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Recent studies have suggested that cells within fracture sites have the potential to induce mesenchymal stem cell (MSC) migration to sites of wound healing indicating that progenitor cells may migrate into bone and initiate osteogenic lineage commitment based on the microenvironmental cues within the bone tissue, itself [12].
Thus, the RANKL/RANK pathway may dictate breast cancer cells to preferentially migrate into bone.
During mammalian development, stem cells first appear in the yolk sac, then migrate into the fetal liver, and finally migrate into bone marrow (BM).
In fact, based on the high constitutive RANK expression in breast cancer specimens and cell lines, recent data suggest that RANK expression status of cancer cells determines whether tumors predominantly migrate into bone, whereas the corresponding ligand RANKL is abundantly expressed.
Recent studies indicated that progenitor cells might migrate into bone fracture sites and initiate osteogenic lineage commitment [ 6].
Recent studies indicate that progenitor cells may migrate into bone fracture sites and initiate osteogenic lineage commitment [ 9].
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This results in a potential passage for bacteria from the skin to migrate into the bone and cause an infection, referred to as pin tract infection [1].
Plasma cells that migrate into the bone marrow or into chronically inflamed tissues can survive for much longer periods of time.
B-lymphocyte ontogeny takes place in lymphoid organs leading to plasma cells that migrate into the bone marrow or mucosa-associated tissues.
These data indicate that expression of CXCR4 and, as a consequence, the potential to migrate into the bone marrow is generally associated with differentiation into plasma cells, whereas the expression of CXCR3 must be induced by the inflammatory cytokine IFN-γ.
Indeed, precursor osteoblasts, but not mature osteoblasts, move and migrate into developing bones along with invading blood vessels that stabilize the bone (Maes et al., 2010).
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