Rk, Rl, Sv, Y.

Inbr (Sv): N8 F45. Genet: Aw c+ p+. Origin:

derived from 129/Sv-lV C P, which was

developed to determine the effect that thegene W+ might have on teratocarcinogene-

sis (none detectable). Wf+ animals wererepeatedly backcrossed to 129. A W/+ 9 ofgen. N8 produced 38 male offspring ofwhich 8 had testicular teratomas. All 129/ter mice are descended from that mating.Charac: about 30% incidence of spontaneous congenital testicular teratomas, appearing between the 12th and 13th day ofgestation. Tumors may occur on either sideor both and may contain tissues derivedfrom all germ layers; rarely metastasize (L.C. Stevens, J. Nati. Cancer Inst., 50: 235,1973). Maintained by: A, Cam, H, Hok, J,Ph, Scr, Sv.

Inbr (R1): 75+. Genet: A*/a pe. Origin: Russell, from PE/RI and noninbred Ay/a stock.Mating is always Ay/a pe/pe $ x a/a pe/pe

6. Charac: occasional somatic reverse mutations pe to +. Maintained by: Rl.

Inbr: 64. Genet: a bC H-2", Akp-1', Amy-1a, Es-1", Es-2", Gdc-1", Got-1", Gof-2",

Gpd-7", Gp/-7", Hbtf, Id-T, Ldr-r, Mod-1-", Mup-1", Pep-y, Pgm-1", Pgm-2", Sep-1",Tam-1c, Trf". Charac: 40XX, 40XY, G-band-

ing pattern standard. Av. litter is 6.7; av.number of weaners is 6.3. Mammary tumorincidence in multiparous mice is 14.3%; pulmonary adenoma and leukemia within 18months are 36.7% and 5.8%, respectively;22 transplantable tumor lines have beenestablished from this strain. These tumorstrains can be used for screening of anti-

cancer drugs, studying tumor immunology,and mechanism of tumor formation. Maintained by: Lab. Exp. Anim., Inst. Hematol-

ogy, Tianjin, China.

Recommended abbreviations for widely used strains; in allcases the full strain designations should always be given in eitherthe Introduction or the Materials and Methods section of anypaper; e.g., ". ..C57BL/6J x DBA/2JF, (hereafter calledB6D2F,)..." In hybrid designations, the female parent should be

listed first.STRAIN ABBREVIATION

AKRBALB/cCBAC3HC57BLC57BL/KSC57BL/6C57BL/10C57BRC57LDBA/1DBA/2HRS/JRill

AKCCBC3BBKsB6B10BRLD1D2HRR3

APPENDIX 2

Abbreviations for use in symbolizing substrains of mice and ratsand for designating holders of strains.

A Antoni van Leeuwenhoekhuis, Amsterdam C, Sarpha-

tistraat 108, The Netherlands (Dr. A. Dux)Aa Cancer Research Institute, Aarhus, DenmarkAai Ace Animals, Inc., P. O. Box 122, Boyertown, PA

19512 (Ms. Ruth Cinaglia)Abg SUNY Albany, Department of Psychology, 1400 Wash

ington Ave., Albany, NY 12222 (Dr. Bruce Dudek)Adr Animal Disease Research Association, Moredun Insti

tute, Gilmerton, Edinburgh, ScotlandAe Dr. H. J. Aeschbacher, NestlÃ©Department de Re

cherche, Case postale 88, CH-1814 La Tour de Peilz,

SwitzerlandAgi Dr. Joe M. Angel, The Jackson Laboratory, Bar Harbor,

ME 04609Ags C.S.I.R.O., Division of Animal Genetics, P. O. Box 90,

Epping, N. S. W., AustraliaAl Dr. R. C. Allen, Department of Pathology, Medical

University of South Carolina, Charleston, SC 29401Alt University of Alberta, Edmonton, Alberta, CanadaAm Dr. J. L. Ambrus, Roswell Park Memorial Institute,

Buffalo, NY 14203An Dr. H. S. Andervont (deceased)Ani Argonne National Laboratory, Division of Biological and

Medical Research, Argonne, IL 60439 (Dr. T. E. Fritz)Ao Dr. D. B. Amos, Duke University School of Medicine,

Department of Immunology, Durham, NC 27710Ar A.R.S.A.L., Via di Valle Caia, 00040 Pomezia (Roma),

Casella Postale 39 Pomezia (dott. Renata Nobili Castelli), Italy

As University of Aarhus, Department of Genetics, Instituteof Ecology and Genetics, DK-8000 Aarhus, Denmark

(Drs. J. Peter Hjorth and J. Tonnes Nielsen)Asl Animal Suppliers (London), Ltd., 685 High Road, North

Finchley, London N 12, EnglandAu Dr. Robert Auerbach, University of Wisconsin, Depart

ment of Zoology, Madison, Wl 53706Ba Instituto de Medicina Experimental, Laboratorio de

Genetica, Avda. San MartÃn5481, Buenos Aires, Argentina


968




Baf Battelle-lnstitut e.V., Postfach 900160, D-6000 Frank

furt am Main 90, BRD (Dr. Anita Schwaier) BscBaz Centro per lo Studio e la Cura dei Tumori, Busto

Arsizio, Italy (Dr. G. Ceriotti) BspBe University of British Columbia, Department of Medical

Genetics, Vancouver, British Colombia V6T1W5, Canada (Muriel J. Harris and Diana M. Juriloff) Bt

Ber University of Birmingham, Department of Cancer Studies, The Medical School, Birmingham, England (Miss BtsV. G. Nash)

Bd Biology Division, Oak Ridge National Laboratory, Bldg.9207, P. O. Box Y, Oak Ridge, TN 37830 Bu

Be Dr. R. A. Beatty, Institute of Animal Genetics, WestMains Road, Edinburgh, Scotland

Ben Dr. Dorothea Bennett, Sloan-Kettering Institute, Lab- Bua

oratory of Developmental Genetics, New York, NY10021 Bw

Bg Behavior Genetics Laboratory, University of Connecticut, Storrs, CT 06268 (Dr. B. E. Ginsburg or Dr. Steven ByMaxson)

Bi Dr. J. J. Bittner (deceased) CaBim Martin-Luther UniversitÃ¤t, Biologisches Institut der

Medizinische, Halle-Wittenberg, DDR Gag

Bk Dr. Sidney L. Beck, Wheaton College, Norton, MA02766 Cam

Bkl Bantin and Kingman, Ltd., The Field Station, Grimston,Aldbrough, Hull 4QE, England (Mr. G. C. Bantin) and Cbi3403/3421 Yale Way, Fremont, CA 94538 (Mr. RobertSchultz) Cd

Bkr Mrs. Helen Bunker, The Jackson Laboratory, Bar Harbor, ME 04609

BI Dr. M. Bielschowsky (deceased)Bin Akademie der Wissenschaften der DDR, Abt. Ver- Cds

suchstiere, Berlin-Buch, DDR

Bis Beatrice L. Snow, Suffolk University, Department ofBiology, Beacon Hill, Boston, MA 02114 Cft

Bm Dr. Wesley G. Beamer, The Jackson Laboratory, BarHarbor, ME 04609 Cg

Bn Dr. S. E. Bernstein, The Jackson Laboratory, BarHarbor, ME 04609

Bnr Abt. Pathologie, UniversitÃ¤tBonn/Rhein, BRD ChBo Biochemical Department of Cancer Institute, Zluty ko- Chi

pec 7, Brno, CzechoslovakiaBog Jerzy Bogajewski, The Breeding Center for Experi

mental Animals, ul. Poznanska 10, 62081 Przezmi- Chp

erowo near Poznan, PolandBom Laboratory Animals Breeding and Research Center, Ci

GÃ¬.Bomholtgard, 8680 Ry, Denmark CibBoo Boots Pure Drug Co., Ltd., Research Department,

Biological Sciences, Nottingham NG2 3AA, England CiuBoy Dr. E. A. Boyse, Sloan-Kettering Institute, Division of

