Abstract
Ovarian carcinoma (OC) is the most lethal gynecological malignancy. Response to platinum-based chemotherapy is poor in some patients and, thus, current research is focusing on new therapy options. The various histological types of OC are characterized by distinctive molecular genetic alterations that are relevant for ovarian tumorigenesis. The understanding of these molecular pathways is essential for the development of novel therapeutic strategies.PurposeWe want to give an overview on the molecular genetic changes of the histopathological types of OC and their role as putative therapeutic targets.In Depth Review of Existing DataIn 2012, the vascular endothelial growth factor (VEGF) inhibitor, bevacizumab, was approved for OC treatment. Bevacizumab has shown promising results as single agent and in combination with conventional chemotherapy, but its target is not distinctive when analyzed before treatment. At present, mammalian target of rapamycin (mTOR) inhibitors, poly-ADP-ribose polymerase (PARP) inhibitors and components of the EGFR pathway are in the focus of clinical research. Interestingly, some phytochemical substances show good synergistic effects when used in combination with chemotherapy.ConclusionOngoing studies of targeted agents in conjunction with chemotherapy will show whether there are alternative options to bevacizumab available for OC patients. Novel targets which can be assessed before therapy to predict efficacy are needed. The assessment of therapeutic targets is continuously improved by molecular pathological analyses on tumor tissue. A careful selection of patients for personalized treatment will help to reduce putative side effects and toxicity.
Highlights
Ovarian carcinoma (OC) is the most lethal gynecological malignancy
follicle stimulating hormone (FSH) and luteinizing hormone (LH) receptors are often expressed on ovarian carcinoma cells, and may contribute to signaling transduction by mitogen-activated protein kinases (MAPKs) [34,35]
It has been demonstrated that the diagnostic value to predict malignancy is higher when a combination of biomarkers, as e.g., Human Epididymal Protein 4 (HE4), CA-125 and carcino-embryonic antigen (CEA) are determined
Summary
Ovarian carcinoma (OC) has been considered as one single disease. ovarian carcinoma comprises a variety of tumors with various histopathological features and expresses different biological behavior. Epithelial ovarian tumors represent the largest group and are basically subdivided into serous, mucinous, endometrioid, clear cell and transitional cell tumors; the latter including Brenner tumors [3]. Among these groups of tumors, three categories are distinguished according to the biological behavior: benign, borderline and malignant. Endometrioid and clear cell carcinomas are frequently associated with endometriosis, which is generally considered a risk factor of ovarian carcinoma. Immunoreactivity for ER and PR is typical for endometrioid and serous carcinomas and less intense or absent in clear cell and mucinous carcinomas. Clear cell carcinoma is characterized by a frequent expression of hepatocyte nuclear factor 1 (HNF1) which is not found in the other histological subtypes
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