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p16INK4a is a beta-...
p16INK4a is a beta-catenin target gene and indicates low survival in human colorectal tumors
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- Wassermann, Stella (författare)
- Pathologisch-Anatomisches Institut der Universität Erlangen-Nürnberg, Erlangen, Germany
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- Scheel, Silvio K (författare)
- Pathologisches Institut der Universität München, Munich, Germany
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- Hiendlmeyer, Elke (författare)
- Pathologisch-Anatomisches Institut der Universität Erlangen-Nürnberg, Erlangen, Germany
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- Palmqvist, Richard (författare)
- Umeå universitet,Patologi
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- Horst, David (författare)
- Pathologisches Institut der Universität München, Munich, Germany
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- Hlubek, Falk (författare)
- Pathologisches Institut der Universität München, Munich, Germany
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- Haynl, Angela (författare)
- Pathologisches Institut der Universität München, Munich, Germany
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- Kriegl, Lydia (författare)
- Pathologisches Institut der Universität München, Munich, Germany
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- Reu, Simone (författare)
- Pathologisches Institut der Universität München, Munich, Germany
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- Merkel, Susanne (författare)
- Chirurgische Kliniken der Universität Erlangen-Nürnberg, Erlangen, Germany
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- Brabletz, Thomas (författare)
- Universitätsklinikum Freiburg, Chirurgische Universitätsklinik, Freiburg, Germany
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- Kirchner, Thomas (författare)
- Pathologisches Institut der Universität München, Munich, Germany
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- Jung, Andreas (författare)
- Pathologisches Institut der Universität München, Munich, Germany
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(creator_code:org_t)
- Elsevier BV, 2009
- 2009
- Engelska.
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Ingår i: Gastroenterology. - : Elsevier BV. - 0016-5085 .- 1528-0012. ; 136:1, s. 196-205.e2
- Relaterad länk:
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- BACKGROUND & AIMS: Human colorectal carcinomas display an infiltrative front of invasion where tumor cells undergo an epithelomesenchymal transition associated with low survival. Epithelomesenchymal transition is regulated by a nuclear beta-catenin accumulation, and subsequently, activation of beta-catenin/TCF4 target genes similar to CYCLIN D(1). Unexpectedly, these tumor cells are characterized by low proliferation, which correlates with the expression of the cell cycle inhibitor p16(INK4A). Therefore, we investigated the molecular mechanism of the transcriptional regulation of p16(INK4A) in colorectal cancer and its correlation with survival. METHODS: Molecular biological techniques were used for investigating the transcriptional mechanisms of the p16(INK4A) gene regulation. Moreover, p16(INK4A) expression was correlated with the 10-year survival of patients with colorectal carcinomas. RESULTS: In colorectal carcinomas, expression of the p16(INK4A) gene is regulated by beta-catenin/TCF4 and correlates with low survival rates of patients with tumors displaying an infiltrative front of invasion. CONCLUSIONS: beta-catenin/TCF4 regulates cell cycle promoting (c-MYC, CYCLIN D(1)) and inhibiting genes (p16(INK4A)) at the same time in the mesenchymally differentiated tumor cells at the front of invasion. The function of p16(INK4A) seems to supersede in this context thus leading to low proliferation. Moreover, these tumor cells seem to govern the outcome of colorectal cancer independently of their proliferation.
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Wassermann, Stel ...
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Scheel, Silvio K
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Hiendlmeyer, Elk ...
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Palmqvist, Richa ...
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Horst, David
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Hlubek, Falk
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visa fler...
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Haynl, Angela
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Kriegl, Lydia
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Reu, Simone
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Merkel, Susanne
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Brabletz, Thomas
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Kirchner, Thomas
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Jung, Andreas
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- Artiklar i publikationen
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Gastroenterology
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Umeå universitet