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Allelotype of Human Ovarian Cancer¹

Departments of Biochemistry [T. S., H. S., R. M., Y. N.] and Gynecology [S. K.], Cancer Institute, Tokyo, 1-37-1, Kami-Ikebukuro, Toshima-ku, Tokyo 170, Japan, and Department of Biochemistry, Korea Cancer Institute Hospital [J-H. L.], Seoul, Korea

In order to determine which chromosome(s) carries a tumor suppressor gene(s) for human ovarian cancer, we examined loss of heterozygosity in 37 tumors with a set of polymorphic DNA markers which cover each autosomal chromosome arm partially.

Frequent losses were observed in chromosomes 4p (42%), 6p (50%), 7p (43%), 8q (31%), 12p (38%), 12q (33%), 16p (33%), 16q (38%), 17p (46%), 17q (39%), and 19p (34%). In addition to these chromosomes, frequent losses of alleles on chromosomes 6q, 13q, and 19q were observed uniquely in serous and serous papillary cystadenocarcinomas; loss of heterozygosity was detected only rarely on these chromosomal arms in nonserous types of tumors. The average (0.12) of fractional allelic loss seen in mucinous cystadenocarcinoma, which usually has a better prognosis than other types, was much lower than that of other tumor phenotypes including serous cystadenocarcinoma (0.31) and clear cell carcinoma (0.20).

These results suggested that (a) a large number of tumor suppressor genes might play a role in ovarian cancer, (b) losses of alleles in different chromosomal regions could account for differences in histopathological features and/or prognoses among patients, and (c) this kind of analysis can contribute to an improved understanding of tumor development and/or progression in human ovarian cancer.

¹ The work was partly supported by a Grant-in-Aid for Cancer Research from the Ministry of Education, Science and Culture of Japan, and the Ministry of Science and Technology of Korea.

² To whom requests for reprints should be addressed, at Department of Biochemistry, Cancer Institute, Tokyo, 1-37-1, Kami-Ikebukuro, Toshima-ku, Tokyo 170, Japan.

Received 4/15/91. Accepted 7/15/91.

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