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ISRN OncologyVolume 2012 2012, Article ID 139268, 19 pages

Review ArticleDepartament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Avenida Diagonal 643, Catalunya, 08028 Barcelona, Spain

Received 23 September 2012; Accepted 11 October 2012

Academic Editors: H. Al-Ali, N. Fujimoto, L. Mutti, and R. Nahta

Copyright © 2012 Josep J. Centelles. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.

Author: Josep J. Centelles



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