Inflammation drives pressure on TP53 mutant clones in myeloproliferative neoplasms

Transformation of a myeloproliferative neoplasm to a secondary acute myeloid leukemia is rare but devastating. Single-cell, multi-omic characterization of hematopoietic stem and progenitor cells now shows the role of inflammation in transformation driven by mutations in TP53, with effects on the mutant clone but also non-mutant counterparts.

Automated summary

Single-cell, multi-omic characterization reveals the role of inflammation in the transformation from myeloproliferative neoplasm to secondary acute myeloid leukemia, affecting both mutant clones and non-mutant counterparts.