Molecular pathogenesis of borderline and invasive ovarian tumors

J BUON. 2009 Jan-Mar;14(1):7-18.


Ovarian cancer still ranks first as the leading cause of death among gynecological malignancies. Malignant transformation of normal ovarian epithelial cells is caused by genetic alterations that disrupt regulation of proliferation, programmed cell death, and senescence. The vast majority of ovarian tumors arise due to accumulation of genetic damage, but the specific genetic pathways for the development of epithelial ovarian tumors, borderline and malignant, are largely unknown. Our results show that in progressive stages of carcinoma, the oxidative stress can contribute to the uncontrolled tumor expansion. Circulating levels of antioxidants may be important to consider when evaluating a woman's risk of cancer, even among women who are at higher predicted risk. The purpose of this article was to review the current approaches to molecular pathogenesis of borderline and invasive epithelial ovarian tumors.

Publication types

  • Review

MeSH terms

  • Biomarkers, Tumor / genetics*
  • Biomarkers, Tumor / metabolism
  • Cell Transformation, Neoplastic / genetics
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Genetic Predisposition to Disease
  • Humans
  • Loss of Heterozygosity
  • Neoplasm Invasiveness
  • Ovarian Neoplasms / genetics*
  • Ovarian Neoplasms / metabolism
  • Ovarian Neoplasms / pathology
  • Oxidative Stress / genetics
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins p21(ras)
  • Risk Factors
  • Signal Transduction / genetics
  • Tumor Suppressor Protein p53 / genetics
  • ras Proteins / genetics


  • Biomarkers, Tumor
  • KRAS protein, human
  • Proto-Oncogene Proteins
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • Proto-Oncogene Proteins p21(ras)
  • ras Proteins