Immunology, New York, NY 10021 CkcBr Dr. G. M. Bonser (deceased) CIBrc Brighton Polytechnic, Department of Pharmacology,

School of Pharmacy, Brighton BN2 4GJ, England ClbBre Dr. E. J. Breyere, Department of Biology, American

University, Washington, DC 20016Brii Prof. P. L. Broadhurst, Department of Psychology, Cm

University of Birmingham, EnglandBrk Dr. Jane Barker, The Jackson Laboratory, Bar Harbor, Cn

ME 04609Birmingham-Southern College, Department of Biology,

Birmingham, AL 35204BÃoterioCentral of the University of Sao Paulo, MedicalSchool, Av. Dr. Arnaldo, 455,01246 SÃ¢oPaulo, Brazil(Dr. Fernando Sogorb Sanchis)Dr. N. Bateman, Field Laboratory, Animal BreedingResearch Organization, Roslin, Midlothian, ScotlandRadiobiology Department, Medical College of St. Bartholomew's Hospital, London EC1M 6BQ, England

(Prof. P. J. Lindop)Dr. Walter J. Burdette, M. D. Anderson Hospital andTumor Insitute, University of Texas, Houston, TX77025Birmingham University, Department of Anatomy, TheMedical School, Birmingham, EnglandDr. Russell V. Brown, Department of Biology, VirginiaCommonwealth University, Richmond, VA 23220Dr. Donald W. Bailey, The Jackson Laboratory, BarHarbor, ME 04609Dr. T. C. Carter, University of Edinburgh, Edinburgh,ScotlandUniversity of Cambridge, School of Agriculture, Downing Street, Cambridge, England (Dr. J. R. Morton)University of Cambridge, Genetics Department, MiltonRoad, Cambridge, EnglandChester Beatty Research Institute, Institute of CancerResearch, Fulham Road, London SW3 6JB, EnglandDr. Albert Claude (deceased). Contact Prof. Paul Ga-

land, UniversitÃ©Libre de Bruxelles, Laboratoire deCytologie et de CancÃ©rologieExperimental, Brussels,BelgiumCenters for Disease Control, Lawrenceville Facility, P.0. Box 363, Lawrenceville, GA 30245 (Dr. James R.Hegner)Central Food Technological Research Institute, AnimalHouse, Mysore, IndiaMrs. A. Cohen, Experimental Oncology Laboratory,Radiation Therapy Department, Johannesburg GeneralHospital, Johannesburg, South AfricaDr. Herman B. Chase (retired)Dr. Jiri Chlumecky, University of Alberta, Health Sciences Small Animal Program, Edmonton, Alberta, Canada T6G 2H7Mrs. Dorothy R. Chapman, The Jackson Laboratory,Bar Harbor, ME 04609Dr. Ernst Caspari (retired)Ciba Research Centre, P. 0. Bag 9002, Aarey Road,Goregaon East, Bombay 63NB, IndiaUnidad de Investigaciones Cancerologicas, Avda.Cuauhtemoc 240, Ciudad de MÃ©xico,MÃ©xicoDr. C. K. Chai (retired)Mrs. Ruth Clayton, Institute of Animal Genetics, WestMains Road, Edinburgh, ScotlandCentral Laboratory of the Blood Transfusion Service,Netherlands Red Cross, Plesmanlaan 129, Amsterdam, The Netherlands (Dr. Paul de Greve)Dr. R. B. Cumming, Biology Division, Oak Ridge National Laboratory, Oak Ridge, TN 37830A. L. Chapman, Ph.D., University of Kansas Medical


969




Center, Kansas City, KS 66103Cnb Centre d'Etude de l'Energie NuclÃ©aire,B-2400 Mol, Db

Belgium (Dr. A. LÃ©onard)Cne Comitato Nazionale per l'Energia Nucleare, Stabulario

C. S. N., Gasacela, C. P. 2400, Rome, Italy DeCo Dr. George A. Carlson, The Jackson Laboratory, Bar Dem

Harbor, ME 04609Col Dr. Robert L. Collins, The Jackson Laboratory, Bar Dg

Harbor, ME 04609Com ARC Institute for Research on Animal Diseases, Comp-

ton, Nr. Newbury, Berkshire, England DiCox Laboratory Supply Co., Inc., 3750 Kentucky Ave., Dk

Indianapolis, IN 46241 (Mr. Eldon J. Cox)Cp Dr. A. B. Chapman, Department of Genetics, University Dm

of Wisconsin, Madison, Wl 53706 DnCpb Centraal Proefdierenbedrijf T.N.O., P. O. B. 167, Zeist,

The Netherlands (Dr. J. C. J. van Vliet) DoCr Division of Cancer Treatment, Animal Genetics and

Production Branch, National Cancer Institute, Freder- Dp

ick, MD 21701 (Dr. Joseph Mayo or Mr. ClarenceReeder)

Crc Clinical Research Centre, Harrow, Middlesex, England Dr(Dr. C. Hetherington)

Crgl Cancer Research Genetics Laboratory, University of DtCalifornia, Berkeley, CA 94720 (Mrs. Kay Yoshiura)

Cri Cancer Research Institute, Tata Memorial Centre, DuParel, Bombay 400 012, India (Dr. H. P. Randelia)

Crj Charles River Japan, Inc., 795 Shimofurusawa, Atsugi- Dvshi, Kanagawa 243-02, Japan

Crl Charles River Breeding Laboratories, Inc., Wilmington, DyMA 01887. And also SociÃ©tÃ©des Elevages CharlesRiver France S.A., B. P. 29, St. Aubin-les-Elbeuf, S.-

M., France ECs R. T. Charles, "Pencincoed," Glynbrochan Rd., Llan-

idloes, Montgomery, WalesCsk Research Laboratories, Chugai Pharmaceutical Co., Ed

Ltd., 8-41-3, Takada, Toshima-ku, Tokyo, Japan (Dr.

Toshima Nobunaga)Csl Commonwealth Serum Laboratories, Poplar Road, Eg

Parkville 3052, Victoria, AustraliaCsr Charles Salt Research Centre, Orthopaedic Hospital, Eh

Oswestry, Shropshire, England EhsCt Dr. Bruce M. Cattanach, M.R.C. Radiobiology Unit,

Harwell, Didcot, OXON OX 11 ORD, EnglandCu Dr. R. L. Curtis, Department of Anatomy, Medical Ei

College of Wisconsin, Wauwatosa, Wl 53226Cub Charles University, Faculty of General Medicine, De- El

partment of Biology, Albertov 4, Prague 2, Czechoslovakia Ep

Cum Cumberland View Farms, Route 3, Clinton, TN 37716(Mr. Kenneth E. Kile, Sr.)

Cv Dr. Verne M. Chapman, Roswell Park Memorial Insti- Ertute, Department of Molelcular Biology, 666 ElmStreet, Buffalo, NY 14203

Cvl Richard H. Civil, Division of Geographic Medicine, Uni- Eru

versity Hospitals, Cleveland, OH 44106Cwr Case Western Reserve University, Animal Facilities, Eup

Cleveland, OH 44106Cy Dr. Marianna Cherry (retired) EusDa Dr. D. A. Davies, Searle Research Laboratories, High

Wycombe, Buckinghamshire HP12 4HL, EnglandDr. David E. Briles, Cellular Immunobiology Unit, TumorInstitute, University of Alabama, Birmingham, AL35294Dr. Margaret K. Deringer (retired)Dr. Peter Demant, Netherlands Cancer Institute, Sar-phatistraat 108, Amsterdam-C, The Netherlands

