ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at the adenoma-carcinoma transition.

Herbst, Andreas;Bommer, Guido;Kriegl, Lydia;Jung, Andreas;Kolligs, Frank T;et.al.
(2009) Gastroenterology — Vol. 137, n° 2, p. 639-648 (2009)

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Authors
  • Herbst, AndreasUniversitaet Muenchen
    Author
  • Bommer, Guidoorcid-logoUCLouvain
    Author
  • Kriegl, LydiaUniversitaet Muenchen
    Author
  • Jung, AndreasUniversitaet Muenchen
    Author
  • Kolligs, Frank T
    Author
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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 p21(Cip1), indicates that ITF-2B is a tumor suppressor that has an important function at the adenoma to carcinoma transition.
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Citations

Herbst, A., Bommer, G., Kriegl, L., Jung, A., Behrens, A., Csanadi, E., Gerhard, M., Bolz, C., Riesenberg, R., Zimmermann, W., Dietmaier, W., Wolf, I., Brabletz, T., Göke, B., & Kolligs, F. T. (2009). ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at the adenoma-carcinoma transition. Gastroenterology, 137(2), 639-648. https://doi.org/10.1053/j.gastro.2009.04.049 (Original work published 2009)