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The Bone Marrow Microenvironment in Myelodysplastic Syndromes—Pathogenesis, Immune Evasion, and Therapeutic Opportunities

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 15 October 2026 | Viewed by 6317

Special Issue Editor

Prof. Dr. Ciro Roberto Rinaldi

E-Mail Website
Guest Editor
United Lincolnshire Hospitals NHS Trust, Lincoln, UK
Interests: haematology; MPN/MDS

Special Issue Information

Dear Colleagues,

Myelodysplastic syndromes (MDS) are clonal hematopoietic disorders characterized by ineffective hematopoiesis, bone marrow dysplasia, and a risk of progression to acute myeloid leukemia. Emerging evidence has underscored the crucial role of the bone marrow microenvironment (BMME) not only as a passive background but as an active participant in disease initiation, maintenance, and progression. The BMME—a complex network of mesenchymal stromal cells, endothelial cells, immune components, and extracellular matrix—is profoundly disrupted in MDS. Dysregulated stromal support, persistent inflammatory cytokine signalling, and immunological dysfunction contribute to the apoptosis of progenitor cell and selective pressure favoring malignant clonal expansion.

This Special Issue aims to explore the multifaceted alterations of the BMME in MDS, including stromal cell dysfunction, inflammatory milieu (e.g., IL-6, TNF-α), immune escape via the overexpression of CD47, and the suppression of “eat-me” signals such as calreticulin. We welcome original research and reviews that focus on molecular mechanisms, in vivo modelling, immunotherapeutic approaches, and stromal-targeting interventions that could restore normal hematopoiesis or reverse immune evasion in MDS.

This Special Issue seeks to stimulate a cross-disciplinary dialogue between hematologists, immunologists, and cancer biologists, and to provide an overview of recent advances in MDS pathophysiology and therapy by focusing on the tumor-supportive ecosystem of the bone marrow.

Prof. Dr. Ciro Roberto Rinaldi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • myelodysplastic syndromes
  • bone marrow microenvironment
  • hematopoietic stem cells
  • mesenchymal stromal cells
  • immune evasion
  • CD47
  • calreticulin
  • inflammatory cytokines
  • clonal hematopoiesis
  • microenvironment-targeted therapy

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Published Papers (2 papers)

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Review

29 pages, 1433 KB  
Review
Myeloid Malignancies Beyond the Cell: Targeting the Tumour Microenvironment with Next-Generation Immunotherapies
by Niloofar Amirian, Anya Squires, Lauretta Azanabor, Claire L. Walker, Matthew J. Simmonds and Ciro Rinaldi
Cancers 2026, 18(11), 1808; https://doi.org/10.3390/cancers18111808 - 1 Jun 2026
Viewed by 369
Abstract
Myeloid malignancies encompass a heterogeneous group of haematological disorders, primarily including myelodysplastic syndromes (MDSs) and myeloproliferative neoplasms (MPNs). MDS is characterised by defective myeloid cell maturation, while MPNs involve the pathological overproduction of myeloid lineage cells. In the absence of timely diagnosis and [...] Read more.
Myeloid malignancies encompass a heterogeneous group of haematological disorders, primarily including myelodysplastic syndromes (MDSs) and myeloproliferative neoplasms (MPNs). MDS is characterised by defective myeloid cell maturation, while MPNs involve the pathological overproduction of myeloid lineage cells. In the absence of timely diagnosis and effective clinical intervention, both entities carry a substantial risk of progression to acute myeloid leukaemia (AML). Although allogeneic haematopoietic stem cell transplantation remains the only potentially curative therapy, its application is frequently constrained by patient-related factors such as advanced age and comorbid conditions. While currently, hypomethylating agent therapy (azacitidine and decitabine) is mainly used in high-risk MDS patients, and ruxolitinib is primarily used in symptomatic primary myelofibrosis (PMF-MPN), their clinical efficacy remains suboptimal. More recently, focus has turned toward the role of the tumour microenvironment (TME) in disease pathogenesis and whether therapeutically targeting the TME, either alone or in combination with conventional therapy, could present a new treatment option. Emerging evidence underscores the significant influence of TME components, particularly macrophages and T cells, in modulating immune responses and shaping the leukaemic niche to either facilitate or hinder malignant progression. In response, a new generation of immune checkpoint inhibitors are being developed to target the TME, including PD-1/CTLA-4 blockers, macrophage-directed agents including CD47 inhibitors, and T cell-targeting checkpoint inhibitors such as TIM-1 and LAG-3. This review will describe the functional role of key TME constituents in the progression of myeloid malignancies and explore the current landscape and future potential of advanced cellular and molecular immunotherapies in the treatment of these disorders. Full article
(This article belongs to the Special Issue The Bone Marrow Microenvironment in Myelodysplastic Syndromes—Pathogenesis, Immune Evasion, and Therapeutic Opportunities)
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19 pages, 1529 KB  
Review
Marrow Microenvironmental Pathobiology and Therapeutic Opportunities for TP53-Mutated Myelodysplastic Syndrome/Acute Myeloid Leukemia
by Cameron J. Hunter, Annie P. Im and Rory M. Shallis
Cancers 2026, 18(2), 275; https://doi.org/10.3390/cancers18020275 - 16 Jan 2026
Cited by 1 | Viewed by 2786
Abstract
Mutations in TP53 inhibit p53 protective behaviors including cell cycle arrest, DNA damage repair protein recruitment, and apoptosis. The ubiquity of p53 in genome-stabilizing functions leads to an aberrant tumor microenvironment in TP53-mutated myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Profound [...] Read more.
Mutations in TP53 inhibit p53 protective behaviors including cell cycle arrest, DNA damage repair protein recruitment, and apoptosis. The ubiquity of p53 in genome-stabilizing functions leads to an aberrant tumor microenvironment in TP53-mutated myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Profound immunosuppression mediated by myeloid-derived suppressor cells, the upregulation of cytokines and cell-surface receptors on leukemic cells, the suppression of native immune regulator cells, and metabolic aberrations in the bone marrow are features of the TP53-mutated AML/MDS marrow microenvironment. These localized changes in the bone marrow microenvironment (BMME) explain why traditional therapies for MDS/AML, including chemotherapeutics and hypomethylating agents, are not as effective in TP53-mutated myeloid neoplasms and demonstrate the dire need for new treatments in this patient population. The unique pathophysiology of TP53-mutated disease also provides new therapeutic approaches which are being studied, including intracellular targets (MDM2, p53), cell-surface protein biologics (immune checkpoint inhibitors, BiTE therapy, and antibody–drug conjugates), cell therapies (CAR-T, NK-cell), signal transduction pathways (Hedgehog, Wnt, NF-κB, CCRL2, and HIF-1α), and co-opted biologic pathways (cholesterol synthesis and glycolysis). In this review, we will discuss the pathophysiologic anomalies of the tumor microenvironment in TP53-mutant MDS/AML, the hypothesized mechanisms of chemoresistance it imparts, and how novel therapies are leveraging diverse therapeutic targets to address this critical area of need. Full article
(This article belongs to the Special Issue The Bone Marrow Microenvironment in Myelodysplastic Syndromes—Pathogenesis, Immune Evasion, and Therapeutic Opportunities)
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