Dr. C. P. Dagg, University of Alabama, College ofGeneral Studies, Department of Biology, Birmingham,AL 35233Dr. Margaret M. Dickie (deceased)Dr. A. G. Dickinson, ARC Animal Breeding ResearchOrganisation, West Mains Road, Edinburgh, ScotlandDr. L. Dmochowski (deceased)Dr. Muriel T. Davisson, The Jackson Laboratory, BarHarbor, ME 04609University of Utah, Radiobiology Division, Salt LakeCity, Utah 84132 (Dr. Charles W. Mays)Dr. Giuseppe Della Porta, Section of ExperimentalCarcinogenesis, Istituto Nazionale per lo Studio e laCura dei Tumori, Milan, ItalyProf. Dr. Med. Herman Druckrey, Laboratorium D.Chirurg. UniversitÃ¤tKlinik, Freiburg im Breisgau, BRDDr. Donald P. Doolittle, Purdue University, PopulationGenetics Institute, Lafayette, IN 47907Dr. Wilhelmina F. Dunning, Papanicolaou Cancer Research Institute, 1445 N. W. 14th St., Miami, FL 33136Dr. Chella S. David, Mayo Clinic, Department of Immunology, Rochester, MN 55901Dr. Raymond Daynes, University of Utah College ofMedicine, Department of Pathology, Salt Lake City, UT84132Dr. Martin Evans, Department of Genetics, Universityof Cambridge, Downing Street, Cambridge CB2 3EH,EnglandCentre for Laboratory Animals, University of Edinburgh, Milton Bridge, Penicuik, Midlothian EH26 OPL,Scotland (T. Graham-Marr)

Dr. I. K. Egorov, The Jackson Laboratory, Bar Harbor,ME 04609Dr. J. Engelbreth-Holm (deceased)

National Institute of Environmental Health Sciences, P.O. Box 12233, Research Triangle Park, NC 27709 (Dr.Conrad B. Richter)Dr. Eva M. Eicher, The Jackson Laboratory, Bar Harbor, ME 04609Dr. U. H. Ehling, Gesellschaft fÃ¼rStrahlen- und Um

weltforschung, 8042 Neuherberg bei MÃ¼nchen,BRDDr. Garios Epper, Radiobiology Laboratory, AtomicEnergy National Commission, Avda. del LibertadorGen. San Martin 8250, Buenos Aires, ArgentinaDr. Robert P. Erickson, Department of Human Genetics, University of Michigan Medical School, AnnArbor, Ml 48109Experimental Radiopathology Unit, Hammersmith Hospital, Ducane Road, London, W12 OHS, EnglandEdinburgh University, Department of Pharmacology, 1George Square, Edinburgh EH8 9JZ, ScotlandEdinburgh University, Department of Surgical Science,Medical School, Teviot Place, Edinburgh EH8 9AG,





ScotlandFa Dr. D. S. Falconer, Institute of Animal Genetics, West Glw

Maine Road, Edinburgh, ScotlandFe Dr. Elizabeth Fekete (deceased)Ffm UniversitÃ¤tFrankfurt, Institut fÃ¼rHumangenetik, 6 Gm

Frankfurt/Main, BRD (Dr. K.-H. Degenhardt)Fg Prof. Frank H. J. Figge (deceased) GnFhc Fred Hutchinson Cancer Research Center, Animal Go

Health Resources, 1124 Columbia Street, Seattle, WA Gr98104 (Ms. Carol Shelmerdine)

Fib The Fibiger-Laboratory, Ndr. Frihavnsgade 70, DK-2100 Copenhagen (3,Denmark Grf

Fis Fisons Agrochemical Division, Chesterford Park Research Station, Nr. Saffron Waiden, Essex, England

Fia Dr. Lorraine Flaherty, New York State Department of GrÃ²Health, Albany, NY 12201

Fn Dr. Paul F. Fenton, Brown University, Biology Department, Providence, Rl 02912 Gs

Fnn Dr. R. H. Finnell, Washington State University, Depart- Gvpment of Veterinary Anatomy, Pullman, WA 99163

Fo Dr. P. Forsthoefel (retired) GwFp Istituto di Patologia Generate della UniversitÃ di Fer- Gy

rara, Via Fossato di Mortara, 64/a, 44100 Ferrara, Italy(Dr. Giorgio Benassi) H

Fr McGill University, Department of Biology, Montreal,Quebec, Canada H3A 1B1 (Dr. Daphne G. Trasler) Ha

Fre Dr. Jeffrey A. Frelinger, Department of Microbiology Haband Immunology, University of North Carolina, ChapelHill, NC 27514

Fs Dr. Morris Foster (deceased) HanFu Dr. Jacob Furth (deceased)Fx Dr. Thomas O. Fox, Department of Neuroscience, Har

Children's Hospital Medical Center, Boston, MA 02115

G Glaxo Laboratories, Ltd., Greenford, Middlesex, Eng- Hbland

Ga Dr. Allen H. Gates, Department of Radiation Biology Heand Biophysics, University of Rochester Medical Cen- Hfter, Rochester, NY 14642

Gb Dr. Donald B. Galbraith, Trinity College, Biology De- Hgpartment, Hartford, CT 06106 Hi

Gbi Glasgow University, Department of Bacteriology andImmunology, Western Infirmary, Glasgow W.1, Scotland HI

Gd Dr. C. M. Goodall, National Cancer Research Laboratories, University of Otago, Dunedin, New Zealand Hlr

Gda Medical Academy Gdansk, Department of Biochemistry, Al. Zwycigstwa 42, Gdansk, Poland Hm

Gen Istituto di Farmacologia, UniversitÃ di Genova, VialeBenedetto XV, N.2, Genova, Italy (Dr. Silvio Parodi) Hn

Gf Anna Goldfeder, D.Sc. M.U.C., Department of Biology,New York University, 952 Brown Bldg., Room 754,Washington Square, New York, NY 10003 Ho

Gg Institute of Genetics, University of Glasgow, GlasgowG11 5JS, Scotland (Dr. J. G. M. Shire) Hok

Gh Dr. Douglas Grahn, Argonne National Laboratory, Division of Biological and Medical Research, 9700 CassAvenue, Argonne, IL 60439 How

Gif see OriGÃ¬ Dr. A. GlÃ¼cksmann(retired)Gli Institute of Oncology, Department of Tumor Biology, Hr

Gliwice 1, PolandDr. S. G. Waelsch, Albert Einstein College of Medicine,Department of Genetics, Eastchester Road and MorrisPark, New York, NY 10461J. P. W. Gilman, DVM, Ontario Veterinary College,Guelph, Ontario, Canada N1G 2W1Drs. E. L. and M. C. Green (retired)Dr. Peter Gorer (deceased)Dr. H. GrÃ¼neberg(deceased).Contact Dr. G. M. Trus-love, University College London, Department of Zoology, Gower Street, London, EnglandDr. Ralph J. Graff, Jewish Hospital of St. Louis, Department of Surgery, 216 South Kingshighway, St.Louis, MO 63110Genetica! Institute, University of Groningen, Kerklaan30, HÃ¤ren(Gr.), The Netherlands (Dr. G. A. van Oort-merssen)Dr. Ludwik Gross (retired)Glasgow University Veterinary School, Department ofVeterinary Pathology, Bearsden, Glasgow, ScotlandDr. John W. Gowen (deceased)Gray Laboratory, Mount Vemon Hospital, Northwood,Middlesex HA6 2RN, England (Dr. J. F. Fowler, Dir.)MRC Radiobiology Unit, Harwell, Didcot, OXON OX11ORD, England (Dr. M. F. Lyon)Dr. T. S. Hauschka (retired)Tumor and Experimental Animals Laboratory, Department of Biology, Instituto Nacional de OncologÃayRadiobiologÃa,Habana-4, Cuba (Dr. Raul Castillo)Zentralinstitut fÃ¼rVersuchstierzucht, Lettrow-Vor-beck-Allee 57, Hannover-Linden, BRD (Dr. W. Heine)University of Northern Iowa, Department of Psychology, Cedar Falls, lA 50613 (Dr. G. M. Harrington)Dr. H. Everett Hrubant, California State University,Department of Biology, Long Beach, CA 90804Dr. W. E. Heston (retired)Dr. Harold A. Hoffman, Animal Genetic Systems, Inc.,11 Taft Court, Rockville, MD 20850Prof. Dr. Paula Hertwig (retired)Dr. Jo Hilgers, Antoni van Leeuwenhoekhuis, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CXAmsterdam, The NetherlandsDr. Liselotte Herberg, Diabetes Forschungsinstitutaufm Hennekamp 65, 4000 DÃ¼sseldorf,BRDHoffman-LaRoche, Bldg. 34, Room 525, 340 Kingsland Street, Nutley, NJ 07116 (Dr. Felix Garcia)Dr. Herbert Morse III, Bldg. 7, Room 304, NationalInstitutes of Health, Washington, DC 20205Dr. F. K. Hoombeek, University of New Hampshire,Zoology Department, Spaulding Bldg., Durham, NH03824Prof. W. F. Hollander, Department of Genetics, IowaState University, Ames, lA 50010Experimental Animal Laboratory, Faculty of Science,Hokkaido University, North 10, West 8, Sapporo 060,Japan (Dr. M. Sasaki)Dr. Alma Howard, Paterson Laboratories, Christie Hospital and Holt Radium Institute, Manchester 20, EnglandDr. G. Hoecker, CÃ¡tedrade Biologia,Av. Zanartu 1042,


