Enhanced susceptibility to chemical induction of ovarian tumors in mice with a germ line p53 mutation

Yian Wang, Zhongqiu Zhang, Yan Lu, Ruisheng Yao, Dongmei Jia, Weidong Wen, Marie LaRegina, Keith Crist, Ronald Lubet, Ming You

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


Mice with a germ line p53 mutation (p53Ala135Val/wt) display increased susceptibility to lung, skin, and colon carcinogenesis. Here, we show that p53Ala135Val/wt mice developed ovarian tumors significantly more rapidly than their wild-type littermates after 7,12-dimethylbenz(a)anthracene (DMBA) treatment. Approximately 50% of the ovarian tumors in p53wt/wt mice and 23% in p53Ala135Val/wt mice are adenocarcinomas and the remaining tumors were adenocarcinoma mixed with sarcoma or ovarian sarcomas. All of the p53Ala135Val/wt mice had died of ovarian tumors 25 weeks after the initial DMBA treatment, whereas >50% of p53wt/wt mice were still alive. These mice not only have a shortened tumor latency but also closely resemble a subset of human ovarian tumors containing the p53 mutation. Microarray and GenMAPP analyses revealed that the mutant p53 (Ala135Val) affected several cellular processes, including the cell cycle, apoptosis, and Wnt pathways. These findings indicate that a germ line p53 mutation significantly enhanced DMBA-induced ovarian tumor development and progression.

Original languageEnglish (US)
Pages (from-to)99-109
Number of pages11
JournalMolecular Cancer Research
Issue number1
StatePublished - Jan 1 2008

ASJC Scopus subject areas

  • Molecular Biology
  • Oncology
  • Cancer Research


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