Aging and disease

Shedding Light on the Interaction Between Rif1 and Telomeres in Ovarian Cancer

Ovarian cancer, more precisely high-grade serous ovarian cancer, is one of the most lethal age-independent gynecologic malignancies in women worldwide, regardless of age. There is mounting evidence that there is a link between telomeres and the RIF1 protein and the proliferation of cancer cells. Telomeres are hexameric (TTAGGG) tandem repeats at the tip of chromosomes that shorten as somatic cells divide, limiting cell proliferation and serving as an important barrier in preventing cancer. RIF1 (Replication Time Regulation Factor 1) plays, among other factors, an important role in the regulation of telomere length. Interestingly, RIF1 appears to influence the DNA double-strand break (DSB) repair pathway. However, detailed knowledge regarding the interplay between RIF1 and telomeres and their degree of engagement in epithelial ovarian cancer (EOC) is still elusive, despite the fact that such knowledge could be of relevance in clinical practice to find novel biomarkers. In this review, we provide an update of recent literature to elucidate the relation between telomere biology and the RIF1 protein during the development of ovarian cancer in women.

ARID1a Gene as a Potential Early Marker to Tackle Endometriosis-Associated Ovarian Cancer

The worries of women with endometriosis - a chronic gynecological disease affecting approximately 10% of women of childbearing age - about the increased risk of ovarian cancer are present worldwide. Endometriosis is a common, often painful, but benign gynecological disease that affects women. However, the pathogenesis remains elusive but is certainly multifactorial. Interestingly, endometriosis shares similarities with cancer. Therefore, women suffering from endometriosis fear an increased risk of ovarian cancer. In addition, these patients suffer from anxiety and depression. Previous studies have provided evidence that epithelial mutations in endometriosis or in the endometrium include certain inactivating mutations responsible for ovarian cancer, such as in the ARID1A gene.