Oncogenes in high grade serous adenocarcinoma of the ovary

Abstract

High grade serous ovarian cancer is characterized by relatively few mutations occurring at low frequency, except in TP53. However other genetic aberrations such as copy number variation alter numerous oncogenes and tumor suppressor genes. Oncogenes are positive regulators of tumorigenesis and play a critical role in cancer cell growth, proliferation, and survival. Accumulating evidence suggests that they are crucial for the development and the progression of high grade serous ovarian carcinoma (HGSOC). Though many oncogenes have been identified, no successful inhibitors targeting these molecules and their associated pathways are available. This review discusses oncogenes that have been identified recently in HGSOC using different screening strategies. All the genes discussed in this review have been functionally characterized both in vitro and in vivo and some of them are able to transform immortalized ovarian surface epithelial and fallopian tube cells upon overexpression. However, it is necessary to delineate the molecular pathways affected by these oncogenes for the development of therapeutic strategies.

Integrating single-cell RNA sequencing and prognostic model revealed the carcinogenicity and clinical significance of FAM83D in ovarian cancer

“…Two groups of epithelial cells accounted for about 80% of the total cells, which supports that OC mostly originates from the epithelium ( 23 ). Through trajectory analysis and CNV analysis ( 24 ), we found that malignant epithelial cells (C1) highly expressed the malignant marker PAX8 and genes related to DNA replication pathways and WNT, KRAS, and other carcinogenic pathways. It has been proven that dysregulated ribosomal organisms occur in the progress of most spontaneous cancers ( 25 ).…”