BMSCs and hematopoiesis

García‐García, Andrés; Castillejo, Carlos L.F. de; Méndez-Ferrer, Simón

doi:10.1016/j.imlet.2015.06.020

Cited by 52 publications

(37 citation statements)

References 96 publications

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“…They possess self-renewal and immunomodulatory capacities and could differentiate into osteoblasts, adipocytes, and chondrocytes under specific conditions (44)(45)(46). Evidence indicates that neoplastic HSCs lead to profound modification of the bone marrow niche, which in turn affects the proliferation and trafficking of HSCs in MF (6,9,11,(47)(48)(49). Although the mechanism for these profound changes in the bone marrow niche are poorly defined, recent studies reported that MSCs in MPN patients have elevated fibronectin levels and exhibit both genetic and functional aberrations (50,51 (53).…”

Section: Discussionmentioning

confidence: 99%

Efficacy of ALK5 inhibition in myelofibrosis

et al. 2017

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Section: Discussionmentioning

confidence: 99%

Efficacy of ALK5 inhibition in myelofibrosis

et al. 2017

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“…Several publications have illustrated that MSCs can sustain MK differentiation and platelet formation through both direct and indirect mechanisms. on the one hand, they can express and secret a wide range of growth factors and chemokines, including TPO, IL-6, IL-11, LIF, SCF, and SDF-1, which can mediate the indirect promoting effects of MSCs on megakaryocytic development and maturation [45,50]. Furthermore, early studies by Cheng et al [51] indicated that MSCs and MKs in the bone marrow have a direct contact with each other.…”

Section: Bone Marrow Mesenchymal Stem Cellsmentioning

confidence: 99%

The role of bone marrow microenvironment in platelet production and their implications for the treatment of thrombocytopenic diseases

Wang

2017

Hematology

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“…MSCs, together with HSCs, are generally described as the cells able to initiate BM reconstitution after mechanical injury [83, 84]. Inside the BM microenvironment, MSCs, mainly localized to line the endosteum and in perivascular region, participate to the hematopoietic niche, being essential for HSCs commitment, mobilization, and exit from the marrow compartment and give origin to all BM stromal elements, such as osteoblasts, adipocytes and chondrocytes.…”

Section: Mesenchymal Stromal Cellsmentioning

confidence: 99%

Tyrosine kinase inhibitors and mesenchymal stromal cells: effects on self-renewal, commitment and functions

et al. 2016

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The hope of selectively targeting cancer cells by therapy and eradicating definitively malignancies is based on the identification of pathways or metabolisms that clearly distinguish “normal” from “transformed” phenotypes. Some tyrosine kinase activities, specifically unregulated and potently activated in malignant cells, might represent important targets of therapy. Consequently, tyrosine kinase inhibitors (TKIs) might be thought as the “vanguard” of molecularly targeted therapy for human neoplasias. Imatinib and the successive generations of inhibitors of Bcr-Abl1 kinase, represent the major successful examples of TKI use in cancer treatment. Other tyrosine kinases have been selected as targets of therapy, but the efficacy of their inhibition, although evident, is less definite. Two major negative effects exist in this therapeutic strategy and are linked to the specificity of the drugs and to the role of the targeted kinase in non-malignant cells. In this review, we will discuss the data available on the TKIs effects on the metabolism and functions of mesenchymal stromal cells (MSCs). MSCs are widely distributed in human tissues and play key physiological roles; nevertheless, they might be responsible for important pathologies. At present, bone marrow (BM) MSCs have been studied in greater detail, for both embryological origins and functions. The available data are evocative of an unexpected degree of complexity and heterogeneity of BM-MSCs. It is conceivable that this grade of intricacy occurs also in MSCs of other organs. Therefore, in perspective, the negative effects of TKIs on MSCs might represent a critical problem in long-term cancer therapies based on such inhibitors.

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BMSCs and hematopoiesis

Cited by 52 publications

References 96 publications

Efficacy of ALK5 inhibition in myelofibrosis

Efficacy of ALK5 inhibition in myelofibrosis

The role of bone marrow microenvironment in platelet production and their implications for the treatment of thrombocytopenic diseases

Tyrosine kinase inhibitors and mesenchymal stromal cells: effects on self-renewal, commitment and functions

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