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Blood, 15 June 2006, Vol. 107, No. 12, pp. 4589-4596. Prepublished online as a Blood First Edition Paper on February 16, 2006; DOI 10.1182/blood-2005-10-4169. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-10-4169v1 107/12/4589    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Dong, M. Articles by Blobe, G. C. Search for Related Content PubMed PubMed Citation Articles by Dong, M. Articles by Blobe, G. C. Related Collections Neoplasia Apoptosis Cell Cycle Oncogenes and Tumor Suppressors Signal Transduction Review Articles Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  REVIEW IN TRANSLATIONAL HEMATOLOGY Role of transforming growth factor- in hematologic malignancies Mei Dong, and Gerard C. Blobe From the Department of Medicine and Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC. Abstract The transforming growth factor- (TGF-) signaling pathway is an essential regulator of cellular processes, including proliferation, differentiation, migration, and cell survival. During hematopoiesis, the TGF- signaling pathway is a potent negative regulator of proliferation while stimulating differentiation and apoptosis when appropriate. In hematologic malignancies, including leukemias, myeloproliferative disorders, lymphomas, and multiple myeloma, resistance to these homeostatic effects of TGF- develops. Mechanisms for this resistance include mutation or deletion of members of the TGF- signaling pathway and disruption of the pathway by oncoproteins. These alterations define a tumor suppressor role for the TGF- pathway in human hematologic malignancies. On the other hand, elevated levels of TGF- can promote myelofibrosis and the pathogenesis of some hematologic malignancies through their effects on the stroma and immune system. Advances in the TGF- signaling field should enable targeting of the TGF- signaling pathway for the treatment of hematologic malignancies. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. B. Baughn, M. Di Liberto, R. Niesvizky, H. J. Cho, D. Jayabalan, J. Lane, F. Liu, and S. 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