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First Department of Internal Medicine, Nagoya University School of Medicine [Y. S., K. S.], Showa-ku, Nagoya 466, and Laboratories of Immunology [Y. O., T. T.] and Chemotherapy [R. U.], and Department of Cardiopulmonary Diseases [T. H., Y. A.] and Thoracic Surgery [M. S.], Aichi Cancer Center, Chikusa-ku, Nagoya 464, Japan
As an initial step to understand rapid growth of small cell lung cancer (SCLC), a complementary DNA library prepared from a SCLC cell line was screened with viral oncogene probes encoding protein-tyrosine kinases, which are known to play an important role in regulation of cell growth. Fifteen clones hybridizing with v-fms probe were isolated, and, by partial sequence analysis, four of them were identified to be c-kit protooncogenes. Northern blot study demonstrated that most of the SCLC tumors and cell lines expressed c-kit transcripts, while non-SCLC tumors and cell lines did not. Neither amplification nor rearrangement of the c-kit gene was demonstrated in SCLC cell lines by Southern blot analysis, however. Our results suggested that c-kit expression in SCLC reflects the unique biological nature of the tumor cells different from non-SCLC and further suggested that the c-kit product may participate in autocrine or paracrine stimulation of SCLC growth.
1 This work was supported in part by a Grant-in-Aid for the Comprehensive Ten-Year Strategy for Cancer Control from the Ministry of Health and Welfare; by Grant-in-Aids for Cancer Research from the Ministries of Education, Science, and Culture and of Health and Welfare in Japan; and by a grant from the Cancer Research Institute, Inc., New York, NY.
2 To whom requests for reprints should be addressed.
Received 10/ 4/90. Accepted 2/19/91.
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