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Hierarchical structure mimicking the natural bone microenvironment has been considered as a promising platform to regulate cell functions.
Bone microenvironment has a significant role in harboring disseminated tumor cells and a source of late relapse [3].
8 The bone microenvironment has become an important focus of basic and clinical research efforts.
PTHrP production by tumor cells in the bone microenvironment has been shown to promote osteoclastic activity and contribute to osteolytic bone metastases [ 5].
In recent years, the idea that osteolytic bone metastasis is driven by intricate cellular and molecular interactions among tumor cells and the host stromal cells commonly found in the bone microenvironment has drawn much attention.
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Transgenic mice over-expressing noggin in the bone microenvironment have decreased trabecular bone volume and impaired osteoblastic function, leading to osteopenia and fractures [ 20].
Thus, ITAM-adapter signaling is not required for estrogen-deficient bone loss in the trabecular rich regions of long bones, indicating that these bone microenvironments have an ITAM-adapter independent mechanism to generate active osteoclasts.
The bone marrow microenvironment has recently been suggested to influence HSC aging, but the underlying mechanisms remain largely unknown.
The bone marrow microenvironment has a key role in regulating haematopoiesis, but its molecular complexity and response to stress are incompletely understood.
A better understanding of the molecular basis of chemotherapy resistance and the molecular sequelae of conventional cytotoxic and novel agents on MM cells and the bone marrow microenvironment has afforded the opportunity to study novel, rationally designed combination therapies in the clinic.
Although the expression of PECAM-1 (CD31) on vascular and haematopoietic cells within the bone marrow microenvironment has been recognized for some time, its physiological role within this niche remains unexplored.
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