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Molecular biology in colorectal cancer.
Clin Transl Oncol. 2006 Jun; 8(6):391-8.CT

Abstract

Cancer is a genetic disease. Colorectal cancer is probably the type of cancer for which the most is known about the genes affected by cancer-causing mutations, their normal functions and their carcinogenic effects when mutated. Most cancer-causing mutations are somatic, occurring in the affected tissue during the course of carcinogenesis. However, most cancers also have a hereditary component that is caused by predisposing mutations that affect the germline, are heritable and contribute to the initiation of carcinogenesis. High-penetrance mutations confer predisposition to colorectal cancer mainly in Lynch syndrome (which involves mutations in mismatch-repair genes) and in familial adenomatous polyposis (which involves mutations in the APC tumour suppressor). Together, these conditions account for 5% or less of all cases of colorectal cancer. Low-penetrance mutations account for a high proportion of all the attributable risk of colorectal cancer, in both familial and sporadic cases. These mutations are more difficult to identify, but mainly due to the implementation of association studies, are increasingly being detected and characterized. The identification of both high- and low-penetrance mutations contributes significantly to our understanding of the molecular genetic processes occurring in cancer. This understanding facilitates the development of therapeutic drugs and preventive strategies.

Authors+Show Affiliations

Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad Complutense, and Servicio de Oncología Médica, Hospital Clínico San Carlos, Madrid, Spain.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

16790391

Citation

Benito, Manuel, and Eduardo Díaz-Rubio. "Molecular Biology in Colorectal Cancer." Clinical & Translational Oncology : Official Publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, vol. 8, no. 6, 2006, pp. 391-8.
Benito M, Díaz-Rubio E. Molecular biology in colorectal cancer. Clin Transl Oncol. 2006;8(6):391-8.
Benito, M., & Díaz-Rubio, E. (2006). Molecular biology in colorectal cancer. Clinical & Translational Oncology : Official Publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 8(6), 391-8.
Benito M, Díaz-Rubio E. Molecular Biology in Colorectal Cancer. Clin Transl Oncol. 2006;8(6):391-8. PubMed PMID: 16790391.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Molecular biology in colorectal cancer. AU - Benito,Manuel, AU - Díaz-Rubio,Eduardo, PY - 2006/6/23/pubmed PY - 2006/9/29/medline PY - 2006/6/23/entrez SP - 391 EP - 8 JF - Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico JO - Clin Transl Oncol VL - 8 IS - 6 N2 - Cancer is a genetic disease. Colorectal cancer is probably the type of cancer for which the most is known about the genes affected by cancer-causing mutations, their normal functions and their carcinogenic effects when mutated. Most cancer-causing mutations are somatic, occurring in the affected tissue during the course of carcinogenesis. However, most cancers also have a hereditary component that is caused by predisposing mutations that affect the germline, are heritable and contribute to the initiation of carcinogenesis. High-penetrance mutations confer predisposition to colorectal cancer mainly in Lynch syndrome (which involves mutations in mismatch-repair genes) and in familial adenomatous polyposis (which involves mutations in the APC tumour suppressor). Together, these conditions account for 5% or less of all cases of colorectal cancer. Low-penetrance mutations account for a high proportion of all the attributable risk of colorectal cancer, in both familial and sporadic cases. These mutations are more difficult to identify, but mainly due to the implementation of association studies, are increasingly being detected and characterized. The identification of both high- and low-penetrance mutations contributes significantly to our understanding of the molecular genetic processes occurring in cancer. This understanding facilitates the development of therapeutic drugs and preventive strategies. SN - 1699-048X UR - https://www.unboundmedicine.com/medline/citation/16790391/Molecular_biology_in_colorectal_cancer_ L2 - http://www.diseaseinfosearch.org/result/1746 DB - PRIME DP - Unbound Medicine ER -