Cargando…
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...
Autores principales: | , , , , , , , |
---|---|
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 |
_version_ | 1783411470506131456 |
---|---|
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. |
format | Online Article Text |
id | pubmed-6468598 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT windischroland oncogenicderegulationofcelladhesionmoleculesinleukemia AT pirschtatnina oncogenicderegulationofcelladhesionmoleculesinleukemia AT kellnerchristian oncogenicderegulationofcelladhesionmoleculesinleukemia AT chenwichmannlinping oncogenicderegulationofcelladhesionmoleculesinleukemia AT lausenjorn oncogenicderegulationofcelladhesionmoleculesinleukemia AT humpeandreas oncogenicderegulationofcelladhesionmoleculesinleukemia AT krausedanielas oncogenicderegulationofcelladhesionmoleculesinleukemia AT wichmannchristian oncogenicderegulationofcelladhesionmoleculesinleukemia |