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Inactivation of p16/CDKN2 and p15/MTS2 is associated with prognosis and response to chemotherapy in ovarian cancer

✍ Scribed by Kazuya Kudoh; Yoshihito Ichikawa; Sadao Yoshida; Misako Hirai; Yoshihiro Kikuchi; Ichiro Nagata; Masanao Miwa; Kazuhiko Uchida

Publisher
John Wiley and Sons
Year
2002
Tongue
French
Weight
130 KB
Volume
99
Category
Article
ISSN
0020-7136

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✦ Synopsis

Abstract

To define the involvement of p16/CDKN2 and p15/MTS2 tumor‐suppressor genes for response to chemotherapy in primary epithelial ovarian cancer, we analyzed alterations of the gene in 45 patients who were treated with primary cytoreductive surgery followed by 6 courses of cis‐diamminedichloroplatinum (II) (cisplatin)‐based combination chemotherapy. Homozygous deletion of p16/CDKN2 and p15/MTS2 genes was found in 8 (18%) and 15 (33%) cases, respectively. Response to the chemotherapy was confirmed by finding at second surgery after the chemotherapy in 26 patients, resulting in 17 responders and 9 nonresponders. The abundance of gene deletion in nonresponders (56%) was significantly higher (p = 0.0463) when compared to that in responders (18%). Moreover, the deletion of genes was a significant poor prognostic factor (p = 0.0441) in advanced ovarian cancer. These results suggest that deletion of p16/CDKN2 and/or p15/MTS2 is a potential indicator for poor chemotherapy response and adverse prognosis in ovarian cancer patients. © 2002 Wiley‐Liss, Inc.

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