Inflammation-driven activation of JAK/STAT signaling reversibly accelerates acute myeloid leukemia in vitro.

ABSTRACT: Acute myeloid leukemia (AML) is characterized by a high relapse rate and dismal long-term overall survival which is related to persistence of leukemia-initiating cells in their niche. Different animal models of myeloid malignancies reveal how neoplastic cells alter the structural and functional characteristics of the hematopoietic stem cell niche to reinforce malignancy. Understanding and disruption of the microenvironmental interactions with AML cells are a vital need. Malignant niches frequently go along with inflammatory responses, but their impact on cancerogenesis often remains unexplored. Here, we uncovered an aberrant production of inflammatory cytokines in untreated AML bone marrow that was proved to promote the proliferation of leukemia cells. This inflammatory response induced an

SUBMITTER: Habbel J 

PROVIDER: S-EPMC7362361 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature