The Hematopoietic Niche in Myeloproliferative Neoplasms
Specialized microanatomical areas of the bone marrow provide the signals that are mandatory for the maintenance and regulation of hematopoietic stem cells (HSCs) and progenitor cells. A complex microenvironment adjacent to the marrow vasculature (vascular niche) and close to the endosteum (endosteal...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2015/347270 |
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| author | Annette H. Schmitt-Graeff Roland Nitschke Robert Zeiser |
| author_facet | Annette H. Schmitt-Graeff Roland Nitschke Robert Zeiser |
| author_sort | Annette H. Schmitt-Graeff |
| collection | DOAJ |
| description | Specialized microanatomical areas of the bone marrow provide the signals that are mandatory for the maintenance and regulation of hematopoietic stem cells (HSCs) and progenitor cells. A complex microenvironment adjacent to the marrow vasculature (vascular niche) and close to the endosteum (endosteal niche) harbors multiple cell types including mesenchymal stromal cells and their derivatives such as CAR cells expressing high levels of chemokines C-X-C motif ligand 12 and early osteoblastic lineage cells, endothelial cells, and megakaryocytes. The characterization of the cellular and molecular networks operating in the HSC niche has opened new perspectives for the understanding of the bidirectional cross-talk between HSCs and stromal cell populations in normal and malignant conditions. A structural and functional remodeling of the niche may contribute to the development of myeloproliferative neoplasms (MPN). Malignant HSCs may alter the function and survival of MSCs that do not belong to the neoplastic clone. For example, a regression of nestin+ MSCs by apoptosis has been attributed to neuroglial damage in MPN. Nonneoplastic MSCs in turn can promote aggressiveness and drug resistance of malignant cells. In the future, strategies to counteract the pathological interaction between the niche and neoplastic HSCs may offer additional treatment strategies for MPN patients. |
| format | Article |
| id | doaj-art-91f2d4754d34494eaf8c11a6e9d26cbd |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-91f2d4754d34494eaf8c11a6e9d26cbd2025-02-03T06:06:35ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/347270347270The Hematopoietic Niche in Myeloproliferative NeoplasmsAnnette H. Schmitt-Graeff0Roland Nitschke1Robert Zeiser2Department of Pathology, Freiburg University Medical Center, Albert-Ludwigs University, 79106 Freiburg, GermanyLife Imaging Center, Center for Biological Systems Analysis (ZBSA), Albert-Ludwigs University, 79104 Freiburg, GermanyDepartment of Hematology and Oncology, Freiburg University Medical Center, Albert-Ludwigs University, 79106 Freiburg, GermanySpecialized microanatomical areas of the bone marrow provide the signals that are mandatory for the maintenance and regulation of hematopoietic stem cells (HSCs) and progenitor cells. A complex microenvironment adjacent to the marrow vasculature (vascular niche) and close to the endosteum (endosteal niche) harbors multiple cell types including mesenchymal stromal cells and their derivatives such as CAR cells expressing high levels of chemokines C-X-C motif ligand 12 and early osteoblastic lineage cells, endothelial cells, and megakaryocytes. The characterization of the cellular and molecular networks operating in the HSC niche has opened new perspectives for the understanding of the bidirectional cross-talk between HSCs and stromal cell populations in normal and malignant conditions. A structural and functional remodeling of the niche may contribute to the development of myeloproliferative neoplasms (MPN). Malignant HSCs may alter the function and survival of MSCs that do not belong to the neoplastic clone. For example, a regression of nestin+ MSCs by apoptosis has been attributed to neuroglial damage in MPN. Nonneoplastic MSCs in turn can promote aggressiveness and drug resistance of malignant cells. In the future, strategies to counteract the pathological interaction between the niche and neoplastic HSCs may offer additional treatment strategies for MPN patients.http://dx.doi.org/10.1155/2015/347270 |
| spellingShingle | Annette H. Schmitt-Graeff Roland Nitschke Robert Zeiser The Hematopoietic Niche in Myeloproliferative Neoplasms Mediators of Inflammation |
| title | The Hematopoietic Niche in Myeloproliferative Neoplasms |
| title_full | The Hematopoietic Niche in Myeloproliferative Neoplasms |
| title_fullStr | The Hematopoietic Niche in Myeloproliferative Neoplasms |
| title_full_unstemmed | The Hematopoietic Niche in Myeloproliferative Neoplasms |
| title_short | The Hematopoietic Niche in Myeloproliferative Neoplasms |
| title_sort | hematopoietic niche in myeloproliferative neoplasms |
| url | http://dx.doi.org/10.1155/2015/347270 |
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