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Background: Leukemic cell adhesion to proteins of the bone marrow microenvironment provides signals which control morphology, motility and cell survival.
The bone marrow microenvironment provides protection to acute lymphoblastic leukemia (ALL) cells against drug treatment and is a frequent site of leukemia relapse.
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While the mechanisms have not been fully elucidated, it is clear that obesity-related chronic inflammatory stimuli to the bone marrow microenvironment provide a unique niche for interaction between mesenchymal stromal/stem cells (BMSCs) and hematopoietic stem cells (HSCs) [ 40].
Therapeutic targeting of these stromal cells within the bone marrow microenvironment, specifically MSCs and osteoblasts, may provide a novel mechanism of inhibiting MM disease progression.
Hematopoietic stem cells reside in specific niches in the bone marrow and give rise to either more stem cells or maturing hematopoietic progeny depending on the signals provided in the bone marrow microenvironment.
The identification of proliferation/survival pathways constitutively activated by genetic alterations in multiple myeloma (MM), or sustained by the bone marrow (BM) microenvironment, provides novel opportunities for the development of targeted therapies.
This review provides an overview of the bone marrow microenvironment and its involvement in normal, physiological HSC maintenance and plasma cell growth throughout MM disease progression.
The lack of efficacy of treatment can be partly attributed to the protection provided to the leukemia cells by the bone marrow microenvironment.
These studies provide insight into how hormonal changes during the menopausal transition might alter the bone marrow microenvironment for BC recurrence.
Interestingly, bone marrow microenvironment is also a critical reservoir for DTCs.
BCP-ALL cells critically depend on interactions with the bone marrow microenvironment.
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