| Article ID | Journal | Published Year | Pages | File Type | 
|---|---|---|---|---|
| 3295292 | Gastroenterology | 2009 | 19 Pages | 
Abstract
												Accumulation of mutations and allelic losses are driving forces of colorectal carcinogenesis. ITF-2B, which is up-regulated during early colorectal carcinogenesis because of loss of adenomatous polyposis coli, is a target for LOH on chromosome 18q, along with deleted in colorectal carcinoma and Smad4. This finding, along with the fact that ITF-2B is a regulator of the key cell cycle inhibitor p21Cip1, indicates that ITF-2B is a tumor suppressor that has an important function at the adenoma to carcinoma transition.
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											Authors
												Andreas Herbst, Guido T. Bommer, Lydia Kriegl, Andreas Jung, Andrea Behrens, Endy Csanadi, Markus Gerhard, Christian Bolz, Rainer Riesenberg, Wolfgang Zimmermann, Wolfgang Dietmaier, Isabella Wolf, Thomas Brabletz, Burkhard Göke, Frank T. Kolligs, 
											