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Oncogenic Deregulation of Cell Adhesion Molecules in Leukemia

Numerous cell–cell and cell–matrix interactions within the bone marrow microenvironment enable the controlled lifelong self-renewal and progeny of hematopoietic stem and progenitor cells (HSPCs). On the cellular level, this highly mutual interaction is granted by cell adhesion molecules (CAMs) integ...

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Autores principales: Windisch, Roland, Pirschtat, Nina, Kellner, Christian, Chen-Wichmann, Linping, Lausen, Jörn, Humpe, Andreas, Krause, Daniela S., Wichmann, Christian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468598/
https://www.ncbi.nlm.nih.gov/pubmed/30841639
http://dx.doi.org/10.3390/cancers11030311
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author Windisch, Roland
Pirschtat, Nina
Kellner, Christian
Chen-Wichmann, Linping
Lausen, Jörn
Humpe, Andreas
Krause, Daniela S.
Wichmann, Christian
author_facet Windisch, Roland
Pirschtat, Nina
Kellner, Christian
Chen-Wichmann, Linping
Lausen, Jörn
Humpe, Andreas
Krause, Daniela S.
Wichmann, Christian
author_sort Windisch, Roland
collection PubMed
description Numerous cell–cell and cell–matrix interactions within the bone marrow microenvironment enable the controlled lifelong self-renewal and progeny of hematopoietic stem and progenitor cells (HSPCs). On the cellular level, this highly mutual interaction is granted by cell adhesion molecules (CAMs) integrating differentiation, proliferation, and pro-survival signals from the surrounding microenvironment to the inner cell. However, cell–cell and cell–matrix interactions are also critically involved during malignant transformation of hematopoietic stem/progenitor cells. It has become increasingly apparent that leukemia-associated gene products, such as activated tyrosine kinases and fusion proteins resulting from chromosomal translocations, directly regulate the activation status of adhesion molecules, thereby directing the leukemic phenotype. These observations imply that interference with adhesion molecule function represents a promising treatment strategy to target pre-leukemic and leukemic lesions within the bone marrow niche. Focusing on myeloid leukemia, we provide a current overview of the mechanisms by which leukemogenic gene products hijack control of cellular adhesion to subsequently disturb normal hematopoiesis and promote leukemia development.
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spelling pubmed-64685982019-04-24 Oncogenic Deregulation of Cell Adhesion Molecules in Leukemia Windisch, Roland Pirschtat, Nina Kellner, Christian Chen-Wichmann, Linping Lausen, Jörn Humpe, Andreas Krause, Daniela S. Wichmann, Christian Cancers (Basel) Review Numerous cell–cell and cell–matrix interactions within the bone marrow microenvironment enable the controlled lifelong self-renewal and progeny of hematopoietic stem and progenitor cells (HSPCs). On the cellular level, this highly mutual interaction is granted by cell adhesion molecules (CAMs) integrating differentiation, proliferation, and pro-survival signals from the surrounding microenvironment to the inner cell. However, cell–cell and cell–matrix interactions are also critically involved during malignant transformation of hematopoietic stem/progenitor cells. It has become increasingly apparent that leukemia-associated gene products, such as activated tyrosine kinases and fusion proteins resulting from chromosomal translocations, directly regulate the activation status of adhesion molecules, thereby directing the leukemic phenotype. These observations imply that interference with adhesion molecule function represents a promising treatment strategy to target pre-leukemic and leukemic lesions within the bone marrow niche. Focusing on myeloid leukemia, we provide a current overview of the mechanisms by which leukemogenic gene products hijack control of cellular adhesion to subsequently disturb normal hematopoiesis and promote leukemia development. MDPI 2019-03-05 /pmc/articles/PMC6468598/ /pubmed/30841639 http://dx.doi.org/10.3390/cancers11030311 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Windisch, Roland
Pirschtat, Nina
Kellner, Christian
Chen-Wichmann, Linping
Lausen, Jörn
Humpe, Andreas
Krause, Daniela S.
Wichmann, Christian
Oncogenic Deregulation of Cell Adhesion Molecules in Leukemia
title Oncogenic Deregulation of Cell Adhesion Molecules in Leukemia
title_full Oncogenic Deregulation of Cell Adhesion Molecules in Leukemia
title_fullStr Oncogenic Deregulation of Cell Adhesion Molecules in Leukemia
title_full_unstemmed Oncogenic Deregulation of Cell Adhesion Molecules in Leukemia
title_short Oncogenic Deregulation of Cell Adhesion Molecules in Leukemia
title_sort oncogenic deregulation of cell adhesion molecules in leukemia
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468598/
https://www.ncbi.nlm.nih.gov/pubmed/30841639
http://dx.doi.org/10.3390/cancers11030311
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