The relevance of the hematopoietic niche for therapy resistance in acute myeloid leukemia

The expansion of acute myeloid leukemia (AML) blasts not only suppresses normal hematopoiesis, but also alters the microenvironment. The interplay of different components of the bone marrow gives rise to altered metabolic states and activates signaling pathways which lead to resistance and impede ef...

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Published inInternational journal of cancer Vol. 154; no. 2; pp. 197 - 209
Main Authors Allert, Catana, Müller‐Tidow, Carsten, Blank, Maximilian Felix
Format Journal Article
LanguageEnglish
Published Hoboken, USA John Wiley & Sons, Inc 15.01.2024
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Abstract The expansion of acute myeloid leukemia (AML) blasts not only suppresses normal hematopoiesis, but also alters the microenvironment. The interplay of different components of the bone marrow gives rise to altered metabolic states and activates signaling pathways which lead to resistance and impede effective therapy. Therefore, the underlying processes and mechanisms represent attractive therapeutic leverage points for overcoming therapy resistance in AML. Here, we briefly discuss resistance mechanisms based on cell interactions and secreted soluble factors in the hematopoietic niche and provide an overview of niche‐related therapeutic targets currently undergoing preclinical and clinical investigation which may help improve the outcome in AML therapy.
AbstractList The expansion of acute myeloid leukemia (AML) blasts not only suppresses normal hematopoiesis, but also alters the microenvironment. The interplay of different components of the bone marrow gives rise to altered metabolic states and activates signaling pathways which lead to resistance and impede effective therapy. Therefore, the underlying processes and mechanisms represent attractive therapeutic leverage points for overcoming therapy resistance in AML. Here, we briefly discuss resistance mechanisms based on cell interactions and secreted soluble factors in the hematopoietic niche and provide an overview of niche‐related therapeutic targets currently undergoing preclinical and clinical investigation which may help improve the outcome in AML therapy.
Abstract The expansion of acute myeloid leukemia (AML) blasts not only suppresses normal hematopoiesis, but also alters the microenvironment. The interplay of different components of the bone marrow gives rise to altered metabolic states and activates signaling pathways which lead to resistance and impede effective therapy. Therefore, the underlying processes and mechanisms represent attractive therapeutic leverage points for overcoming therapy resistance in AML. Here, we briefly discuss resistance mechanisms based on cell interactions and secreted soluble factors in the hematopoietic niche and provide an overview of niche‐related therapeutic targets currently undergoing preclinical and clinical investigation which may help improve the outcome in AML therapy.
Author Müller‐Tidow, Carsten
Blank, Maximilian Felix
Allert, Catana
Author_xml – sequence: 1
  givenname: Catana
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  givenname: Carsten
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  fullname: Müller‐Tidow, Carsten
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  surname: Blank
  fullname: Blank, Maximilian Felix
  email: maximilianfelix.blank@med.uni-heidelberg.de
  organization: German Cancer Research Center (DKFZ)
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Keywords cell adhesion-mediated drug resistance
niche related therapies
soluble factor-mediated drug resistance
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Snippet The expansion of acute myeloid leukemia (AML) blasts not only suppresses normal hematopoiesis, but also alters the microenvironment. The interplay of different...
Abstract The expansion of acute myeloid leukemia (AML) blasts not only suppresses normal hematopoiesis, but also alters the microenvironment. The interplay of...
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SubjectTerms Acute myeloid leukemia
Cancer
Cancer research
cell adhesion‐mediated drug resistance
Cell interactions
Clinical trials
Hematology
Hemopoiesis
Medical research
Microenvironments
niche related therapies
soluble factor‐mediated drug resistance
Targeted cancer therapy
Therapeutic targets
Title The relevance of the hematopoietic niche for therapy resistance in acute myeloid leukemia
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fijc.34684
https://www.ncbi.nlm.nih.gov/pubmed/37565773
https://www.proquest.com/docview/2892161109
https://search.proquest.com/docview/2850311771
Volume 154
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