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1 ous multicellular interactions in the cancer-bone microenvironment.
2 medicine hold promises in delivering drug to bone microenvironment.
3 one cell/cancer cell interactions within the bone microenvironment.
4 skeletal CAFs and conditions the surrounding bone microenvironment.
5 e matrix homeostasis and the prostate cancer-bone microenvironment.
6 stem cell development are independent of the bone microenvironment.
7 activator of NF-kappaB (RANK)-ligand in the bone microenvironment.
8 in the communication between tumors and the bone microenvironment.
9 regulating local response to changes in the bone microenvironment.
10 ht to act through the osteoclast by changing bone microenvironment.
11 on breast cancer cells in bone by the local bone microenvironment.
12 ells blocked their ability to survive in the bone microenvironment.
13 umor cells and resident stromal cells in the bone microenvironment.
14 uppression of canonical Wnt signaling in the bone microenvironment.
15 clasts, and proinflammatory cells within the bone microenvironment.
16 en I and by cleavage of other factors in the bone microenvironment.
17 ng are likely mediated by alterations in the bone microenvironment.
18 ow, suggesting a potential alteration of the bone microenvironment.
19 ranching morphogenesis and metastasis to the bone microenvironment.
20 henotypes with a growth advantage within the bone microenvironment.
21 Bone metastases interact with the bone microenvironment.
22 be functionally suppressed by factors in the bone microenvironment.
23 es of cancer cells and their activity in the bone microenvironment.
24 argeting both the cancer cell as well as the bone microenvironment.
25 s, osteoblasts, and endothelial cells of the bone microenvironment.
26 ession and inhibition of OCL activity in the bone microenvironment.
27 y of the prostate cancer cells to invade the bone microenvironment.
28 e in modulating RANKL gene expression in the bone microenvironment.
29 esumably, both pathways are activated in the bone microenvironment.
30 f tumor cells to colonize and survive in the bone microenvironment.
31 timuli modulate RANKL gene expression in the bone microenvironment.
32 bition of prostate cancer cell growth in the bone microenvironment.
33 cytoplasm and nucleus of cancer cells in the bone microenvironment.
34 and cells of osteoblastic lineage within the bone microenvironment.
35 the dormancy of prostate cancer cells in the bone microenvironment.
36 mib, as a pretreatment regimen, modified the bone microenvironment and enhanced bone strength and vol
37 pivotal in the maintenance of a homeostatic bone microenvironment and for proper osteoblast-osteocla
39 nocarrier, which can sequentially target the bone microenvironment and myeloma cells to enhance the d
40 strategies for targeting the prostate cancer-bone microenvironment and several single- and multiagent
41 one marrow endothelium, extravasate into the bone microenvironment, and destroy bone tissue to allow
42 on the potential cell sources of TNF in the bone microenvironment, and on the mechanism of TNF actio
43 and MMP-13 are highly expressed in the tumor-bone microenvironment, and, of these, MMP-7 and MMP-9 we
44 he understanding of the biology of the tumor-bone microenvironment are leading to the development of
46 n tumor cells and myeloid progenitors in the bone microenvironment as a requirement for osteoclast di
48 a serine protease, plays a vital role in the bone microenvironment by modulating tumor-stromal intera
49 provides tumor cell growth advantages in the bone microenvironment by stimulating interleukin-6 (IL6)
50 randomised study shows that targeting of the bone microenvironment can delay bone metastasis in men w
51 hat osteosarcoma tumor-driven changes in the bone microenvironment contribute to the chemotherapy-res
52 o elucidate tumor-stroma interactions in the bone microenvironment contributing to invasion and proli
53 confirmed that MDSC isolated from the tumor-bone microenvironment differentiated into functional ost
56 e function, implicating a role for the tumor-bone microenvironment in cancer-associated muscle weakne
57 paracrine signaling cascade to modulate the bone microenvironment in favor of osteoclastogenesis and
60 breast cancer shows extreme tropism for the bone microenvironment, leading to the establishment of o
61 ined the role of proteases in modulating the bone microenvironment, little is currently known about t
62 ex temporal and cellular interactions in the bone microenvironment make drug development challenging.
63 e selective inhibition of MMP-7 in the tumor-bone microenvironment may be of benefit for the treatmen
66 ed novel experimental systems that model the bone microenvironment of the breast cancer metastatic ni
67 sting a link between primary cancers and the bone microenvironment prior to metastasis, and this link
70 ls increases tumor cell interaction with the bone microenvironment, resulting in greater formation of
73 ctions between prostate cancer cells and the bone microenvironment that can explain the tendency of p
74 of osteoclast precursors migrating into the bone microenvironment that can subsequently differentiat
75 the interactions between tumor cells and the bone microenvironment that lead to osteolytic disease.
76 itamin D deficiency, contribute to a fertile bone microenvironment that might promote bone metastases
77 of host-derived MMP-7 and MMP-9 in the tumor-bone microenvironment, the tibias of MMP-7 and MMP-9 nul
78 cursors to rapidly respond to signals in the bone microenvironment to promote specifically osteoclast
79 tumor-generated pressure acts to modify the bone microenvironment to promote the growth of prostate
80 iogenic factors that are secreted within the bone microenvironment to regulate osteoporosis is lackin
82 alized synthetic matrix mimicking a CaP-rich bone microenvironment, we examine a molecular mechanism
83 bone and the accompanying enrichment of the bone microenvironment with growth-promoting factors that
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