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Laboratories of Chemotherapy [O. W., H. O., R. U., Ta. T.], and Immunology [M. N., To. T.], Aichi Cancer Center Research Institute, Chikusa-ku, Nagoya 464; Departments of Pathology and Clinical Laboratories [T. K.], Aichi Cancer Center Hospital, Chikusa-ku, Nagoya 464; and Department of Orthopedic Surgery, Fujita Health University Second (Ban Buntane Houtokukai) Hospital, Otobashi, Nakagawa-ku, Nagoya 454 [O. W., T. S.], Japan
Frequent homozygous deletions of the p16 (MTS1) gene encoding a cyclin-dependent kinase inhibitor were recently reported in various tumor cell lines including examples derived from lung cancers, but direct evidence for their occurrence in lung cancer patients has not been reported thus far. In the present study, alterations of p16 and/or p15, a p16-related cyclin-dependent kinase, were observed not only in lung cancer cell lines but also in the corresponding tumor specimens in vivo, excluding the possibility of in vitro artifacts. Interestingly, a clear specificity was also noted in terms of the affected histological subtype; i.e., only non-small cell lung cancers carried alterations (6 of 20 as compared to 0 of 20 small cell lung cancer cell lines).
1 This work was supported in part by a Grant-in-Aid for the Second Term Comprehensive Ten-Year Strategy for Cancer Control from the Ministry of Health and Welfare, Japan; and by Grants-in-Aid for Cancer Research from the Ministry of Education, Science, and Culture and the Ministry of Health and Welfare, Japan.
2 To whom requests for reprints should be addressed.
Received 11/30/94. Accepted 12/19/94.
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