Transforming growth factor-beta signaling in normal and malignant hematopoiesis

J Interferon Cytokine Res. 2007 Jul;27(7):543-52. doi: 10.1089/jir.2007.0009.

Abstract

Transforming growth factor-beta (TGF-beta) is an important physiologic regulator of cell growth and differentiation. TGF-beta has been shown to inhibit the proliferation of quiescent hematopoietic stem cells and stimulate the differentiation of late progenitors to erythroid and myeloid cells. Insensitivity to TGF-beta is implicated in the pathogenesis of many myeloid and lymphoid neoplasms. Loss of extracellular TGF receptors and disruption of intracellular TGF-beta signaling by oncogenes is seen in a variety of malignant and premalignant states. TGF-beta can also affect tumor growth and survival by influencing the secretion of other growth factors and manipulation of the tumor microenvironment. Recent development of small molecule inhibitors of TGF-beta receptors and other signaling intermediaries may allow us to modulate TGF signaling for future therapeutic interventions in cancer.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Hematopoiesis*
  • Humans
  • Leukemia / blood
  • Leukemia / drug therapy
  • Leukemia / metabolism*
  • Lymphoma / blood
  • Lymphoma / drug therapy
  • Lymphoma / metabolism*
  • Multiple Myeloma / blood
  • Multiple Myeloma / drug therapy
  • Multiple Myeloma / metabolism
  • Myelodysplastic Syndromes / blood
  • Myelodysplastic Syndromes / drug therapy*
  • Myelodysplastic Syndromes / metabolism*
  • Receptors, Transforming Growth Factor beta / blood
  • Receptors, Transforming Growth Factor beta / metabolism*
  • Signal Transduction
  • Transforming Growth Factor beta / biosynthesis
  • Transforming Growth Factor beta / blood
  • Transforming Growth Factor beta / metabolism*

Substances

  • Receptors, Transforming Growth Factor beta
  • Transforming Growth Factor beta