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Santiago de ChileHsd Hartan/Sprague-Dawley, Box 29176, Indianapolis, IN

46229Ht Dr. H. B. Hewitt (retired) JfcHu Dr. Katharine P. Hummel (retired)Hul Hull University,Department of Zoology, Hull,Yorkshire,

England JkoHz Dr. L. A. Herzenberg, Department of Genetics, Stan

ford University School of Medicine, Palo Alto, CA94304 Jms

Ibg Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80302 (Dr. G. E. McCleam)

Ibm Institute for Bio-Medical Research, Ltd., CH-4402 Ful- Jslinsdorf, Switzerland

Ibr Israel Institute for Biological Research, P.O. Box 19,Ness-Ziona, Israel Ka

loo Iffa Credo, les Oncins, 69/Saint Germain-sur-l'Arbre- Kam

sie, France (Dr. Vet. A. Perrot)1er Institute for Cancer Research, 7701 Burholme Ave., Kb

Fox Chase, Philadelphia,PA 19111 (Dr. Timothy Poote)Icrc Indian Cancer Research Centre, Parel, Bombay 12,

India (Dr. B. K. Batra) KchIcrf Imperial Cancer Research Fund, Burtonhde Lane,

London WC2A 3PX, Englandlei Institute for Experimental Immunology, University of Kd

Copenhagen, Norre Allee 71, DK 2100 Copenhagen0, Denmark Kfm

Ig Dr. Rigoberto Iglesias, Instituto de Medicina Experimental, Avda. Irarrazaval 849, Casilla 3401, Santiago Kgade Chile

Igg Institute of General Genetics, Division of Histocompa-tibility Genetics, USSRAcademy of Sciences, Moscow Kh117333, USSR (L. E. Pospelov) Ki

Imr Institute for Medical Research, Copewood Street,Camden, NJ 08103 (Ms. Jane A. Holben)

Inns Institut de Recherches sur les Maladies du Sang, La- Klboratoire d'ExpÃ©rimentationanimale,HÃ´pitalSt. Louis,

2 place du Dr. Foumier, 75010 Paris, France (Dr. G. KljMahouy)

Irr Institute for Research in Reproduction, Jehangir Mer-wanji Street, Parel, Bombay 12, India Km

Itx INTOX Laboratory, 914 Barber Street, Little Rock, AR72202 (Dr. Lloyd Jeck)

Iw Institut fÃ¼rVersuchstierkunde und Versuchstierkran- Kn

kheiten der Freien UniversitÃ¤t Berlin, Tietzenweg 85/87,1 Berlin 45, BRD

JorJax The Jackson Laboratory, Bar Harbor, ME 04609 KOJÃ¤h National Institute of Animal Health, Kodaira, Tokyo-to, Kon

Japan (Dr. Takayoshi Ino)Jb Dr. Jan Bruell, Psychology Department, Case Western Â«p

Reserve University, Cleveland, OH 44106Jd A. Jurand, University of Edinburgh, Department of KS

Genetics, West Mains Road, Edinburgh 9, Scotland KsbJe Dr. Nancy Jenkins, University of Cincinnati School of

Medicine, Department of Microbiology and MolecularGenetics, 231 Bethesda Ave., Cincinnati, OH 45267

Jem Hebrew University-Hadassah Medical School, Experi- Â«su

mental Medicine and Cancer Research, Jerusalem,Israel (Dr. Michael Schlesinger)

Jena Institut fÃ¼rMikrobiologie und experimentelle Therapie Kt

der Deutschen Akademie der Wissenschaften zu Berlin, Beuthenbergstrasse 11, DDR 69 Jena, DDR (Dr.H. HÃŸinGCKG)

Department of Genetics and Breeding, Central Institutefor Experimental Animals, 17-2, Aobadi-2, Meguro,

Tokyo, JapanKeio University School of Medicine, Department ofMicrobiology, Shinanomachi, Shinjuku-ku, Tokyo, Ja

pan (Dr. Daizo Ushiba)Animal Breeding Unit, Institute of Medical Science,University of Tokyo, Shiba Shirokane-Daimachi, Min-ato-ku, Tokyo, Japan (Dr. Yoshio Tajima)

Dr. Judy M. Strum, University of Maryland School ofMedicine, Department of Anatomy, John Eager Howard Hall, 655 W. Baltimore St., Baltimore, MD 21201Dr. H. S. Kaplan (deceased)Kathryn A. Mason, Department of Radiation Oncology,UCLA School of Medicine, Los Angeles, CA 90024Dr. Berenice Kindred, German Cancer Research Center, Institute for Immunology and Genetics, D-6900

Heidelberg, BRDDr. Walter Kocher, Freie UniversitÃ¤t Berlin, InstitutfÃ¼rToxicologie und Embryonalpharmakologie, Gary-strasse 1-9,1000 Berlin 33, BRD

Dr. J. F. Kidwell, Division of Biology and Medical Science, Brown University, Providence, Rl 02912Kleintierfarm MadÃ¶rin AG, WÃ¶lferweg 34, CH 4414FÃ¼llinsdorf,SwitzerlandKagashim University, Laboratory of Animal Breeding,Faculty of Agriculture, Kagoshima, Japan (Dr. ManjiroTaketomi)Dr. Henry I. Kohn (retired)Kirschbaum Memorial Colony, Kagawa MedicalSchool, Ikenobe, Miki, Kagawa 761-07, Japan (Dr.

Masaki Ohmori)Drs. G. and E. Klein, Department of Cell Research,Karolinska Institute!, Stockholm 60, SwedenDr. Jan Klein, Department of Immunogenetics, MaxPlanck Institute for Biology, Corrensstr. 42,7400 TÃ¼bingen 1, BRDDr. Robert F. Kallman, Department of Radiology, Stanford University School of Medicine, Palo Alta, CA94304Dr. Fr. KrÃ¶ning,Medizinische Forschungsanstalt, Phar-

makologische Abteilung, Bunsenstr. 10, GÃ¶ttingen,BRDDr. N. Kobozieff (retired)UniversitÃ¤tKonstanz. Fachbereich Biologie, 775 Konstanz, Postfach 7733, BRD (Dr. Eberhard! Weiler)Dr. Hilary Koprowski, The Wistar Institute, 36th atSpruce, Philadelphia, PA 19104Dr. N. Kaliss (retired)Dr. Kenneth S. Brown, Laboratory of DevelopmentalBiology and Anomalies, National Institute of DentalResearch, Bldg. 30, Room 412, Washington, DC20205Kansas State University, Animal Resources Facility,Department of Laboratory Animal Medicine, Manhattan, KS 66502Dr. Harold Kalter, Children's Hospital Research Foun-


