Background: The MCP-1/CCR2 axis is one of the major chemokine signaling pathways that play a crucial role in the tumor microenvironment and has been involved in triggering various tumor progression mechanisms, such as increasing the immunosuppressive cells recruitment and promoting tumor cell proliferation and invasiveness.
Aim: The current study investigated the association of MCP1 (rs1024611) and CCR2 (rs1799864) genes variants with the risk as well as prognosis of colorectal cancer (CRC) and colorectal liver metastases (CRLM).
Subjects And Methods: A retrospective cohort study involved 408 patients (284 CRC and 124 CRLM), and 284 healthy control was conducted.
Background: Recent studies suggest that SDF-1 and CXCR4 are expressed in certain cancer cells, and malignant cells use this chemokine/receptor system to promote tumor progression and metastasis. However, the pathophysiological significance of their expression in colorectal cancer (CRC) tissue has not been fully elucidated.
Objective: The purpose of this study was to assess SDF-1/CXCR4 expression and to explore its contribution to colorectal cancer.
J Immunoassay Immunochem
September 2015
The aim was to evaluate the relationship between SDF-1G801A polymorphism and its immunohistochemical expression in colorectal cancer tissues in the Tunisian cohort. The molecular and immunohistochemical analysis showed that SDF-1G801A polymorphic variant was higher in CRC patients with TNM stage II and III, the SDF-1 expression was significantly increased from normal mucosa to primary tumor (p < 0.05).
View Article and Find Full Text PDFOne of the most important pathways which are frequently affected in colorectal cancer is p53/ (MDM2)/p14ARF pathway. We aim to determine the methylation pattern of p14/ARF in relation to mutation of p53. This correlation was studied to investigate whether their alterations could be considered as a predictor factor of prognosis in colorectal cancer and whether it can be useful in early-stage diagnosis.
View Article and Find Full Text PDFBackground: About 10% to 15% of sporadic colorectal cancers demonstrate high level of microsatellite instability that is generally associated with aberrant methylation of hMLH1 promoter.
Aim: To investigate the association between MSI status, hMLH1 protein expression and methylation status of the hMLH1 promoter in a cohort of Tunisian sporadic colorectal cancer.
Methods: Expression of MLH1 and MSH2 was determined by immunohistochemistry and the MSI status was analysed by microfluid-based on-chip electrophoresis.
Background: The prevalence of p53 mutations in colorectal cancer could reach 90%. The most important regulator of this protein that was identified originally was the Murine Double Minute2 (MDM2) oncoprotein, by which the levels of p53 were fixed through an autoregulatory feedback loop. In cancer cases, the overexpression of MDM2 deregulates this feedback, and the signaling pathway between MDM2 and p53 is blocked.
View Article and Find Full Text PDFIntroduction: MDM2 was originally identified as an oncoprotein that binds to p53 and inhibits p53-mediated transactivation. Scientists have described functional single-nucleotide polymorphisms (SNP) in the MDM2 gene. They showed that the genotype of SNP 309 induces an increase in the level of MDM2 protein, which causes attenuation of the p53 pathway.
View Article and Find Full Text PDFBeta-catenin plays a critical role with E-cadherin in cell-cell adhesion and is also a key molecule of the highly conserved Wnt signaling pathway that regulates cell proliferation and differentiation. Abrogation of this pathway is implicated in the carcinogenesis of several malignancies, especially colorectal cancer. The objective of this study was to determine the prognostic value of β-catenin/E-cadherin complex in Tunisian patients with colorectal cancer.
View Article and Find Full Text PDFThe β-galactoside-binding protein galectin-3 (gal-3) has pleitropic biological functions and has been implicated in cell growth, differentiation, adhesion, RNA processing, apoptosis, and malignant transformation. To investigate the pattern of inactivation of the gal-3 gene (LGALS3) in colorectal cancers (CRC), we studied a series of Tunisian patients with CRC to identify abnormal methylation in LGALS3 promoter using a methylation-specific PCR. We also examined the gal-3 gene expression by reverse transcription-PCR and the expression of gal-3 protein by immunohistochemistry.
View Article and Find Full Text PDFAppl Immunohistochem Mol Morphol
December 2010
Background: We examined the association of one linked GC/AT polymorphism at p73 with the risk of colorectal cancer.
Aim: In this study, we investigated whether this polymorphism was related to the risk of colorectal cancer, and whether there were relationships between the polymorphism and loss of heterozygosity, protein expression, or clinicopathologic variables.
Materials And Methods: The p73 genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism in 150 Tunisian patients with colorectal cancer and in 204 healthy control subjects.
Introduction: The protein p73 is the first identified homolog of the tumor suppressor gene p53, but its function in tumor development has not been established. Indeed, the results regarding the p73 implication in colorectal cancers is still controversial.
Aim: We investigated whether the p73 is implicated in colorectal cancer, whether the p73 expression is related to prognosis and whether the p73 expression is correlated with p21-ras or p53.
Background: The p73 gene encodes a nuclear protein that is highy homologous to p53. p73 also shares some common functions with p53 protein indicating that p73 gene is a p53-like tumor suppressor.
Aim: In this study, we examined by immunohistochemestry the p73 expression on 120 cases of colorectal carcinomas and evaluated its implication in carcinogenesis.
Anatomical and functional results were evaluated at 3 and 5 years after surgery for chronic cholesteatomatous otitis media in 94 patients treated by the same surgeon between 1975 and 1983. Open techniques predominated and were justified by seven clinical or epidemiologic factors present alone or in association in 80% of cases. Many patients were non-attenders at follow up (40% at 3 years and 70% at 5 years), recovery from their cholesteatoma being noted in 84% and 78% of those attending at 3 and 5 years respectively.
View Article and Find Full Text PDFAnatomic and functional results are reported after 3 and 5 year follow up of 94 cases of chronic cholesteatomatous otitis operated upon and kept under surveillance by the same surgeon between 1975 and 1983. Open technics dominated and were justified by seven clinical and epidemiologic factors found alone or in combination in 80% of patients. Results must allow for the high rate of non-attenders (40% at 3 years and 70% at 5 years).
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