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cytotoxic attack by purified mouse natural killer cells than those clones lacking these carbohydrates, suggesting that the tumorigenicity of the former clones may be influcnccd by immunoprotective effects of these novel carbohydrates.

Polymorphic N-acetylation capacity in lung cancer. Philip PA, Fitzgerald DL, Cartwright RA, Peake MD, Rogers HJ. Department ofMedical Oncology, Charing Cross Hospital. London W6 8RF. Carcinogenesis 1988;9:491-3.

Hepatic N-acetylation phenotype has been suggested to be an impor- tant risk factor in the aetiology of bladder cancer. This study explores the N-acetylation capacity of a series of lung cancer cases (126) and two control groups. Nooverall association of slow orrapid acetylatorsexists between cancer patients and controls. There is also no difference in the distribution of acctylation phenotypes amongst the histological subtypes.

Clinical prognostic relevance of growth of human adenocarcinomas of the lung in nude mice. Volm M, Mattem J. German Cancer Research Center, lnsriture of Experimental Pathology, D-6900 Heidelberg. Anticancer Res 1987;7:1129-32.

Forty-nine adenocarcinomas of tbe lung were transplanted into nude mice in order to examine whether the growth of these tumors or the establishment of tumor lines might be of clinical prognostic value. Twenty-one of the tumors showed growth (=43%) and 7 (=14%) could be maintaind by serial transplantation. There was no difference in the survival of patients whether their tumors showed growth in the first passage or not. On the other hand, the patients died significantly earlier ifa tumorline byserialtransplantation couldbeestablished(p<0.0001). Tumors which could be established had a higher proliferative activity in the primary tumor and in the xenografted tumor in the first passage. Therefore, the establishment of a tumor line might be an additional prognostic indicator for patients with adenocarcinomas of the lung.

Natural killer activity of lymphocytes infiltrating human lung cancers following preoperative systemic recombinant interleukin 2 Anderson TM, Ibayashi Y, Tokuda Y, Colquhoun S, Holmes C, Golub SH. Division ofdurgical Oncology, UCLA School of Medicine. Los An- geles, CA 90024. Arch Surg 1987; 122: 1446-50.

Tumor-infiltrating lymphocytes (TILs) show depressed natural killer (NK) activity compared with peripheral blood lymphocytes (PBLs). To determineifTILNKfunctioncanbereactivatedinvivo, 11 patientswith tumors metastatic to the lung were treated with systemic recombinant intcrleukin2(rIL-2).SpontaneousTILNKactivityandNKactivityafter three days incubation with 100 U/mL orrIL-2 were increased in patients reccivmg 15,000 U/kg of rIL-2 preoperatively compared with those receiving between loo0 and 10,000 U/kg. Histologically, higher doses of rIL-2 increased the number of intratumoral lymphocytes, the level of peritumoral lymphocytic transferrin, and the expression of HLA-DR. Spontaneous PBL NK activity in patients receiving between 10,ooO and 15,000 U/kg of rIL-2 was also incrcasedand was further increased by in vitro culture with rIL-2. Thus, PBL NK activity and TIL NK function invivocanbcaugmcntedwith l5,0OOU/kgofsystemicrIL-2.BothTIL- and PBL-inducible cytotoxicitics were further enhanced by in vitro

culture with rtL-2.

Alloantibodies, autoantibodies, and immune complexes in patients with lung cancer. Gomy MK, Lawniczak M. Jenek R, Slowik-Gabryelska A, Kaczmarek E, Zeromski J. Department of Clinical Pathomorphology, Academy of Medicine, Poznan. Lung 1988;166:97-105.

The sera of patients with lung cancer, nonmalignant lung disease, and blood donors were subjcctcd to various immunologic assays. Nine

assays, based on immunoradiometric (IRMA) and immunoenzymatic (ELISA) principles, included 3 types of fetal cell antibodies, 2 estab- lishcd lung cancer cell antibodies, anti-DNA, anti-IgG autoantibodies, andimmunecomplexassays basedonclq bindingandanti-C3activity. Antitumor cell antibody level was significantly lower in patients with lung cancer compared to blood donors. In the remaining 7 assays, the lung cancer patients tended towards higher median values compared to both control patients and blood donors, but witbout statistical signifi- cance, with the exception ofanti-DNA antibodies. Statistical analysis of all9assaystaken together hasshown significantdifferencesbetweenthe 3 groups. When only 5 assays were used to assess 3 types of fetal cell antibodies, anti-DNA antibodies, and immune complexes by means of ELISA antiC3, the margins between groups increased. A range of values for theselectedassayswasestablished thatmaydiscriminate701 of tested individuals of the 3 groups. These results suggest the existence of a characteristic profile of deranged humoral immunity in lung cancer patients.

Loss of heterozygosity on chromosomes 3,13, and 17 in small-cell carcinoma and on chromosome 3 in adenocarcinoma of the lung. Yokota J, Wada M, Shimosato Y, Terada M, Sugimura T. National Cancer CenterResearchInstitute. Chuo-ku, Tokyo 104. F’roc Natl Acad Sci USA 1987;84:9252-6.

By a molecular genetic approach using polymorphic DNA markers that detect allelic dcledon of specific chromosomal regions, we ana- lyzed for possible loss of chromosomal heterozygosity in five different histological types of lung cancer obtained from 47 patients. In small-cell carcinomas, the incidence of allclic deletions at tbreedifferentchromo- somal loci was extremely high; loss of heterozygosity was detected on chromosomes 3p in 7 of 7 patients (100%) 13q in 10 of 11 patients (91%). and 17p in 5 of 5 patients (100%). The deletions at these loci in small-ccl1 carcinomas were observed even in the tumors without any clinical evidence of metastasis. Furthermore, loss of heterozygosity on chromosomes 3p and 13q occurred prior to NMYC amplification and chromosome 1 lp deletion. Loss of heterozygosity on chromosome 3p was also detected with high frequency in adenocarcinomas [5 of 6 patients (83%)]. Hetcrozygositj of chromosomes 13q and 17p was lost in 10 of 3 1 patients (32%) and in 3 of 12 patients (25%). respectively, of lung cancers other than small-cell carcmomas. These results indicate that recessive gcnctic changes involving sequences on chromosomes 3, 13q. and l7p may play important roles in the genesis of small-cell carcinoma, and those on chromosomes 3p may play an important role in the genesis of adenocarcinoma.

The cytotoxic activity of cisplatin, carboplatin and teniposide alone and corn bined determined on four human small cell lung cancer cell lines by the clonogenic assay. Roed H, Vindelov LL, Christensen IJ, Spang-Thomsen M, Hansen HH. DepartmentofOncologyB.Finsenlnstitute,DK-2l~Copen~gen.E~ J Cancer Clin Oncol 1988;24:247-53.

Using the clonogenic assay to compare the cytotoxic activity of cisplatin andcarboplatinon four human smallcell lungcancercell lines, cisplatin was shown to be equally or more potent than carboplatin at equitoxic doses with 1 h incubation. Increased potency of carboplatin was revealed when the drugs were tested with continuous incubation, although cisplatin still was the most potent drug when compared on a microgram to microgram basis. This relative increase in potency of carboplatin can at least partly be cxplaincd by thedevelopmentofa more reactive form of the drug when stored in tissue culture medium. By combining either cisplatin or carboplatin with teniposide additive cell kill was obtained. Additivity was also obtained when cisplatin was combined with carboplatin. Since the two drugs haveadifferent toxicity pattern a clinical synergy may be obtained by combined use of these two analogucs.