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dation, Eiland Ave. and Bethesda, Cincinnati, OH |_sh45229

Kun Katholteke UniversitÃ¤t, Central Animal Laboratory, LtNijmegen, The Netherlands (F. G. J. Janssen)

Kw Department of Animal Genetics and Organic Evolution, LubJagiellonian University, Karasia 6,30-060 Krakow, Po

land (Dr. Haiina Krzanowska) LwKx Dr. W. Eugene Knox, Cancer Research Institute, New

England Deaconess Hospital, 194 Pilgrim Road, Bos- Lws

ton, MA 02115L Lilly Research Laboratories, Eli Lilly and Co., Indian

apolis, IN 46206 (Dr. T. T. Yen) LyLac Experimental Embryology and Teratology Unit, MRC M

Laboratories, Woodmansterne Road, Carshalton, Surrey SM5 4EF, England (Dr. D. Whittingham) Ma

Lati Laboratory Animals Institute, Tancsics M. Road, Go-

dÃ¶llÃ¶,Hungary MacLay W. M. Layton, Department of Anatomy, Dartmouth

Medical School, Hanover, NH 03755Lb Dr. Miriam Ueberman, Department of Radiology, Stan- Mai

ford University School of Medicine, Palo Alto, CA94305 Man

Ld Dr. J. Russell Undsey, University of Alabama, Department of Comparative Medicine, 1919 7th Ave. South,Birmingham, AL 35233 Mar

Le Mrs. Priscilla W. Lane, The Jackson Laboratory, BarHarbor, ME 04609 Mas

Lee Leeds University School of Medicine, Laboratory Animals Department, Thoresby Place, Leeds LS2 9NL, MaxEngland

Lei Dr. W. Hijmans, Research Laboratories, Department Mbof Rheumatology, University Hosital, Leiden, The Netherlands Mcd

Lhm London Hospital Medical College, Department of Cancer Research, Ashfield Street, Whitechapel, London E.I.England Mel

Lhr London Hospital Research Laboratories, AnimalHouse, Ashfield Street, Whitechapel, London E. 1., MeEngland

U Dr. C. C. Little (deceased)Lia Liverpool University, Department of Anatomy, P. O. Mei

Box 147, Liverpool L69 3BX, EnglandLid Liverpool University, School of Dental Surgery, Bound

ary Place, Liverpool 7, England MelLJI Dr. Frank Lilly, Department of Genetics, Albert Einstein

College of Medicine, Bronx, NY 10461U Laboratory Animals Centre, Polish Academy of Sei- Mg

enees, Lomna Las k. Warsaw, PolandLn Dr. J. B. Lyon, Department of Biochemistry, Emory Mib

University, Atlanta, GA 30322Lo Los Alamos Scientific Laboratory, P. O. Box 1663, Los

Alamos, NM 87544 (Dr. J. F. Spalding)Lp Dr. W. S. Lapp. Department of Physiology, McGill Mk

University, Montreal, Quebec, Canada H3A 1B1 MlLs Dr. Edwin P. Les, The Jackson Laboratory, Bar Harbor,

ME 04609Lsb Division of Health Effects, Environmental Health Mo

Centre, Department of National Health and Welfare,Tunney's Pasture, Ottawa, Ontario, Canada K1A OL2 Mob

(Dr. Souheil Laham)

London School of Hygiene and Tropical Medicine, 395Hatfield Road, St. Albans, Hertfordshire, EnglandDr. Edward H. Leiter, The Jackson Laboratory, BarHarbor, ME 04609Medizinische Hochschule LÃ¼beck,2400 LÃ¼beck1,BRDDr. L. W. Law, National Cancer Institute, Washington,DC 20205Dr. Susan E. Lewis, Life Science and Toxicology Division, Research Triangle Institute, Research TrianglePark, NC 27709Dr. Clara Lynch (retired)Memorial Sloan-Kettering Institute Cancer Center, 410E. 68th Street, New York, NY 10021Dr. E. A. Mirand, Roswell Park Memorial Institute,Buffalo, NY 14203Massey Universityof Manawatu and Palmerston NorthGeneral Hospital, Palmerston North, New Zealand (Dr.R. E. Munford)M.A. Bioproducts, Biggs Ford Road, Walkersville, MD21793 (W. L Athey)Dr. Stanley J. Mann, Temple University Health Sciences Center, Central Animal Facilities, 3400 NorthBroad Street, Philadelphia,PA 19140Royal Marsden Hospital, Radiotherapy Research Unit,Downs Road, Sutton, Surrey, EnglandUniversity of Massachusetts, Department of Zoology,Amherst, MA 01002 (Dr. H. Rauch)Max-Planck-Institut fÃ¼rImmun biologie, StÃ¼beweg51,Freiburg i Br., BRDMax-Planck-lnstitut fÃ¼rBiochemistry, D-8033 Martinsried, BRDDr. Hugh 0. McDevitt, Stanford University School ofMedicine, Department of Medical Microbiology, Stanford, CA 94305Dr. Anne McLaren, UniversityCollege London, WolfsonHouse, 4, Stephenson Way, London, EnglandSir Peter B. Medawar, Clinical ResearchCentre, North-wick Park Hospital, Watford Road, Harrow, MiddlesexHA1 3UJ, EnglandExperimental Animal Research Laboratory, Meiji University, Tama-ku, Kawasaki, Kanagawa 214, Japan(Dr. Hiroshi Nagasawa)Dr. Roger Melvold, Department of Microbiology andImmunology, Northwestern University School of Medicine, 303 E. Chicago Ave., Chicago, IL 60611Prof. Walter Morgan, South Dakota State College,Department of Animal Science, Brookings, SD 57006Genetic Laboratory of the Institute of ExperimentalBiology, Academy of Medical Sciences of the USSR,Baltiskaya 8, Moscow A-315, USSR (Dr. B. V. Konyu-khov)seeHokDr. James R. Miller, Central Research Division,TakedaChemical Industries, Ltd., 2-17-85 Jusohonmachi, Yo-dogawa-ku, Osaka 532, JapanDr. R. H. Mole, Radiobiology Unit, Harwell, Didcot,OXON 0X11 ORD, EnglandDr. Larry E. Mobraaten, The Jackson Laboratory, BarHarbor, ME 04609


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Mol Veterinary Surgeon Mollegaard's Breeding LabÃ³ralo- Nip

ries, Ltd., 4623 LI. Skensved., Ejby, DenmarkMp Dr. E. D. Murphy (deceased). Contact Mr. John Roths, Nmg

The Jackson Laboratory, Bar Harbor, ME 04609Mq Dr. Jacqueline Mouriquand, Centre d'Etudes Nu- Nnd

clÃ©airesde Grenoble, B.P. 269, Grenoble, FranceMr Dr. E. W. Miller, Cancer Research Laboratory, Depart

ment of Pathology, Royal Victoria Infirmary, Newcastle Noupon Tyne 1, England

Ms National Institute of Genetics, Yata 1111, Misima, Si-zuoka-ken, Japan Not

Mts MTS Laboratories, P. O. Box 22091, San Diego, CA92122 (Marc H. layman) Nrs

Mu Dr. Irving Mauer, Environmental Protection Agency,1400 S. Joyce St., Suite B-1605, Arlington, VA 22202 Ns

Mv Dr. N. N. Medvedev (retired)My Dr. W. S. Murray (deceased) NvsMza Dr. J. Echave Llanos, Instituto de Patologia General y Nya

Experimental, Facultad de Ciencias MÃ©dicas,Universidad Nacional de Cuyo, Mendoza, Argentina

N Veterinary Resources Branch, Bldg. 14A, Room 102, ONational Institutes of Health, Washington, DC 20205(Dr. Cari Hansen) Oci

