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Carcinogenesis Advance Access originally published online on May 12, 2006
Carcinogenesis 2006 27(11):2148-2156; doi:10.1093/carcin/bgl068
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Escaping from the TGFß anti-proliferative control

Joan Seoane

Institució Catalana de Recerca i Estudis Avançats (ICREA), Medical Oncology Program Vall d'Hebron University Hospital Research Institute, Barcelona, Spain

*To whom correspondence should be addressed at: Medical Oncology Program, Vall d'Hebron University Hospital Research Institute, Psg. Vall d'Hebron 119-129, 08035 Barcelona, Spain. Email: jseoane{at}ir.vhebron.net

Transforming growth factor-ß (TGFß) has a crucial role in tissue homeostasis and disruption of the TGFß pathway has been implicated in many human diseases including cancer. As a potent inhibitor of epithelial cell proliferation, TGFß is a tumor suppressor. Tumor cells evade the antitumoral effect of TGFß, either by acquiring somatic mutations that blunt TGFß signaling or by selectively preventing the cytostatic responses to TGFß. During tumor progression, TGFß not only loses the anti-proliferative response but can also become an oncogenic factor. Recent work has provided insights into the specific molecular mechanisms involved in the loss of the TGFß anti-proliferative response. This review is an overview of the mechanisms that lead to the impairment of the tumor-suppressive function of TGFß in cancer. The understanding of how the TGFß signal is disrupted in cancer might facilitate the design and development of rational and successful therapeutic strategies.


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