Mutant allele-specific imbalance modulates prognostic impact of KRAS mutations in colorectal adenocarcinoma and is associated with worse overall survival.
Furthermore, we compared the quality, labor input, and applicability of the method for diagnostic purposes with those of a laboratory-validated manual method in a clinical setting by screening a set of 45 colorectal adenocarcinoma for the KRAS mutation.
EGFR gene copy number gains and KRAS/BRAF mutations have been reported to act as positive and negative predictors, respectively, of therapeutic response to EGFR targeted therapies in colorectal adenocarcinoma, a tumour type claimed to be genetically similar to ITAC.
Sanger sequencing is one of several reliable methods in use to detect KRAS and BRAF mutations to facilitate clinical patient selection for anti-epidermal growth factor receptor (EGFR) monoclonal antibody therapy in unresectable metastatic colorectal adenocarcinoma (CRC).
Cetuximab is an anti-epidermal growth factor receptor that helps effectively treat patients with advanced colorectal adenocarcinoma without KRAS activating mutations.
In this study, we investigated early hypomagnesemia as a predictor of efficacy and outcome in terms of time to progression (TtP) and overall survival (OS) in a cohort of patients affected by advanced colorectal adenocarcinomaKRAS wild-type cetuximab-treated.
Expression of mutant p53 and of the multidrug resistant proteins P-glycoprotein and glutathione S-transferase-pi correlated in colorectal adenocarcinoma.
Metalloproteinase-1, metalloproteinase-7, and p53 immunoexpression and their correlation with clinicopathological prognostic factors in colorectal adenocarcinoma.
To assess and compare immunohistochemical expression of epidermal growth factor receptor (EGFR) with gene amplification as demonstrated by chromogenic in situ hybridisation (CISH), in colorectal adenocarcinoma.
Maspin expression correlated negatively with liver metastasis of CRA (p < 0.05), positively with tenascin expression (p < 0.05), but not with tumor size, depth of invasion, local invasion via vessels, lymph node metastasis, differentiation, expression of Ki-67 and p53 or MVD (p > 0.05).
All the patients with colorectal mucinous adenocarcinoma and colorectal signet-ring cell carcinoma with a positive family history of colorectal adenocarcinoma had tumors that showed p53 expression (P = 0.012).
Immunohistochemical detection of expression of the epidermal growth factor receptor (EGFR) has been utilized to identify eligible patients with solid malignant tumors, including colorectal adenocarcinoma, for monoclonal antibody therapy (eg, cetuximab).
Multiple sample areas in colorectal adenocarcinoma at early and advanced stages and in metastases were studied for the well-known genetic alterations: K-ras and p53 point mutations and loss of heterozygosity (LOH) on chromosomes 5q and 18q.
The high frequency of transitions among K-RAS mutation suggests that G/T mismatches play an important role in the oncogenesis of colorectal adenocarcinoma, implying that alkylating carcinogens may be involved in the colorectal carcinogenesis.
Genetic alteration of p53, but not overexpression of intratumoral p53 protein, or serum p53 antibody is a prognostic factor in sporadic colorectal adenocarcinoma.
These results reveal that immunohistochemical assessment does not predictTP53 mutation status in colorectal adenocarcinoma, mainly in cases displaying absence of nuclear staining.
Therefore, the purpose of our study was to determine the prognostic value of BAX protein expression and the mutational status of its upstream regulator p53 in primary colorectal adenocarcinoma.
Taken together, these data imply that deregulated expression of Id proteins in colorectal adenocarcinoma arises at least in part as a consequence of loss of p53 function and contributes to the uncontrolled proliferation of tumor cells in colorectal cancer.
Archival formalin-fixed, paraffin-embedded tissues from seven cases of colorectal adenocarcinoma were laser- and hand-microdissected and subsequently evaluated by PCR/SSCP/sequencing for Ki-ras exon 1 and p53 exons 5, 7, and 8.Results.