v-Raf murine sarcoma viral oncogene mutation status in serous borderline ovarian tumors and the effect on clinical behavior.

Aims: To determine the incidence of activating v-raf murine sarcoma viral oncogene (BRAF) mutations in 30 serous borderline tumors (SBTs) of the ovary and the accompanying implants and to link BRAF mutation status to the clinical behavior of these tumors.

Methods And Results: Serous borderline tumors and noninvasive implants of 30 patients were analyzed for the presence of the BRAF V599E mutation, and mutation status was correlated to 70 months of clinical follow-up. Mutation status could be assessed in 27 SBTs.

Differential gene expression in ovarian tumors reveals Dusp 4 and Serpina 5 as key regulators for benign behavior of serous borderline tumors.

Purpose: Ovarian serous borderline tumors (SBT) are characterized by arborizing papillae lined by stratified epithelial cells, varying atypia, and absence of stromal invasion. Originally, these tumors have been classified as borderline because they behaved in a remarkably indolent manner, even with widespread tumor deposits called implants and the presence of lymph node involvement. The molecular biology of these lesions has just begun to be explored.

In ovarian neoplasms, BRAF, but not KRAS, mutations are restricted to low-grade serous tumours.

Genes of the RAF family, which mediate cellular responses to growth signals, encode kinases that are regulated by RAS and participate in the RAS/RAF/MEK/ERK/MAP-kinase pathway. Activating mutations in BRAF have recently been identified in melanomas, colorectal cancers, and thyroid and ovarian tumours. In the present study, an extensive characterization of BRAF and KRAS mutations has been performed in 264 epithelial and non-epithelial ovarian neoplasms.

Molecular genetic evidence for monoclonal origin of bilateral ovarian serous borderline tumors.

Patients with serous borderline tumors of the ovary often present with multiple tumors at different sites in the abdominal cavity. Whether different foci of ovarian serous borderline tumors are monoclonal in origin, arising as a consequence of spread from a single ovarian site, or whether such deposits are polyclonal and explained by independent molecular genetic alterations on the background of a field defect, is unknown. So far, only X-chromosome inactivation studies were performed to study this issue.