الفهرس 
Title : Immunohistochemical Application and Exploration of the Role of MMR genes, BRAF mutation and Beta-Catenin in colorectal carcinoma
AbstractOnly 14 pages are availabe for public view
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Abstract
Background: The tumorigenesis of colorectal carcinoma is a multistep process. It arises from accumulation of genetic alteration that transforms normal glandular epithelium to invasive adenocarcinoma (Worthley et al., 2007). Defect in DNA mismatch repair genes (dMMR) as well as BRAF mutation are forms of genomic instability that involved in CRC development. Although genetic testing remains the gold standard for the detection of MSI, the College of American Pathologists (CAP) recommends an initial immunohistochemical workup with a four-antibody panel (MLH1, PMS2, MSH2, and MSH6) to screen for a defective mismatch repair system (Hashmi et al., 2017). Also Immunohistochemistry has recently been validated for the detection of BRAFV600E mutation (Toon et al., 2014). Beta-Catenin is another factor that plays a key role in CRC tumorigenesis. However, its prognostic significance remains controversial. We conduct this study to examine the expression of MMR proteins, BRAF and Beta-Catenin in colorectal cancer and look for association with other clinico-pathological parameters and survival. Material and methods: It is a retrospective study that carried out on 83 cases, pathologically diagnosed as colorectal carcinoma, presented to the National Cancer Institute, Cairo University during the period from 2008-2013 by performing MMR proteins, BRAF and Beta-Catenin immunohistochemistry. Correlation with clinico-pathologic characteristics as well as overall survival (OS) and progression free survival (PFS) was done. Results: dMMR, BRAFV600E mutation and nuclear Beta-Catenin expression were identified in 40 out of 83 (48.2%), 17 out of 83 (20.5%) and 4 out of 83 (4.8%). For MMR and BRAF, none of the clinicopathologic parameters were significantly correlated with their status. 7 out of 40 (17.5%) tumors with dMMR carried BRAF mutation while 10 out of 43 (23.3%) tumors with pMMR harbor the mutation (P = 0.516)