Mechanisms of inactivation of the receptor tyrosine kinase EPHB2 in colorectal tumors

The receptor tyrosine kinase EPHB2 has recently been shown to be a direct transcriptional target of TCF/beta-catenin. Premalignant lesions of the colon express high levels of EPHB2 but the expression of this kinase is reduced or lost in most colorectal carcinomas. In addition, inactivation of EPHB2...

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Veröffentlicht in:	Cancer research (Chicago, Ill.) Ill.), 2005-11, Vol.65 (22), p.10170-10173
Hauptverfasser:	ALAZZOUZI, Hafid, DAVALOS, Veronica, IMAI, Kohzoh, YAMAMOTO, Hiroyuki, MARIADASON, John M, GEBERT, Johannes F, AALTONEN, Lauri A, SCHWARTZ, Simo JR, ARANGO, Diego, KOKKO, Antti, DOMINGO, Enric, WOERNER, Stefan M, WILSON, Andrew J, KONRAD, Lars, LAIHO, Päivi, ESPIN, Eloi, ARMENGOL, Manel
Format:	Artikel
Sprache:	eng
Schlagworte:	Adenoma - enzymology Adenoma - genetics Biological and medical sciences Colorectal Neoplasms - enzymology Colorectal Neoplasms - genetics CpG Islands DNA Methylation Enzyme Activation Exons Frameshift Mutation Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation, Enzymologic Gene Silencing Humans Medical sciences Microsatellite Repeats - genetics Promoter Regions, Genetic Receptor, EphB2 - genetics Receptor, EphB2 - metabolism Repetitive Sequences, Nucleic Acid Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors
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