A tale of two alleles: TP53 and transformation in MPNs

In this issue of Blood, Li et al harness an elegant series of preclinical models to address 3 questions in the biology of myeloproliferative neoplasms (MPNs). They ask how the TP53 allelic state promotes leukemic transformation; what the cellular origin of the resultant leukemia is; and whether the TP53 mutant clones bear specific vulnerabilities amenable to therapeutic exploitation.(1)

Automated summary

In this study, Li et al used preclinical models to address three questions in the biology of myeloproliferative neoplasms (MPNs): how the TP53 allelic state promotes leukemic transformation, the cellular origin of the resultant leukemia, and whether TP53 mutant clones have specific vulnerabilities for therapeutic exploitation.