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National Cancer Center Research Institute, 1-1, Tsukiji 5-chome, Chuo-ku, Tokyo 104 [N. M., J. Y., M.N., Y. S., T.S., M. T.]; Department of Medicine, Tokyo Women's Medical College, 1 1, Kavada-cho 8-chome, Shinjuku-ku, Tokyo 162 [N. M., H. M.j; Kanagawa Cancer Center, Clinical Research Institute, Nakao-cho 54-2, Asahiku, Yokohama 241 [M. O.], Japan; and Ludwig Institute for Cancer Research, Royal Victoria Hospital and McGill University Faculty of Medicine, Montreal H3A 1A1 [W. K. C.]. Canada
Common regions of loss of heterozygosity on chromosomes 3, 13, and 17 were determined by restriction fragment length polymorphism analysis in 34 tumors and nine cell lines from 27 patients with small cell lung carcinoma. The common regions of loss of heterozygosity on chromosomes 3, 13, and 17 reside between D3S2 (3p14p21) and EKBAß (3p22p24.1), between D13S1 (13q12)and D13S2 (13q22), and distal to MYH2 (17p13.1), respectively. Allele loss in each of these regions has been previously shown in several human tumors. Thus, the present findings indicate the pleiotropy of recessive genetic lesions in these genomic areas. Cytogenetic analysis was performed on three small cell lung carcinoma cell lines which had allele loss on all three chromosomes, and although chromosome 3p deletions were observed in two of three cell lines, no obvious structural abnormalities involving chromosomes 13 and 17 were detected. Mitotic recombination or mitotic nondisjunction rather than deletion may thus be the frequent chromosomal mechanism for attaining homozygosity of chromosomes 13 and 17 in small cell lung carcinoma.
1 This work was supported in part by a Grant-in-Aid for a Comprehensive 10-Year Strategy for Cancer Control from the Ministry of Health and Welfare of Japan, and Grants-in-Aid from the Ministry of Health and Welfare and from the Ministry of Education, Science, and Culture of Japan.
2 Recipient of a Research Resident Fellowship from the Foundation for Promotion of Cancer Research. To whom requests for reprints should be addressed, at Genetics Division, National Cancer Center Research Institute, 1-1 Tsukiji 5-chome, Chuo-ku, Tokyo 104, Japan.
Received 3/27/89. Accepted 6/19/89.
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