Abstract
Epigenetic aberrations are now well established in the development and progression of ovarian cancer, including DNA methylation, histone modifications, and microRNA dysregulation, and their progressive accumulation is correlated with the progression of the stage grade of disease. Epigenetic aberrations are relatively stable, linked to various subtypes of the disease, and present in circulating serum, representing promising diagnostic, prognostic, and pharmacodynamic biomarkers. Unlike DNA mutations and deletions, aberrant gene-repressive epigenetic changes, including DNA methylation inhibitors or histone-modifying enzymes, are theoretically reversible by epigenetic therapies. While no action against solid tumors, including ovarian cancer, has been shown in epigenetic monotherapies, preclinical studies indicate that they may be successful when used in conjunction with one another or with conventional chemotherapy, and combinatorial epigenetic therapy regiments are being investigated in cancer clinical trials. Improved interventions against this debilitating malignancy will provide a greater understanding of epigenetics’ role in ovarian cancer.
Highlights
IntroductionOvarian cancer, a molecularly heterogeneous condition associated with poorest prognosis
Among gynecological malignancies, ovarian cancer, a molecularly heterogeneous condition associated with poorest prognosis
The complete epigenetic state corresponding to a particular cell phenotype (e.g., DNA methylation, histone modification, and miRNA expression) is referred to as the epigenome [8]
Summary
Ovarian cancer, a molecularly heterogeneous condition associated with poorest prognosis. The highest mortality rates are associated with ovarian cancer, reflecting the third most prevalent cancer in female carcinomas of the gynecologic system. An ovarian cancer diagnosis at the localized level is considerable curable (over 95 percent five-year survival rate; [5]). The complete epigenetic state corresponding to a particular cell phenotype (e.g., DNA methylation, histone modification, and miRNA expression) is referred to as the epigenome [8]. Though repressive epigenetic changes (including DNA methylation) control genes in normal tissues (e.g., imprinted genes and inactivation of female X-chromosomes), they are dramatically altered in cancer [6, 9]. Global DNA hypomethylation and localized hypermethylation of promoter-associated CpG islands occur primarily in cancer cells, with the latter acting as a replacement for point mutations or deletions to induce transcriptional silencing of tumor suppressor genes [6]
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