By Jonathan S. Berek MD MMS, Neville F. Hacker AM MD
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Additional resources for Berek and Hacker's Gynecologic Oncology
35 36 Hereditary Ovarian Cancer It had long been suspected based on epidemiologic and family studies that approximately 10% of epithelial ovarian cancers are attributable to inheritance of mutations in high-penetrance cancer susceptibility genes. The BRCA1 gene was identified on chromosome 17q in 1994, and BRCA2 was identified on chromosome 13q in 1995. Inherited mutations in these two breast and ovarian cancer susceptibility genes are responsible for approximately 6% and 3% of ovarian cancers, respectively (167).
It is conceivable that these chromosomal alterations may be frequent sequelae of infection with oncogenic HPVs while playing no significant role in the pathogenesis of cervical cancers. Abnormalities 44 45 seen in invasive cancers using comparative genomic hybridization also have been identified in high-grade dysplasias, however, suggesting that these are early events in cervical carcinogenesis (307,309,310). Oncogenes and Tumor Suppressor Genes Only a small fraction of HPV-infected women develop cervical cancer.
High-risk HPV types contain E7 oncoproteins that bind Rb with more affinity than E7 from low-risk types. The transforming activity of E7 may be increased by CKII mutation, implying a role for this binding site in the development of HPV-mediated neoplasias. The E6 proteins of oncogenic HPV subtypes bind to and inactivate the TP53 tumor suppressor gene product (302,303). There also is a correlation between oncogenicity of various HPV strains and the ability of their E6 oncoproteins to inactivate p53.
Berek and Hacker's Gynecologic Oncology by Jonathan S. Berek MD MMS, Neville F. Hacker AM MD