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Updated: Oct 23, 2025

Bioengineering of Humanized Bone Marrow Microenvironments in Mouse and Their Visualization by Live Imaging
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Published on: August 1, 2017

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NFĸB Targeting in Bone Marrow Mesenchymal Stem Cell-Mediated Support of Age-Linked Hematological Malignancies

Lauren S Sherman1,2, Shyam A Patel3, Marianne D Castillo1,2

  • 1Department of Medicine, Hematology/Oncology, Rutgers New Jersey Medical School, Newark, NJ, USA.

Stem Cell Reviews and Reports
|August 19, 2021
PubMed

Insights

Mesenchymal stem cells (MSCs) dysfunction in hematological disorders, particularly acute myeloid leukemia (AML), impacts bone marrow microenvironment. Targeting NFκB in MSCs may offer new therapeutic strategies for leukemia.

Area of Science:

  • Hematology
  • Stem Cell Biology
  • Immunology

Background:

  • Mesenchymal stem cells (MSCs) play a crucial role in the bone marrow (BM) microenvironment.
  • MSC dysfunction is observed in various hematological disorders.
  • The interplay between MSCs and hematological malignancies, especially during disease progression, remains incompletely understood.

Purpose of the Study:

  • To investigate the functional status of MSCs in patients with hematological disorders.
  • To explore the role of MSCs in the transition to acute myeloid leukemia (AML).
  • To identify potential therapeutic targets within MSCs for leukemia treatment.

Main Methods:

  • Analysis of MSC function, including MHC-II expression and differentiation capacity, in patients with hematological disorders.
  • Retrospective study evaluating MSC phenotype in patients with bone marrow fibrosis.
  • Investigation of NFκB signaling pathway in MSCs and its impact on leukemic cells.

Main Results:

  • MSCs from most hematological disorder patients showed decreased MHC-II expression, except in one AML case.
  • AML MSCs exhibited impaired differentiation and increased proliferation, forming foci-like structures.
  • A significant increase in MSCs was observed in patients with bone marrow fibrosis, suggesting a role in leukemia transition.
  • NFκB was identified as crucial for MSC function and a potential target to sensitize leukemic cells to azacitidine.

Conclusions:

  • MSC dysfunction is a feature of hematological disorders, with unique alterations in AML.
  • MSCs may contribute to the progression of hematological disorders towards AML.
  • Targeting the NFκB pathway in MSCs presents a promising strategy for combination therapy against leukemia stem cells.
Keywords:
AzacytidineBone marrowBortezomibLeukemiaMesenchymal stem cellMyelodysplasiaMyeloproliferative disorder

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