Frequent alteration of DNA damage signalling and repair pathways in human colorectal cancers with microsatellite instability

Accumulation of frameshift mutations at genes containing coding mononucleotide repeats is thought to be the major molecular mechanism by which mismatch repair-deficient cells accumulate functional alterations. These mutations resulting from microsatellite instability (MSI) can affect genes involved...

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Veröffentlicht in:	Oncogene 2007-08, Vol.26 (40), p.5919-5926
Hauptverfasser:	Miquel, C, Jacob, S, Grandjouan, S, Aimé, A, Viguier, J, Sabourin, J-C, Sarasin, A, Duval, A, Praz, F
Format:	Artikel
Sprache:	eng
Schlagworte:	Adult Aged Antineoplastic Agents - pharmacology Apoptosis Biological and medical sciences Carcinogenesis Cell Biology Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cellular signal transduction Chemotherapy Colorectal cancer Colorectal Neoplasms - genetics Control Deoxyribonucleic acid Disease Progression DNA DNA Damage DNA Repair DNA-dependent protein kinase Double-strand break repair Female Frameshift mutation Fundamental and applied biological sciences. Psychology Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation, Neoplastic Genetic aspects Genetics Human Genetics Humans Internal Medicine Male Medical sciences Medicine Medicine & Public Health Microsatellite Instability Middle Aged Mismatch repair Molecular and cellular biology MRE11 protein MSH6 protein Mutation Oncology original-article Physiological aspects Protein kinase C Risk factors Signal Transduction Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors
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