Case for inflammatory memory for hematopoietic stem and progenitor cells in AML niche

“In this research perspective, we discuss recent work from our lab describing an active role of HSPCs in AML and the potential implications.”

BUFFALO, NY- September 5, 2024 – A new research perspective was published in Oncotarget's Volume 15 on September 4, 2024, entitled, “Trained and ready - the case for an inflammatory memory for hematopoietic stem and progenitor cells in the AML niche.”

As noted in the abstract of this paper, lifelong hematopoiesis is sustained by the crosstalk between hematopoietic stem and progenitor cells (HSPCs) and specialized bone marrow niches. Acute myeloid leukemia (AML) disrupts this balance, as leukemic blasts secrete factors that remodel the bone marrow into a self-reinforcing leukemic niche. Additionally, HSPCs are key components of the innate immune system. Over the past decade, elegant studies of infection and experimental inflammation have demonstrated the generation of an adoptively transferable, innate immune memory.

In their research perspective, Ding-Wen Chen, Eric K. Wafula, and Peter Kurre from the Department of Pediatrics, Comprehensive Bone Marrow Failure Center, Division of Hematology and the Department of Biomedical and Health Informatics at the Children’s Hospital of Philadelphia, and the Perelman School of Medicine at the University of Pennsylvania, discuss recent findings from their lab on the active role of HSPCs in AML and its potential implications.

“Considering the abundant evidence for AML associated inflammation, and the involvement of healthy HSPCs discussed in our study, the question arises whether sterile cancer-associated inflammation also has long-term functional consequences.”

Continue reading: DOI: https://doi.org/10.18632/oncotarget.28642

Correspondence to: Ding-Wen Chen - chend5@chop.edu, and Peter Kurre - kurrep@chop.edu

Video short: https://www.youtube.com/watch?v=lY382scWJUI

Keywords: cancer, hematopoietic stem and progenitor cells, acute myeloid leukemia, inflammation, innate immune reprogramming, trained immunity

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