Radon progeny exposure and lung cancer risk in New Mexico c’ miners: A case-control study Samei JM, Pathak DR. Morgan MV, Marbury MC, Key CR, Valdivia AA.DepartmentofMedicine.CancerCenter. UniversltyofNewMexlco Medica/ C‘rwrrr. Albuquerque, NM 87131. Health Phys 1989;56:415- ?I.

A case-control study was conducted to describe lung cancer risk in a cohort of New Mexico underground U miners. The subjects Included 65 cases and 230 age-matched controls, mos1 with exposures below 3.50 J h m 3 (IO(x) WLM). The risk for lung cancer was Increased for all cumulauvc exposures to Rn Progeny of 0.35 J h m ’ (100 WLM) or greater. The odds ratios wcrc unchanged with control for cigarette smokmg. Wnh exclusion of subjects with exposures above 3.50 J h m ’ ( IO(X) WLM), the estimated ~YCCSS relative risk was 0.3% per mJ h m ’ (I. I % per WLM). The risk was grcatcr for younger \ubJccts and the

data were consistent with a multiplicative interaction bctwccn cigarellc smoking and exposure to Rn progeny.

Radon and lung cancer Sam~l JM. liruversily of New Mex~o, New Mexico 7’umor Registry, Alhuyuerqw, NM87131 J Nat1 Cancer Ins1 1989:X1:745-57.

Radon, an inert gas released during the decay of uramum-238, IS ubiquitous m indoor and outdoor air and contamina1es many undcr- groundmmcs.Exlcnsiveepidemiologicevidencefrom studresofunder- ground miners and complementary animal data have documented that radon causes lung cancer in smokers and nonsmokers. Radon must also he considered a potentially important cause of lung cancer for the general population, which is cxposcd through contammation of indoor air by radon from soil, water, and budding materials. This review dcscrihes radon’s sources, levels m U.S. homes, dosimetry, the epidc- miologic evidence from studies of miners and the general populalion. and the prmcipal, rcccnt risk assessments.

Basic biology

Differential expression ofthe c-erbR-2 gene in human small cell and non-small cell lung cancer Schneider PM, Hung M-C, Chmcca SM c1 al. Deparrnznl ofThoracic Surgery, Unwerstty ofTexas. M.D. Anderson Cancer Center, llouston. TX 77030. Cancer Res 1989;49:4968-71.

WC studied non-small cell lung cancers (NSCLC) from 60 palicnls for abnormalities in the c-erbB-2 gene. Eleven human lung cancer cell lines. Including four derived from small cell lung cancer (SCLC) and scvcn derived from NSCLC wcrc also cxamincd for altcred c-erbB-2 gcnc expression. Southern blot analysis of paired tumor and normal lung samples demonstrated that amplificauon of the c-erbB-2 gene is rare In NSCLC (2/6l)) and not rccuictcd to adcnocarcmomas. One patient showed an EcoRl rcstricuon fragment length polymorphism for the c-crbB-2 locus, Four of four SCLC cell lmes demonstrated mimmal or nondctcctahle expression of c-erbB-2 mRNA compared to high Irvcls of cxprcssion by icvcn of seven NSCLC Imcs. The highest cxprc\sion lcvcls wcrc seen in four of four adcnocarcmomas. We conclude that c-erbB-2 expression IS diffcrcnt in SCLC compared 10 NSU C and high cxpresslon ol L-crbB-2 IS consistently prcscnl In lung adcnocarcinomas.

Antiproliferative and differentiative effect of granulocytc-macro- phage colony-stimulating factor on a variant human small cell lung cancer cell line Yamashila Y, Nara N, Aoki N. I;irs~ Department of Internal Medirinr. 70!~0 Medical and Dental Cinrvers~ty. Bunkw-ku. I’okw 113. Cancer Re\ iY)x9:-195334-X.

A variant clone was adopted durmg passages oi a small cell lung cancer cell line, GKTB- I .3. The variant clone cxhibitcd distinct charac- teristics with alterations m morphology, pos~tlve stammg with non- specific esterase stain, and an incrcasc m surface specific markers 0KM5, HLA-DR. Mol, and My7, usually found on monocytesor their precursors. However, it cxcrtcd a very raprd proliferation just like immature cells. This new clone, GKT3l.iV, was shown to have specific bindmg capacity togranulocyt~~macrophagz colony-stimulat- mg factor (GM-CSF), wnh a number of hmdmg sib.“; comparable 10 that of myelomonocylcs or monocytic cell Ime\. Thuh it\ prollferaiioll was mhibitcd by GM-CSF in clonogenic assay and suspension culture. Increase m the pcrccntagc of cells with surlacc marker Mol hy the addition of GM-CSF suggcstcd its diffcrentiaiivc cffcfcci. Cell cycle analysis showed that the antiproliferatrvc effect ol GMCSF was due to a block in G, or Cl,. The antiprohfcrative effect (Ii GM-CSF was abolished by the addition of anti-GM-(‘SF antibody.

Concordant deletions of chromosome 3p and loss of heterozygosity for chromosomes 13 and 17 in small cell lung carcinoma Mori N, Yokota I, Oshimura M et al. Natmnal Cancer Center Research Instrtute, Chum-ku. Tokyc~ 104. Cancer Rca 1989:49:S130-5.

Common regions ol~loss of hetcroyygosny on chromosomes 3, 13, and I7 were determined by restriction fragment length polymorphism analysrs m 34 tumors and ninecell lines from 27 pa1ients with small cell lung carcinoma. The common regions of loss of hctero/ygosity on chromosomes 3, 13, and I7 reside hctween DIS2 (3p14-~21) and ERBALI (3~22.p24.1), between D13SI (13q12) and Dl3S2 (1 iq22). anddistal to MYH2 (17pl3.1). rcspectivcly. Allclc loss mcachol these regions has been prcvrously shown in hcveral human tumors. Thus, the present findings indicate the pleiotropy of rcccssrvc genetic lesions in 1hesc genomic areas. Cytogenctic analysis was performed on three small cell lung carcinoma cell lines which hdd allclc lo\s on all three chromosomes, and although chromosome 3p dclctrorrs were observed m two of three cell lines. no obvious structural abnormalities mvolvmg chromosomes 13 and 17 wcrc detected. Mitoric rzcombmauon or mnolrc nondisJunction rather than deletion may thus be 1he frequent chromosomal mechamsm lorattaming homo/yposity 01 Lhromosomes 13 and 17 in small cell lung carcinoma.

Immunological and pharmacological removal of small cell lung cancer cells from bone marrow autografts Humblct Y, Feyens A-M, Sckhavat M, .4gahous D, Canon J-L, Symann ML. Experunental Oncology and Hemutology Lalor~ltory, St. Luc University Ifospital, Catholic (Jniversrtv cfl.ouvaw. B-1-300 Brursels. Cancer Res 1989;49:5058-61.

Autologous bone marrow transplantation is u\ed m \mall cell lung cancer (SCLC) to reverse the hcmatological toxicny induced by high dose therapy even though the prcscncs ofcanccrous .cllc m the graft 1s potentially dangerous by remfusion of the dr,ica\i% along with the hematoporctrc stem cells. The prcscn1 studic\ wcrc undertaken lo cxaminc the ef~fcctivcncss of anti-SC’LC’ rat monoilonal anubodics LCAI and LCh6 plus human complement combmcd with a derivative of cyclophosphamidc (As&Z 7557) lor 1hc clm~mation of cancerous clonogemc cells from the graft. In a scrics of assays Lonductcd with three SCLC cell lines, used alone or mixed with normal bone marrow cells, the addition of As&-Z 7557 to two cycles ol treatment with monoclonal antibodies plus complcmcnt rc\ults in a 4- top 5-loganth- mic reductron of the clonogemc SCLC cell\ dctcLtahle by limump dilution analysis. This w’as superior 10 clthcr trcatmcnt used alone. When normal bone marrow was suhmutrd to 1111‘ ~.anic trcatmcnt, a median (range) of34% (15.77%) ol 1hc colony-lorming unit, granulo- cytc-macrophagc was rccovcrcd. Thc\c rc\uI~s \uggc\l that the a\wla- bon of immunological (LCAI and L.Chh pIti\ human complcmcnt) and pharmacological (AstaZ 7557) removal mcthocl~ I\ clflxilvc furpurg- mg mctastatlc clonogcmc cell> from bone matx~ trf!it‘l.C’ paticnls and

could hc considered hcforc autologou~ hone marro\k u~muplantatron.