The SPS affair: a complex tale of illicit proliferation

Cancer Cell. 2009 Aug 4;16(2):87-8. doi: 10.1016/j.ccr.2009.07.005.

Abstract

In this issue of Cancer Cell, Xiao et al. report that PLC-beta3 mutant mice develop myeloprolfierative neoplasms and show that tumor suppressor activity does not require PLC-beta3 catalytic activity. Instead, PLC-beta3 forms a complex with SHP-1 and Stat5 that facilitates Stat5 dephosphorylation. A similar mechanism may be operative in some human leukemias.

Publication types

  • Comment

MeSH terms

  • Animals
  • Cell Differentiation
  • Cell Proliferation*
  • Cell Survival / genetics
  • Lymphoma / genetics
  • Lymphoma / metabolism*
  • Lymphoma / pathology
  • Mice
  • Mutation
  • Myeloproliferative Disorders / genetics
  • Myeloproliferative Disorders / metabolism*
  • Myeloproliferative Disorders / pathology
  • Phospholipase C beta / genetics
  • Phospholipase C beta / metabolism
  • Phospholipase C beta / physiology*
  • Phosphorylation
  • Protein Tyrosine Phosphatase, Non-Receptor Type 6 / genetics
  • Protein Tyrosine Phosphatase, Non-Receptor Type 6 / metabolism
  • Protein Tyrosine Phosphatase, Non-Receptor Type 6 / physiology*
  • STAT5 Transcription Factor / genetics
  • STAT5 Transcription Factor / metabolism*
  • STAT5 Transcription Factor / physiology
  • Signal Transduction

Substances

  • STAT5 Transcription Factor
  • Protein Tyrosine Phosphatase, Non-Receptor Type 6
  • Ptpn6 protein, mouse
  • Phospholipase C beta