scholarly journals Are clinicopathological features of colorectal cancers with methylation in half of CPG island methylator phenotype panel markers different from those of CPG island methylator phenotype-high colorectal cancers?

Pathology ◽  
2016 ◽  
Vol 48 ◽  
pp. S153
Author(s):  
Ye-Young Rhee ◽  
Jeong-Mo Bae ◽  
Kyung-Ju Kim ◽  
Xianyu Wen ◽  
Young-Seok Song ◽  
...  
Keyword(s):  
Cpg Island ◽  
Clinicopathological Features ◽  
Colorectal Cancers ◽  
Cpg Island Methylator Phenotype ◽  
Methylator Phenotype

scholarly journals Ethnicity and Risk for Colorectal Cancers Showing Somatic BRAF V600E Mutation or CpG Island Methylator Phenotype

2008 ◽  
Vol 17 (7) ◽  
pp. 1774-1780 ◽  
Author(s):  
Dallas R. English ◽  
Joanne P. Young ◽  
Julie A. Simpson ◽  
Mark A. Jenkins ◽  
Melissa C. Southey ◽  
...  
Keyword(s):  
Cpg Island ◽  
Braf V600e Mutation ◽  
Braf V600e ◽  
Colorectal Cancers ◽  
Cpg Island Methylator Phenotype ◽  
Methylator Phenotype

scholarly journals 745 Colorectal Cancers (CRCs) With the CpG Island Methylator Phenotype (CIMP) Do Not Show Improved Survival With 5-Fluorouracil (5FU)-Based Adjuvant Chemotherapy

2010 ◽  
Vol 138 (5) ◽  
pp. S-102
Author(s):  
Rodrigo Jover ◽  
Thuy-Phuong T. Nguyen ◽  
Lucía Pérez-Carbonell ◽  
Artemio Payá ◽  
Cristina Alenda ◽  
...  
Keyword(s):  
Adjuvant Chemotherapy ◽  
Cpg Island ◽  
Colorectal Cancers ◽  
Cpg Island Methylator Phenotype ◽  
Methylator Phenotype

CpG Island Methylator Phenotype in Colorectal Cancers: Comparison of the New and Classic CpG Island Methylator Phenotype Marker Panels

2008 ◽  
Vol 132 (10) ◽  
pp. 1657-1665 ◽  
Author(s):  
Sun Lee ◽  
Nam-Yun Cho ◽  
Eun Joo Yoo ◽  
Jung Ho Kim ◽  
Gyeong Hoon Kang
Keyword(s):  
Clinical Outcome ◽  
Microsatellite Instability ◽  
Braf Mutation ◽  
Cpg Island ◽  
Tumor Location ◽  
Colorectal Cancers ◽  
Clinicopathologic Features ◽  
Cpg Island Methylator Phenotype ◽  
P Values ◽  
Methylator Phenotype

Abstract Context.—CpG island methylator phenotype (CIMP) designates a subset of colorectal cancers featuring concordant hypermethylation of multiple promoter CpG islands. Little is known about the clinical outcome or histologic characteristics of CIMP-positive colorectal cancers defined by recently identified CpG island methylator phenotype panels. Objective.—To investigate and compare the molecular and clinicopathologic features of CIMP-positive colorectal cancers defined by classic (p16, hMLH1, MINT1, MINT2, MINT31) and new (CACNA1G, IGF2, NEUROG1, RUNX3, SOCS1) CIMP panels. Design.—We analyzed 130 colorectal cancers for hypermethylation of both panels using methylation-specific polymerase chain reaction. Results.—With at least 2 markers methylated, both classic (39/130; 23.1%) and new (23.1%) CIMP-positive colorectal cancers were significantly associated with proximal tumor location, microsatellite instability, and BRAF mutation (all P values were less than .05). The new panel outperformed the classic panel in detecting these features. With at least 3 markers methylated, new CIMP-positive colorectal cancers (16.9%) were closely associated with proximal tumor location, low frequency of KRAS mutation, and high frequency of BRAF mutation (all P values were less than .05), whereas classic CIMP-positive colorectal cancers (18.5%) were closely associated with proximal tumor location, frequent microsatellite instability, and frequent BRAF mutation (all P values were less than .05). Analyzing a combination of CIMP and microsatellite instability status, CIMP-positive/microsatellite instability–negative colorectal cancers had the worst clinical outcomes. Conclusions.—Whereas the classic panel outperformed in predicting clinical outcome, the new panel was superior in detecting known clinicopathologic features of CIMP but inferior in prognostication power.

Abstract 2889: Distinct microbiome in colorectal cancers with the CpG Island Methylator Phenotype

2015 ◽  
Author(s):  
Ang Sun ◽  
Matteo Cesaroni ◽  
Christian Jobin ◽  
Carlos Barrero ◽  
Jaroslav Jelinek ◽  
...  
Keyword(s):  
Cpg Island ◽  
Colorectal Cancers ◽  
Cpg Island Methylator Phenotype ◽  
Methylator Phenotype

CPG island methylator phenotype and patients with multiple colorectal cancers

2000 ◽  
Vol 118 (4) ◽  
pp. A46
Author(s):  
William Mallory Grady ◽  
Sanford Markowitz ◽  
Joseph Willis
Keyword(s):  
Cpg Island ◽  
Colorectal Cancers ◽  
Cpg Island Methylator Phenotype ◽  
Methylator Phenotype

scholarly journals Molecular Subtypes of Colorectal Cancer and Their Clinicopathologic Features, With an Emphasis on the Serrated Neoplasia Pathway

2016 ◽  
Vol 140 (5) ◽  
pp. 406-412 ◽  
Author(s):  
Jeong Mo Bae ◽  
Jung Ho Kim ◽  
Gyeong Hoon Kang
Keyword(s):  
Colorectal Cancer ◽  
Complex Disease ◽  
Molecular Subtypes ◽  
Cpg Island ◽  
Colorectal Cancers ◽  
Cpg Island Methylator Phenotype ◽  
Molecular Features ◽  
Methylator Phenotype ◽  
Serrated Neoplasia Pathway ◽  
Molecular Carcinogenesis

Context.—Colorectal cancer is a heterogeneous disease entity with 3 molecular carcinogenesis pathways and 2 morphologic multistep pathways. Right-sided colon cancers and left-sided colon and rectal cancers exhibit differences in their incidence rates according to geographic region, age, and sex. A linear tendency toward increasing frequencies of microsatellite instability–high or CpG island methylator phenotype–high cancers in subsites along the bowel from the rectum to the cecum or the ascending colon accounts for the differences in tumor phenotypes associated with these subsites. The molecular subtypes of colorectal cancers exhibit different responses to adjuvant therapy, which might be responsible for differences in subtype-specific survival. Objectives.—To review the clinicopathologic and molecular features of the molecular subtypes of colorectal cancer generated by combined CpG island methylator phenotype and microsatellite statuses, to integrate these features with the most recent findings in the context of the prognostic implications of molecular subtypes, and to emphasize the necessity of developing molecular markers that enable the identification of adenocarcinomas involving the serrated neoplasia pathway. Data Sources.—Based on the authors' own experimental data and a review of the pertinent literature. Conclusions.—Because colorectal cancers arise from 2 different morphologic multistep carcinogenesis pathways with varying contributions from 3 different molecular carcinogenesis pathways, colorectal cancer is a heterogeneous and complex disease. Thus, molecular subtyping of colorectal cancers is an important approach to characterizing their heterogeneity with respect to not only prognosis and therapeutic response but also biology and natural history.

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