<b>Conclusions:</b><i>TBC1D8</i> drives OVCA tumorigenesis and metabolic reprogramming, and TBC1D8 serves as an independent prognosis factor for OVCA patients.
<b>Materials and Methods:</b> We collected EOC samples from 204 patients and examined tumor SIK3 expression by immunohistochemistry (IHC) and CA125 expression in tumors and serum.
<b>Methods:</b> 255 <i>BRCA1/2</i>-negative Chinese familial breast and/or ovarian cancer (FBOC) patients were recruited for <i>FANCC</i> germline mutations screen.
<b>Methods:</b> Patients with Breast Cancer (BC) and/or Ovarian Cancer (OC) fulfilling established criteria were offered genetic counseling and BRCA1/2 testing; VUSs identified in index cases were checked in other relatives affected by BC/OC whenever possible.
<b>Objective</b> To detect the expression of microRNA-338-3p (miR-338-3p) and MET transcriptional regulator MACC1 (MACC1) gene in different ovarian tissues, to analyze their relationships, their correlations to the clinicopathologic characteristics of epithelial ovarian cancer and their significant to the progression of ovarian cancer.
<b>Objective</b> To detect the expression of microRNA-338-3p (miR-338-3p) and MET transcriptional regulator MACC1 (MACC1) gene in different ovarian tissues, to analyze their relationships, their correlations to the clinicopathologic characteristics of epithelial ovarian cancer and their significant to the progression of ovarian cancer.
<b>Objective:</b> We carried out a meta-analysis of case-control studies to determine whether epoxide hydrolase 1 (<i>EPHX1</i>) gene polymorphism rs1051740 was related to the risk of ovarian cancer.
<b>Purpose:</b> Acquired resistance to cisplatin is a major barrier to success in treatment of various cancers, and understanding mitotic mechanisms unique to cisplatin-resistant cancer cells can provide the basis for developing novel mitotic targeted therapies aimed at eradicating these cells.<b>Experimental Design:</b> Using cisplatin-resistant models derived from primary patient epithelial ovarian cancer (EOC) cells, we have explored the status of mitotic exit mechanisms in cisplatin-resistant cells.<b>Results:</b> We have uncovered an unexpected role of long-term cisplatin treatment in inducing mitotic exit vulnerability characterized by increased spindle checkpoint activity and functional dependency on Polo-like kinase 1 (PLK1) for mitotic exit in the presence of anaphase promoting complex/cyclosome (APC/C) dysfunction in a cisplatin-resistant state.
<i>KRAS</i> mutations and the protein expression of EGFR and PKC-alpha should be evaluated as predictive biomarkers in patients with LGSC treated with MEKi.
<i>SUSD2</i>, a secreted tumor suppressor downregulated by promoter CpG island methylation in adipocytes, was upregulated after guadecitabine treatment, and recombinant SUSD2 decreased OC cell migration and invasion.
<i>TP53</i>WT endometrioid OC highly expressed CXCL14 compared to <i>TP53</i>m, showing better progression-free survival but no difference in overall survival (OS).
(3) Univariate and multivariate analyses showed that tumor size, tumor grade, tumor stage, plasma fibrinogen, serum albumin, FA score and tumor marker CA125 were statistically correlated with OS of EOC patients after surgery (<i>P</i><0.05).
1) Coding DNA instability is likely to be a very rare event in OC and, therefore, may not significantly contribute to the development of OC, and 2) the high frequency of LOH at hMLH1 observed in our ovarian tumors suggests that further investigation is needed to determine if such a trend exists in other mismatch DNA repair and/or critical genes.
17 beta Hydroxysteroid dehydrogenase 1 "pseudogene" is differentially transcribed: still a candidate for the breast-ovarian cancer susceptibility gene (BRCA1).