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Publications

Journal Article Review Ppublish

PubMed: 42594808 DOI: 10.1016/j.cytogfr.2026.08.001

Inflammatory mechanisms in the AML bone marrow niche: From pathogenesis to therapy.

Cytokine Growth Factor Rev 91:99-109

Authors: Toon Suls, Eva Lion, Florian Van Oers, Eva De Backer, Elena Lasorsa, Sébastien Anguille

Affiliations

  • Laboratory of Experimental Hematology, Vaccine & Infectious Disease Institute (VAXINFECTIO), Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium; Johnson & Johnson, Oncology Discovery, Beerse, Belgium.
  • Laboratory of Experimental Hematology, Vaccine & Infectious Disease Institute (VAXINFECTIO), Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium.
  • Laboratory of Experimental Hematology, Vaccine & Infectious Disease Institute (VAXINFECTIO), Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium; Center for Cell Therapy & Regenerative Medicine and Division of Hematology, Antwerp University Hospital, Edegem, Belgium.
  • Johnson & Johnson, Oncology Discovery, Beerse, Belgium.
  • Laboratory of Experimental Hematology, Vaccine & Infectious Disease Institute (VAXINFECTIO), Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium; Center for Cell Therapy & Regenerative Medicine and Division of Hematology, Antwerp University Hospital, Edegem, Belgium.

Abstract

Acute myeloid leukemia (AML) is a highly aggressive hematologic malignancy in which inflammatory signaling plays a pivotal role in disease pathogenesis. The dysregulation of the cytokine network leads to an increased abundance of pro-inflammatory mediators, such as IL-1β, TNF-α and IL-6, relative to anti-inflammatory cytokines like TGF-β and CXCL12. This disbalance in cytokine levels is closely associated with tumor development and fosters a pro-tumorigenic microenvironment by facilitating leukemic cell proliferation, reducing survival rates, and promoting drug resistance. In addition, inflammatory cytokines have been shown to preferentially support hematopoietic stem and progenitor cell populations harboring mutations associated with clonal hematopoiesis. This review summarizes the current knowledge on inflammatory cytokines and signaling pathways in AML, focusing on: (i) their mechanisms of action and implications for immune tolerance and clonal hematopoiesis and (ii) the emerging therapeutic strategies targeting these pathways to improve clinical outcomes for patients with AML.

MeSH

Cytokines, Cells, Hematopoiesis, Bone Marrow, Neoplasms, Clonal Hematopoiesis, Therapeutics