Role of transforming growth factor-beta in hematologic malignancies

Blood. 2006 Jun 15;107(12):4589-96. doi: 10.1182/blood-2005-10-4169. Epub 2006 Feb 16.

Abstract

The transforming growth factor-beta (TGF-beta) signaling pathway is an essential regulator of cellular processes, including proliferation, differentiation, migration, and cell survival. During hematopoiesis, the TGF-beta 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-beta develops. Mechanisms for this resistance include mutation or deletion of members of the TGF-beta signaling pathway and disruption of the pathway by oncoproteins. These alterations define a tumor suppressor role for the TGF-beta pathway in human hematologic malignancies. On the other hand, elevated levels of TGF-beta can promote myelofibrosis and the pathogenesis of some hematologic malignancies through their effects on the stroma and immune system. Advances in the TGF-beta signaling field should enable targeting of the TGF-beta signaling pathway for the treatment of hematologic malignancies.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Differentiation* / drug effects
  • Cell Differentiation* / genetics
  • Cell Movement / drug effects
  • Cell Movement / genetics
  • Cell Proliferation / drug effects
  • Drug Resistance, Neoplasm / drug effects
  • Drug Resistance, Neoplasm / genetics
  • Hematologic Neoplasms / drug therapy
  • Hematologic Neoplasms / genetics
  • Hematologic Neoplasms / metabolism*
  • Hematologic Neoplasms / pathology
  • Hematopoiesis* / drug effects
  • Hematopoiesis* / genetics
  • Humans
  • Mutation / drug effects
  • Oncogene Proteins / genetics
  • Oncogene Proteins / metabolism*
  • Signal Transduction* / drug effects
  • Signal Transduction* / genetics
  • Transforming Growth Factor beta / genetics
  • Transforming Growth Factor beta / metabolism*

Substances

  • Oncogene Proteins
  • Transforming Growth Factor beta