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MAP3K7 is recurrently deleted in pediatric T-lymphoblastic leukemia and affects cell proliferation independently of NF-κB.

David M Cordas Dos SantosJuliane EilersAlfonso Sosa VizcainoElena OrlovaMartin ZimmermannMartin StanullaMartin SchrappeKathleen BörnerDirk GrimmMartina U MuckenthalerAndreas E KulozikJoachim B Kunz
Published in: BMC cancer (2018)
This study revealed that the recurrent deletion of MAP3K7/CASP8AP2 is associated with SIL-TAL1 fusions and a mature immunophenotype, but not with response to treatment and risk of relapse. Homozygous deletions of MAP3K7 were not observed, and efficient depletion of MAP3K7 interfered with viability of T-ALL cells, indicating that a residual expression of MAP3K7 is indispensable for T-lymphoblasts.
Keyphrases
  • high density
  • cell proliferation
  • signaling pathway
  • induced apoptosis
  • poor prognosis
  • pi k akt
  • cell cycle arrest
  • single cell
  • young adults
  • immune response
  • cell cycle
  • toll like receptor