Na Dr. Joseph H. Nadeau, The Jackson Laboratory, BarHarbor, ME 04609 Odn

Nac National Cancer Center, Research Institute, Chuo-ku,

Tokyo, Japan (Dr. Hiroshi Nagasawa) OkNag Nottingham University, School of Agriculture, Joint An

imal Breeding Unit, Sutton Bonington, Nr. Loughbor-

ough, Leicestershire, England OlaNar Nara Medical College, Department of Pathology, 840

Shijo-cho, Nara-ken, Japan (Prof. Dr. Y. Tsubura) Omr

Nav Naval Medical Research Institute, Laboratory AnimalScience Branch, Bldg. 21, Bethesda, MD 20814

Nb Dr. R. L. Noble, Cancer Research Centre, University Onlof British Columbia, Vancouver V6T 1W5, British Columbia, Canada Org

Ncr Nottingham University, Cancer Research Campaign,Nottingham, England Ori

Nctr National Center for Toxicological Research, Jefferson,AR 72079 (Mr. Harvey Kalbach) Ort

Ndri Naval Dental Research Institute, Great Lakes NavalBase, Great Lakes, IL 60088

Nem Nagoya University, Research Institute of Environmen- Ostal Medicine, Furo-cho, Chikusa-ku, Nagoya (Sen-ichi

Oda)Nga Nagoya University School of Agriculture, Department Osb

of Animal Genetics, Furo-cho, Chikusa-ku, Nagoya-

shi, JapanNi Dr. Robertha van Nie, Antoni van Leeuwenhoekhuis,

Netherlands Cancer Institute, Plesmanlaan 121, 1066 OsuCX Amsterdam, The Netherlands

Nia National Institute of Aging, Bldg. 31, Washington, DC Ott20205 (Dr. Don Gibson)

Nii National Institute of Immunology, P. 0. Box 4922, NewDelhi 11029, India (Dr. R. K. Anand) Ou

Nimr National Institute for Medical Research, Mill Hill, London NW7 1AA, England

Nin National Institute of Nutrition, Indian Council of Medical OwResearch,Jamei-Osmania,Hyderabad7, India

Nippon Rat Co., Ltd., 608-3, Negishi, Urawa, Saitama,

JapanDepartment of Zoology, Toemooiveld, Nijmegen, TheNetherlands (Dr. J. H. F. van Abeelen)National Institute for Nutritional Diseases, S. A. MedicalResearch Council, Private Bag 380, Pretoria, SouthAfricaDr. D. J. Nolte, University of the Witwatersrand, Genetics Laboratory, Milner Park, Johannesburg, SouthAfricaCancer Research Laboratory, The University, University Park, Nottingham, EnglandNational Institute of Radiological Sciences, 4-9-1, An-

agawa, Chiba, Japan 280 (F. Nagasawa)Dr. Muriel Nesbitt, Department of Biology, Universityof California at San Diego, San Diego, CA 92037Nevis Biological Station, Irvington, NY 10533New York State Department of Health, Tower Bldg.,Empire State Plaza, Albany, NY 12201 (Dr. Ronald F.Gruhn)Universitetets Institutt for Generell og EksperimentalPatologi, Oslo, Norway (Dr. K. Amesen)Ontario Cancer Institute, University of Toronto, 500Sherboume St., Toronto, Ontario M4X 1K9, CanadaOdense Universitet, Laboratory Animal Unit, J. B. Wins-

lows vej 21, 5000 Odense C, DenmarkDivision of Inbred Strains of Experimental Animals,Animal Experiment Center, Okayama University Medical School, Okayama 700, JapanOxfordshire Laboratory Animal Colonies, Shaws Farm,Bicester, OXON, EnglandUniversity of Otago Medical School, Department ofMedicine, Wellcome Medical Research Institute, P. O.Box 913, Dunedin, New ZealandOncological Institute, Bd I Mac II, P3 5916, Bucharest12, RomaniaOrganon Laboratories, Ltd., Newhouse, Lanarkshire,ScotlandCentre de L'Ã‰lectionet d'Elevage d'Animaux de La

boratoire, 45 OriÃ©ans-la-Source, France [formerly Gif]

Institute of Orthopaedics, Royal National OrthopaedicHospital, Brockley Hill, Stanmore, HA7 4LP England(Dr. S. Yousuf Ali)Osaka University, Institute for Cancer Research, Do-jima-HamadÃ´ri, Fukushima-ku, Osaka, Japan (Dr. Ya-

suyuji Akamatsu)Osaka University, Department of Experimental Chemotherapy, Research Institute for Microbial Diseases,Yamadakami, Suita, Osaka-fu, Japan (Dr. Jun-ichi Ka-

wamata)University of Otago Medical School, Department ofSurgery, Dunedin, New ZealandGenetics Section, Animal Research Institute, CentralExperimental Farm, Ottawa, Ontario, Canada (Dr. R.S. Gowe)Dr. Henry C. Outzen, Department of Medical Pathology, University of California College of Medicine, Davis,CA95616Dr. Ray D. Owen, Division of Biological Sciences,California Institute of Technology, Pasadena, CA

CANCER RESEARCH VOL.974

45 MARCH 1985




91109 Rap

Oxf Oxford University Cellular Immunology Unit, Sir WilliamDunn School of Pathology, Oxford, England

Pa Dr. Virginia Papaioannou, Tufts University School of RbMedicine, Department of Pathology, 136 HarrisonAve., Boston, MA 02111

Pap Papanikolaou's Research Center of Oncology and Ex- Rbt

perimental Surgery, Hellenic Anticancer Institute, 171Alexandras Av. 603, Athens, Greece (Dr. T. Sirmake- Rdchian-Karra) Re

Pas Pasteur Institute, UnitÃ©de GÃ©nÃ©tiqueCellulaire, DÃ©- Rgpartment de Biologie MolÃ©culaire,25, rue du DocteurRoux, 75015 Paris, France (J. L. GuÃ©net) RhÃ´

Pat Paterson Laboratories, Christie Hospital and Holt Radium Institute, Manchester, England M20 9BX

Pe Dr. P. R. Peacock (retired) RijPer Division of Cancer Research, University of Perugia,

Perugia, Italy (Prof. Lucio Severi) RkPfd Proefdierencentrum K.U.L., deCroylaan 34, B-3030

Heverlee (Leuven), Belgium RkuPfi Pfizer, Ltd., Parasitology Research Department, Sand

wich, Kent, England RlPgi Population Genetics Institute, Life Science Bldg., G-

117, Purdue University, Lafayette, IN 47907 (Dr. T. G. RmaMartin)

Ph Czechoslovak Academy of Sciences, Institute of Ex- Rn

perimental Biology and Genetics, Budejovicka 1083,Prague 4, Czechoslovakia (Doc. MUDr. Milan Hasek) Ro

Pha Slovak Academy of Sciences, Institute for Experimental Pharmacology, DobrÃ¡Voda pri Trnave, Czechoslo- Ros

vakiaPi Dr. H. I. Pilgrim, University of Utah College of Medicine,

Department of Surgery, Salt Lake City, UT 84112 RotPm Dr. Paul C. Montgomery, Department of Microbiology,

School of Dental Medicine, University of Pennsylvania,Philadelphia, PA 19104 Rp

Pms Royal Postgraduate Medical School, HammersmithHospital, Ducane Rd., London, W. 12, England

PÃ´ Dr. E. E. Pogosianz, Institute of Experimental and RrClinical Oncology, Kashirskoje sh.6, Moscow M-478,

USSR RtPol School of Pharmacy, The Polytechnic, Department of

Pharmacology, Chester Road, Sunderiand, Durham, SEngland

Pp Drs. Raymond and Diana Popp, Biology Division, Oak SaRidge National Laboratory, Oak Ridge, TN 37830

Pr Dr. Louis J. Pierre, University of Connecticut, Department of Animal Genetics, Storrs, CT 06268 Sab

Ps Dr. Donald D. Porteous, SUNY Downstate MedicalCenter, Department of Radiology, 450 Clarkson Ave., SafBrooklyn, NY 11235

Psy Institute of Psychiatry, Animal Psychology Laboratory, SbBethlem Royal Hospital, Monks Orchard Road, Beck-enham, Kent, England Sbh

