DNA distress creates lethal opportunity in MPN

Research output: Contribution to journalReview article

Abstract

In this issue of Blood, Nieborowska-Skorska et al show that exposure of myeloproliferative neoplasm (MPN) cells to the JAK inhibitor, ruxolitinib, results in blockage of DNA damage repair pathways, thereby exacerbating double-strand DNA breaks and creating a synthetic lethal susceptibility to poly-ADP-ribose polymerase (PARP) inhibitors. Consequently, the combination of ruxolitinib with PARP inhibitors leads to elimination of quiescent and proliferating MPN leukemic stem/progenitor cells in vitro and in mouse models.

Original languageEnglish (US)
Pages (from-to)2814-2816
Number of pages3
JournalBlood
Volume130
Issue number26
DOIs
StatePublished - Dec 28 2017

Fingerprint

Stem Cells
Double-Stranded DNA Breaks
DNA
Stem cells
DNA Repair
DNA Damage
Neoplasms
Repair
Blood
INCB018424
Poly(ADP-ribose) Polymerase Inhibitors
In Vitro Techniques

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

Cite this

DNA distress creates lethal opportunity in MPN. / Tyner, Jeffrey.

In: Blood, Vol. 130, No. 26, 28.12.2017, p. 2814-2816.

Research output: Contribution to journalReview article

Tyner, Jeffrey. / DNA distress creates lethal opportunity in MPN. In: Blood. 2017 ; Vol. 130, No. 26. pp. 2814-2816.
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