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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Related Experiment Video

Updated: Dec 13, 2025

Author Spotlight: Analyzing Bone Marrow Microenvironment in Murine Hematological Malignancies
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Targeting the Microenvironment in MDS: The Final Frontier.

Patric Teodorescu1,2, Sergiu Pasca1, Delia Dima1

  • 1Department of Hematology, Iuliu Hategan University of Medicine and Pharmacy, Cluj-Napoca, Romania.

Frontiers in Pharmacology
|August 4, 2020
PubMed
Summary
This summary is machine-generated.

Myelodysplastic syndromes (MDS) involve malignant cells disrupting the bone marrow microenvironment (BME), harming normal cells. Therapies should target both malignant cells and the BME for successful treatment.

Keywords:
CYP26 enzymesall-trans retinoic acidazacytidinelenalidomideluspaterceptmicroenvironmentmyelodyslastic syndromesrigosertib

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Area of Science:

  • Hematology
  • Oncology
  • Stem Cell Biology

Background:

  • Myelodysplastic syndromes (MDS) are clonal hematopoietic stem and progenitor cell (HSPC) disorders.
  • MDS is characterized by ineffective hematopoiesis, leading to peripheral cytopenias and bone marrow failure.
  • Malignant MDS cells manipulate the bone marrow microenvironment (BME) to maintain clonal dominance.

Purpose of the Study:

  • To review how current and emerging MDS therapies may reprogram the bone marrow microenvironment (BME).
  • To understand the role of the BME in MDS pathogenesis and treatment resistance.

Main Methods:

  • Review of current literature on MDS pathogenesis and therapeutic strategies.
  • Analysis of the impact of malignant cells on the BME in MDS.
  • Synopsis of drug mechanisms targeting both malignant cells and the BME.

Main Results:

  • MDS cells create a BME detrimental to normal hematopoiesis and allogeneic HSPC engraftment.
  • The disturbed BME contributes to cytopenias and treatment challenges in MDS.
  • Current and investigational MDS drugs show potential for BME modulation.

Conclusions:

  • Targeting the BME is crucial for effective MDS therapy.
  • Reprogramming the BME alongside direct anti-MDS cell action offers a promising therapeutic avenue.
  • Future MDS treatments should integrate BME-modulating strategies for improved patient outcomes.