Differential colorectal carcinogenesis:Molecular basis and clinical relevance

Colorectal cancer(CCR) is one of the most frequent cancers in developed countries.It poses a major public health problem and there is renewed interest in understanding the basic principles of the molecular biology of colorectal cancer.It has been established that sporadic CCRs can arise from at leas...

Full description

Saved in:
Bibliographic Details
Published inWorld journal of gastrointestinal oncology Vol. 2; no. 3; pp. 151 - 158
Main Authors Morán, Alberto, Ortega, Paloma, de Juan, Carmen, Fernández-Marcelo, Tamara, Frías, Cristina, Sánchez-Pernaute, Andrés, Torres, Antonio José, Díaz-Rubio, Eduardo, Iniesta, Pilar, Benito, Manuel
Format Journal Article
LanguageEnglish
Published China Baishideng Publishing Group Co., Limited 15.03.2010
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Colorectal cancer(CCR) is one of the most frequent cancers in developed countries.It poses a major public health problem and there is renewed interest in understanding the basic principles of the molecular biology of colorectal cancer.It has been established that sporadic CCRs can arise from at least two different carcinogenic pathways.The traditional pathway,also called the suppressor or chromosomal instability pathway,follows the Fearon and Vogelstein model and shows mutation in classical oncogenes and tumour suppressor genes,such as K-ras,adenomatous polyposis coli,deleted in colorectal cancer,or p53.Alterations in the Wnt pathway are also very common in this type of tumour.The second main colorectal carcinogenesis pathway is the mutator pathway.This pathway is present in nearly 15% of all cases of sporadic colorectal cancer.It is characterized by the presence of mutations in the microsatellite sequences caused by a defect in the DNA mismatch repair genes,mostly in hMLH1 or hMSH2.These two pathways have clear molecular differences,which will be reviewed in this article,but they also present distinct histopathological features.More strikingly,their clinical behaviours are completely different,having the "mutator" tumours a better outcome than the "suppressor" tumours.
Bibliography:Alberto Morán,Paloma Ortega,Carmen de Juan,Tamara Fernández-Marcelo,Cristina Frías,Pilar Iniesta,Manuel Benito,the second Department of Biochemistry and Molecular Biology,School of Pharmacy,Complutense University,28040-Madrid,Spain Andrés Sánchez-Pernaute,Antonio José Torres,Surgery Service II,Clínico San Carlos Hospital,28040-Madrid,Spain Eduardo Díaz-Rubio,Oncology Service,Clínico San Carlos Hospital,28040-Madrid,Spain
Correspondence to: Manuel Benito, PhD, the second Department of Biochemistry and Molecular Biology, School of Pharmacy, Complutense University, 28040-Madrid, Spain. benito@farm.ucm.es
Author contributions: Morán A, de Juan C, Frías C, Ortega P and Fernández-Marcelo T performed the molecular analyses; Sánchez-Pernaute A and Torres AJ assessed the clinical correlations; Díaz-Rubio E was assessor of this work; Benito M directed and coordinated this work; Benito M, Iniesta P and Morán A were involved in writing the manuscript.
Telephone: +34-91-3941777 Fax: +34-91-3941779
ISSN:1948-5204
1948-5204
DOI:10.4251/wjgo.v2.i3.151