scholarly journals Cross talk of chromosome instability, CpG island methylator phenotype and mismatch repair in colorectal cancer

2018 ◽  
Author(s):  
Tian‑Ming Zhang ◽  
Tao Huang ◽  
Rong‑Fei Wang
Keyword(s):  
Colorectal Cancer ◽  
Mismatch Repair ◽  
Cross Talk ◽  
Cpg Island ◽  
Chromosome Instability ◽  
Cpg Island Methylator Phenotype ◽  
Methylator Phenotype

scholarly journals Reduced FHIT Expression Is Associated with Mismatch Repair Deficient and High CpG Island Methylator Phenotype Colorectal Cancer

2013 ◽  
Vol 61 (9) ◽  
pp. 627-638 ◽  
Author(s):  
Rabeah Abbas Al-Temaimi ◽  
Sindhu Jacob ◽  
Waleed Al-Ali ◽  
Diana Ann Thomas ◽  
Fahd Al-Mulla
Keyword(s):  
Colorectal Cancer ◽  
Mismatch Repair ◽  
Cpg Island ◽  
Cpg Island Methylator Phenotype ◽  
Methylator Phenotype

scholarly journals General Aspects of Colorectal Cancer

ISRN Oncology ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-19 ◽  
Author(s):  
Josep J. Centelles
Keyword(s):  
Colorectal Cancer ◽  
Cpg Island ◽  
Chromosome Instability ◽  
Tumour Suppressor Genes ◽  
Cpg Island Methylator Phenotype ◽  
Dna Damages ◽  
Hereditary Nonpolyposis ◽  
Methylator Phenotype ◽  
Peutz Jeghers Syndrome ◽  
General Aspects

Colorectal cancer (CRC) is one of the main causes of death. Cancer is initiated by several DNA damages, affecting proto-oncogenes, tumour suppressor genes, and DNA repairing genes. The molecular origins of CRC are chromosome instability (CIN), microsatellite instability (MSI), and CpG island methylator phenotype (CIMP). A brief description of types of CRC cancer is presented, including sporadic CRC, hereditary nonpolyposis colorectal cancer (HNPCC) or Lynch syndromes, familiar adenomatous polyposis (FAP), MYH-associated polyposis (MAP), Peutz-Jeghers syndrome (PJS), and juvenile polyposis syndrome (JPS). Some signalling systems for CRC are also described, including Wnt-β-catenin pathway, tyrosine kinase receptors pathway, TGF-β pathway, and Hedgehog pathway. Finally, this paper describes also some CRC treatments.

scholarly journals The Role of the CpG Island Methylator Phenotype in Colorectal Cancer Prognosis Depends on Microsatellite Instability Screening Status

2010 ◽  
Vol 16 (6) ◽  
pp. 1845-1855 ◽  
Author(s):  
Anna M. Dahlin ◽  
Richard Palmqvist ◽  
Maria L. Henriksson ◽  
Maria Jacobsson ◽  
Vincy Eklöf ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Microsatellite Instability ◽  
Cpg Island ◽  
Cancer Prognosis ◽  
Cpg Island Methylator Phenotype ◽  
Methylator Phenotype

scholarly journals CpG Island Methylator Phenotype-Low (CIMP-Low) in Colorectal Cancer: Possible Associations with Male Sex and KRAS Mutations

2006 ◽  
Vol 8 (5) ◽  
pp. 582-588 ◽  
Author(s):  
Shuji Ogino ◽  
Takako Kawasaki ◽  
Gregory J. Kirkner ◽  
Massimo Loda ◽  
Charles S. Fuchs
Keyword(s):  
Colorectal Cancer ◽  
Cpg Island ◽  
Cpg Island Methylator Phenotype ◽  
Kras Mutations ◽  
Male Sex ◽  
Methylator Phenotype

scholarly journals IGFBP7 is a p53-responsive gene specifically silenced in colorectal cancer with CpG island methylator phenotype

