Biomakers in the ovary

Authors

  • Andrew Brechuck MD

    Corresponding author
    1. Division of Gynecologic Oncology, Duke University Medical Centre Durham, NC 27710
    • Division of Gynecologic Oncology, Duke University Medical Center, Box 3079, Durham, NC 27710
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Abstract

Alterations in specific oncogenes and tumor suppressor genes that serve as surrogate makers of malignant transformation have been identified in ovarian cancers. Overexpression of the HER-2/neuoncogene occurs in approximately 30% of breast and ovarian cancers. In most studies, HER-2/neu overexpression has correlated with poor survival. Although mutation of the K-ras oncogene has been found in some mucinous ovarian cancers, mutations in this gene appear to be more common in borderline ovarian tumors. Amplification of c-myc occurs in approximately 30% of ovarian cancers and is more frequently seen in serous cancers. Mutation of the p53 tumor suppressor gene, with resultant over experssion of mutant p53 protein, occurs in 50% of stage III/IV and 15% of Stage I/II ovarian cancers. Most p53 mutations in ovarian cancers are transitations, which suggest that they arise spontaneously rather than due to exogenous carcinogens. In contrast to the acquired genetic alterations described above that are a feature of sporadic ovarian cancers, a small fraction of epithelial ovarian cancers arise due to inherited genetic defects. Recently, the BRCAI tumor suppressor gene on chromosome 17q was identified and shown to be responsible for some cases of hereditary breast and ovarian cancer. Families in which mutations in this gene exist are usually characterized by early age of diease on set. Presently, it remains unclear what fraction of herediatry ovarian cancers are due to BRCAI mutations.

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