Pt Dr. Michael Potter, Laboratory of Genetics, NationalCancer Institute, Bldg. 37, Room 2B03, Washington, ScDC 20205

Pu Dr. B. D. Pullinger (retired) ScrRa Dr. Harold Rauch, Zoology Department, University of

Massachusetts, Amherst, MA 01003

Breeding Farm Rappolova, Laboratory of Inbred Animals, Academy of Medical Science, Solyanka 14, Moscow, USSRDr. R. G. Busnel, Institut National de la RechercheAgronomique, Laboratoire de Physiologie Acoustique,Jouy-en-Josas (S. & 0.), France

Dr. Roy RiWet, Institute of Cancer Research, 7701Burholme Ave., Philadelphia, PA 19111Dr. G. Rudali (deceased)Dr. Elizabeth S. Russell (retired)University of Reading, Department of Physiology andBiochemistry, Reading, Berkshire, England (R. Batt)RhÃ´ne-Poulenc SantÃ©,Department of Biology, Re

search Centre, B. P. 14, F94407 Vitry sur Seine Cedex,France (Dr. Lavelle)Radiobidogical Institute TNO, P. O. Box 5815, NL-2280 HV Rijswijk, The NetherlandsDr. Thomas H. Roderick, The Jackson Laboratory, BarHarbor, ME 04609Rockefeller University, 1230 York Ave., New York, NY10021 (Dennis Stark)Drs. W. L. and L. B. Russell, Biology Division, OakRidge National Laboratory, Oak Ridge, TN 37830Istituto di Anatomia Comparata, UniversitÃ di Roma,Via Alfonso Borelli, 50, Rome, Italy (Dr. M-V. Civitelli)Dr. Eugene M. Rinchik, Division of Immunology, DukeUniversity Medical Center, Durham, NC 27710Dr. U. Roth, Zoologisches Institut, Jungiusstr. 6, Hamburg 36, BRDRoswell Park Memorial Institute, West Seneca Laboratory, 2863 Clinton St., West Seneca, NY 14224(Barbara Holdridge)Dr. Med. W. Rotzsch, Physiologisch-Chemisches In

stitut der UniversitÃ¤t Leipzig, Ã¼ebigstr. 16, Leipzig,DDRDr. Rosemary W. Elliott, Department of Molecular Biology, Roswell Park Memorial Institute, Buffalo, NY14263Dr. M. N. Runner, University of Colorado, Departmentof Biology, Boulder, CO 80304Mr. John B. Roths, The Jackson Laboratory, Bar Harbor, ME 04609Department of Life Sciences, Bar-Han University, Ra-mat-Gan, Israel (Dr. Kurt Stern)

Research Institute for Tuberculosis, Leprosy and Cancer, Cancer Research Laboratory, Tohoku University,Sendai, Japan (Dr. Haruo Sato)S.A. Bureau of Standards, Private Bag 191, Pretoria,South AfricaSouthern Animal Farms, 475 E. Main St., Prattville, AL36067Dr. Arthur G. Steinberg, Biological Laboratory, Case-Western Reserve University, Cleveland, OH 44106Department of Serology and Bacteriology, Universityof Helsinki, Helsinki, Finland (Prof. O. MÃ¤kelÃ¤)Dr. J. P. Scott, Tufts University, Department of Psychology, Medford, MA 02155Scripps Clinic and Research Foundation, Departmentof Experimental Pathology, 476 Prospect St., La Jolla,CA 92037 (Mr. Steven Wilson)


975




Sd Dr. K. L. Sydnor, Department of Medicine, Universityof Kentucky College of Medicine, Lexington, KY 40506 Sx

Sda Tohoku University, Laboratory of Animal Breeding,Department of Animal Husbandry, Faculty of Agriculture, 210 Kita-6-bancho, Sendai, Japan (Dr. Shusaku Sy

Nishida)Se Prof. Lucio Severi, Istituto di Anatomia e Istologia

Patologica dell' UniversitÃ degli Studi di Perugia, Pe- Sz

rugia, ItalySed Dr. Robert S. Sedlacek, Massachusetts General Hos- T

pital, Department of Radiation Medicine, Boston, MA02114 Ta

Seg Dr. Albert SegaloÂ«, Division of Endocrinology, AltonOchsner Medical Foundation, 1520 Jefferson Hwy., TacNew Orleans, LA 70121

Sel Laboratorio Bioterapico Milanese, Selvi and C., Milan, TachItaly (Dr. W. Murmann)

Sf Dr. Donald C. Shreffler, Washington University Schoolof Mediane, Department of Genetics, St. Louis, MO Tar63110

Sfd Stanford University School of Medicine, Department ofAnatomy, Pato Alto, CA 94304 Tb

Sg Dr. Jack Stimpfling, The Mclaughlin Research Institute, Columbus Hospital, Great Falls, MT 59401 Tbi

Shi Shionogi and Co., Ltd., Research Laboratory, Sagisu-kamidori, Fukushima-ku, Osaka, Japan (Dr. Yasunao Tbr

Ogawa)Si Dr. Morten Simonsen, Queen Victoria Hospital, East Ten

Grinstead, Sussex RH19 3DZ, EnglandSid Dr. Richard L. Sidman, Department of Neuroscience Th

G-2, Children's Hospital Medical Center, Boston, MA

02115 TifSim Simonsen Laboratories, Inc., Route 1, Box 129, Day Toni

Road, Gilroy, CA 95020 (Dr. James Russell)Sk Dr. H. E. Skipper, Southern Research Institute, Bir- Tor

mingham, AL 35205Skh Skin and Cancer Hospital, Temple University, Health

Services Center, Philadelphia, PA 19140 ToxSm Dr. David Steinmuller, Mayo Clinic, Department of Im

munology, Rochester, MN 55901Smh St. Mary's Hospital Medical School, Department of Tr

Pathology, Paddington, London W2 1PG, EnglandSmn Dr. Charles L. Sidman, The Jackson Laboratory, Bar

Harbor, ME 04609 TruSn Dr. George D. Snell (retired)Sp Dr. William L. Simpson, Wayne State University School Tu

of Medicine, Detroit, Ml 48202Sr Dr. Howard A. Schneider (retired) TwSri Stanford Research Institute, Department of Experi

mental Therapeutics, Mento Park, CA 94025Ss Dr. Willys K. Silvers, Department of Human Genetics, Ty

University of Pennsylvania School of Medicine, Philadelphia, PA 19104 Ucsd

Ssc State Seruminstitute, Copenhagen S, Denmark (Dr.Fennestad)

St Dr. Leonell C. Strong (deceased) UctSto Breeding Farm Stolbovaya, Laboratory of Inbred Ani

mals, Academy of Medical Science, Solyanka 14, Moscow, USSR Uip

Sv Dr. L. C. Stevens, The Jackson Laboratory, Bar Har

bor, ME 04609Dr. David H. Sachs, Transplantation Biology Section,Immunology Branch, National Cancer Institute, Washington, DC 20205Dr. A. Symeonidis (deceased). Contact Dr. C. G. Ga-

brielides, Cancer Institute, Theagenion Memorial,Thessaloniki, GreeceDr. Leonard D. Schultz, The Jackson Laboratory, BarHarbor, ME 04609Department of Zoology, University of Toronto, TorontoM5S 1A8, Ontario, CanadaTakatsuki Animal Farm, Takeda Chemical Industries,Kyoto, JapanTaconic Farms, Inc., Hover Ave., Germantown, NY12526 (Mr. Joseph W. Phelan)Dr. Takehiko Tachibana, Virology Division, NationalCancer Center Research Institute, Chuo-ku, Tokyo

104, JapanDr. A. K. Tarkowski, Department of Embryology, Institute of Zoology, University of Warsaw, 00-927 War

saw, PolandDr. S. A. Bamett, Australian National University, Department of Zoology, Canberra ACT 2600, AustraliaTokyo Biochemical Research Institute, 41-8 Takada 3,