2009 ◽  
Vol 31 (3) ◽  
pp. 342-349 ◽  
Author(s):  
Hiromu Suzuki ◽  
Shinichi Igarashi ◽  
Masanori Nojima ◽  
Reo Maruyama ◽  
Eiichiro Yamamoto ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cpg Island ◽  
Cpg Island Methylator Phenotype ◽  
Responsive Gene ◽  
Methylator Phenotype

Determination & expression of chimeric protein in colorectal cancer: A bioinformatics Approach

2021 ◽  
Vol 2 (3) ◽  
pp. 35-67
Author(s):  
Gargi Bhattacharyya ◽  
Amit Chattopadhay
Keyword(s):  
Colorectal Cancer ◽  
Cpg Island ◽  
Therapeutic Process ◽  
Chimeric Protein ◽  
Ageing Population ◽  
Cpg Island Methylator Phenotype ◽  
High Risk Factors ◽  
Bowel Movements ◽  
Methylator Phenotype ◽  
New Treatments

Colorectal cancer (CRC) accounts for about 10% of cancer-related mortality in western countries. Increasing ageing population, undesirable modern dietary and high-risk factors like smoking, obesity and low exercise. Chromosomal instability (CIN), CpG island methylator phenotype (CIMP), and microsatellite instability are the three different mechanism that give rise to CRC. It often grow slowly, and customarily doesn’t produce symptoms until reaching a substantial size of several centimeters, which can block the passage of feces and cause cramping, pain, or bleeding which can present as visible bleeding with bowel movements or, rarely, dark “tarry” stools. Most colon tumors develop via a several different processes involving a series of histological, morphological, and genetical changes that accumulate over time to time. New treatments for primary and metastatic colorectal cancer have emerged, like in variety of therapeutic process by preparing chimeric proteins that triggers the cells and stop it from getting severe.

scholarly journals Clinicopathological and Molecular Profiles of Sporadic Microsatellite Unstable Colorectal Cancer with or without the CpG Island Methylator Phenotype (CIMP)

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3487
Author(s):  
Shih-Ching Chang ◽  
Anna Fen-Yau Li ◽  
Pei-Ching Lin ◽  
Chun-Chi Lin ◽  
Hung-Hsin Lin ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cpg Island ◽  
Gene Mutations ◽  
Proximal Colon ◽  
Tnm Stage ◽  
Cpg Island Methylator Phenotype ◽  
Kras Mutations ◽  
Methylator Phenotype ◽  
Next Generation Sequencing Ngs ◽  
Mutation Spectra

Background: The 5’-C-phosphate-G-3’ island methylator phenotype (CIMP) is a specific phenotype of colorectal cancer (CRC) associated with microsatellite instability-high (MSI-high) tumors. Methods: In this study, we determined the CIMP status using eight methylation markers in 92 MSI-high CRC patients after excluding five germline mismatch repair (MMR) gene mutations analyzed by next-generation sequencing (NGS) and confirmed by Sanger sequencing. The mutation spectra of 22 common CRC-associated genes were analyzed by NGS. Results: Of the 92 sporadic MSI-high tumors, 23 (25%) were considered CIMP-high (expressed more than 5 of 8 markers). CIMP-high tumors showed proximal colon preponderance and female predominance. The mutation profiles of CIMP-high tumors were significantly different from those of CIMP-low or CIMP-0 tumors (i.e., higher frequencies of BRAF, POLD1, MSH3, and SMAD4 mutations but lower frequencies of APC, TP53, and KRAS mutations). Multivariate analysis demonstrated that tumor, node, metastasis (TNM) stage was the independent prognostic factor affecting overall survival (OS). Among the MSI-high cases, the CIMP status did not impact the outcome of patients with MSI-high tumors. Conclusions: Only TNM stage was a statistically significant predictor of outcomes independent of CIMP profiles in MSI-high CRC patients. Sporadic MSI-high CRCs with different mechanisms of carcinogenesis have specific mutation profiles and clinicopathological features.

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