Ovarian cancer

Insilico investigation of TNFSF10 signaling cascade in ovarian serous cystadenocarcinoma

Published on: 2nd July, 2019

OCLC Number/Unique Identifier: 8259199051

The ovarian serous Cystadenocarcinoma shared large number of deaths in gynecologic carcinoma. It has various numbers of molecular events from initiation to progression and at advance stage, surgery is the end product of such molecular signaling. We assess in this study the whole mechanistic view of TNFSF10 network which has the ideal apoptotic causing identity. We used fresh insilico strategy to uncover the secrets and inter-links from its protein-protein interaction complex. We retrieved the TNFSF10 signaling network from STRING database (www.string-db.org). The network contains 25 nodes and 152 edges with clustering presentation. After retrieval, we performed gene enrichment and characterization analysis of network from WebGestalt toolkit (www.webgestalt.com). Finally, we examined the participation of whole network in ovarian cancer progression from cBioPortal, a cancer genomic data portal (www.cbioportal.org). Our results showed that majority of cases have loss of function of death receptors (DR4 and DR5) that are the main unit of initiation of apoptotic signaling. Most of downstream signaling members showed amplification that regulates cell proliferative pathways including NFkB pathway. TNFSF10 cluster has loss of function and in future it gain attention for further research studies to discover its interactome level view for valuable therapy. FAS cluster has large number of members and majority showed amplification rendering them as co-targets for combinational drug designing.
Cite this ArticleCrossMarkPublonsHarvard Library HOLLISGrowKudosResearchGateBase SearchOAI PMHAcademic MicrosoftScilitSemantic ScholarUniversite de ParisUW LibrariesSJSU King LibrarySJSU King LibraryNUS LibraryMcGillDET KGL BIBLiOTEKJCU DiscoveryUniversidad De LimaWorldCatVU on WorldCat

And p53 in epithelial immunohisto- chemical expression of Forkhead Box (FOX) A1 ovarian cancer

Published on: 20th May, 2022

Background: Ovarian cancer (OC) is the fifth cause of cancer mortality in females. There were an estimated 300,000 new cases of OC diagnosed worldwide in 2018, corresponding to 3.4% of all cancer cases among women. The high mortality rate of OC attributed to asymptomatic growth of the tumor leads to its diagnosis at advanced stages. About 85% - 90% of OC are epithelial including serous, endometrioid, clear cell, and mucinous carcinoma. Aim: To study the immunohistochemical (IHC) expression of FOXA1 and p53 in epithelial OC and its association with prognostic indicators such as age, tumor size, stage, grade, and histological type.Materials and methods: The study included 52 cases with EOC from the pathology department, faculty of medicine, Aswan, and Sohag Universities, in the period from January 2017 to December 2019. This study involved 52 patients with OC and a median age of 53 years. Different histological types were included as 37 serous, 12 mucinous, 1 case endometroid 2 cases clear cell OC. The study cases were classified into 22 Grade I, 16 Grade II, and 20 Grade III. About 22 cases were at stage I, 9 at stage II, 11 at stage III, and 10 at stage IV. Tissue sections were stained using the IHC technique with FOX A1 at a dilution of 1:100 and p53 at 1:100. Results: A statistically significant correlation was found between FOX A1 expression and advanced patient's age, high grade, advanced stage, ruptured capsule, and ascites, regardless of tumor laterality. No significant association was found between p53 immunoexpression and the same clinic-pathological parameters although p53 was associated with serious type. Conclusion: FOXA1 immunoexpression in EOC is considered a poor prognostic factor in EOC. FOXA1 could be a potential therapeutic target and prognostic marker in EOC.
Cite this ArticleCrossMarkPublonsHarvard Library HOLLISGrowKudosResearchGateBase SearchOAI PMHAcademic MicrosoftScilitSemantic ScholarUniversite de ParisUW LibrariesSJSU King LibrarySJSU King LibraryNUS LibraryMcGillDET KGL BIBLiOTEKJCU DiscoveryUniversidad De LimaWorldCatVU on WorldCat