Toshima, Tokyo, JapanDr. Yoshihiko Tsubura, 2nd Department of Pathology,Nara Medical College, Kashihara-shi, Nara-ken, Japan

University of Tennessee, Memorial Research Center,Knoxville, TN 37920 (Dr. J. B. Jones)Dr. Karl Theiler, Anatomisches Institute der UniversitÃ¤t,Gloriastr. 19, 8006 Zurich, SwitzerlandTierfarm AG, 4334 Sisseln, Switzerland (Dr. H. Humi)Tohoku University School of Medicine, Central Farmfor Experimental Animals, Sendai, JapanDr. S. Tores, Instituto Nacional do CÃ¡ncer, Sezao dePesquisas, Pea, da Druz Vermelha 23, Rio de Janeiro,Guanabara, BrazilMRC Toxicology Unit, MRC Laboratories, Woodman-

steme Road, Carshalton, Surrey SM5 4EF, England(Dr. J. B. Greig)Dr. John J. Trentin, Division of Experimental Biology,Baylor University College of Medicine, Houston, TX77025Trudeau Institute, P. O. Box 59, Saranac Lake, NY12983 (David P. Kirstein)Max-Planck-lnstitut fÃ¼rBiologie, Abt. Immungenetik,

7400 TÃ¼bingen1, BRD (Dr. Jan Klein)Dr. Noboru Takasugi, Zoological Institute, Faculty ofScience, University of Tokyo, Hongo, Bunkyo-ku, To

kyo, JapanDr. Benjamin A. Taylor, The Jackson Laboratory, BarHarbor, ME 04609University of California at San Diego, Department ofPediatrics, P. 0. Box 3548, San Diego, CA 92103 (Dr.G. F. Chemoff)Animal Unit, Medical School, University of Cape Town,Observatory, 7925, Cape Town, South Africa (M. E.Howard-Tripp)UnitÃ©d'lmmunopathologie IRSE, C.N.R.S., B. P. 8,94

Villejuif, France


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Urne University of Minnesota, Department of Laboratory WmrMedicine and Pathology, Minneapolis, MN 55455 (MissJune Smith) Wms

Umm University of Missouri-Columbia, School of Medicine,

Columbia, MO 65201 (Dr. Ronald M. Mclaughlin)Un Dr. A. C. Upton, Institute of Environmental Medicine, Wn

NYU Medical Center, New York, NY 10021Uni Unilever Research Laboratories, Biology Division, Col- Wo

worth House, Sharnbrook, Bedford, EnglandUp Miss Delta E. Uphoff, National Cancer Institute, Wash

ington, DC 20204 WqUpj Upjohn Co., Animal Rearing and Procurement Unit,

Kalamazoo, Ml 49001Urd Urology Research, Duke University, Durham, NC Wr

27710 (Susan Poulton)Vir Institute of Virology, Church Street, Glasgow, ScotlandVsp Dr. Michale E. Keeling, University of Texas System Wrm

Cancer Center, Science Park, Veterinary ResourceDivision, Box 151 B1, Bastrop, TX 78602 Ws

W Instytut Onkologii Â¡mMarii Sklowdowskiej-Curie, Zak-

lad Biologii Nowotworow, Warszawa, ul. Wawelska15, Poland (Dr. Alina Czamomska) Wsl

Wa Department of Genetics, Agricultural University, Gen.Foulkesweg 53, 6703 BM Wageningen, The Netherlands (Dr. P. de Boer) Wt

Wak Wakayama Medical College, Department of Phystol- Wts

ogy, Wakayama, Japan (Dr. H. Matsushita)Wai Wallaceville Animal Research Centre, Department of Ww

Agriculture, Private Bag, Wellington, New Zealand WyWe Dr. J. A. Weir, University of Kansas, Department of

Zoology, Lawrence, KS 66045Wehi Walter and Eliza Hall Institute of Medical Research, Y

Melbourne 3050, Australia (Dr. G. J. V. Nossal)Wf Dr. George L. Wolff, National Center for Toxicological

Research, Division of Mutagenic Research, Jefferson, YokAR 72079

Wg Dr. H. E. Walburg, Jr., Oak Ridge National Laboratory,Comparative Animal Research Laboratory, Oak Ridge, ZalTN 37830

Wh Dr. Abraham White, Department of Biochemistry, Al- Zbz

bert Einstein College of Medicine, 1300 Morris ParkAve., Bronx, NY 10461 Zgm

Wi Dr. J. W. Wilson (deceased)Wim Drs. Richard E. and Cynthia Wimer, City of Hope Zgr

Medical Center, Quarte, CA 91010Wis Wistar Institute of Anatomy and Biology, 36th Street ztk

at Spruce, Philadelphia, PA 19104WI Dr. H. J. Wolfe, University of Kansas, Department of

Zoology, Lawrence, KS 66045 ZtmWm Dr. William H. Murphy, University of Michigan, Depart

ment of Microbiology, East Medical Bldg., Ann Arbor, ZurMl 48104

Dr. Willie M. Reams, Jr., Department of Biology, University of Richmond, Richmond, VA 23137Dr. R. Michael Williams, Sidney Farber Cancer Institute, Division of Tumor Immunology, 44 Binney St.,Boston, MA 02115Weizmann Institute of Science, Laboratory AnimalsBreeding Center, Rehovot, IsraelDr. James E. Womack, Institute of Comparative Medicine, Texas A and M University, College Station, TX77843Dr. Walter C. Quevedo, Jr., Brown University, Divisionof Biological and Medical Sciences, Providence, Rl02912University of Wisconsin Medical Center, Departmentof Radiology, 1300 University Ave., Madison, WI 53706(Dr. Kelly H. Clifton)Walter Reed Army Institute of Research, Chief, Department of Animal Resources, Washington, DC 20307Dr. John West, Sir William Dunn School of Pathology,University of Oxford, South Parks Road, Oxford, 0X13RE, EnglandDr. H. Bazin, UniversitÃ©Catholique de Louvain, Ecolede SantÃ©Publique, Ave. Chapelle aux Champs 4,1200Brussels, BelgiumDr. Wesley K. Whitten, Hobart, TasmaniaDr. Peter J. Wettstein, Department of Microbiology,USC School of Medicine, Los Angeles, CA 90033Mrs. E. F. Woodworth (retired)Dr. G. W. Woolley, Institute of General Medical Sciences, National Institutes of Health, Washington, DC20205Yuriovo Laboratory of Experimental Animals, Department of Genetics, Yurtovo Post Office, Khimki Town,Moscow Region, USSRDepartment of Veterinary Science, National Institute ofHealth (Yoken), Kamiosaki, Shinagawa-ku, Tokyo 141,

Japan (Drs. Masara Nakagawa and Toshihiko Asano)Dr. M. B. Zaleski, Department of Microbiology, SUNYBuffalo, Buffalo, NY 14214UniversitÃ¤t Zurich, Biologisches Zentrallaboratorium,Kantonsspital, Ramistr. 100, Zurich, SwitzerlandMedical Faculty, Department of Physiology, Salata 3,41000 Zagreb, Yugoslavia (Prof. Dr. Filip Culo)Institut "Ruder Boskovic," 41001 Zagreb, Bijenicka 54,

Yugoslavia (Dr. Lidija Suman)Zentrale Tierversuchsanlage des Klinikums der JohannWolfgang Goethe-UniversitÃ¤t, D600 Frankfurt, Theo-dor-Stein-Kai 7, BRD

Zentrales Tierlaboratorium der Medizinischen Hochschule, Roderbruchstr. 101, 3 Hannover, BRDInstitut fÃ¼rZuchthygiene der UniversitÃ¤t ZÃ¼rich,Win-

terthurerstr. 260, CH 8057 ZÃ¼rich,Switzerland


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standardizednomenclaturefor inbredstrainsof …...[cancer research 45, 945-977, march 1985]...

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