Smad4 haploinsufficiency in mouse models for intestinal cancer

The Smad4 +/E6sad mouse carries a null mutation in the endogenous Smad4 gene resulting in serrated adenomas and mixed polyposis of the upper gastrointestinal (GI) tract with 100% penetrance. Here, we show by loss of heterozygosity (LOH) analysis and immunohistochemistry (IHC) that, although the majo...

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Veröffentlicht in:	Oncogene 2006-03, Vol.25 (13), p.1841-1851
Hauptverfasser:	Alberici, P, Jagmohan-Changur, S, De Pater, E, Van Der Valk, M, Smits, R, Hohenstein, P, Fodde, R
Format:	Artikel
Sprache:	eng
Schlagworte:	Adenomatous polyposis coli Age of Onset Animal models Animals Apoptosis Biological and medical sciences Cancer Cell Biology Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Chromosome 18 Chromosomes Colorectal cancer Disease Progression DNA Mutational Analysis Fundamental and applied biological sciences. Psychology Gastroenterology. Liver. Pancreas. Abdomen Gastrointestinal tract Genes, APC Haploinsufficiency Heterozygosity Human Genetics Immunohistochemistry Internal Medicine Intestinal Neoplasms - genetics Intestinal Neoplasms - physiopathology Loss of Heterozygosity Medical sciences Medicine & Public Health Mice Mice, Inbred C57BL Molecular and cellular biology Mutation Oncology original-article Pathology Phenotype Polyposis Polyps Signal Transduction Smad4 protein Smad4 Protein - genetics Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Transforming Growth Factor beta - physiology Tumor suppressor genes Tumorigenesis Tumors Wnt Proteins - physiology
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