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1 mor cells and properties appertaining to the bone microenvironment.
2 osphatases to kill cancer cells in a mimetic bone microenvironment.
3 otemporal hybrid agent-based model of the MM-bone microenvironment.
4 ogical interactions between MM cells and the bone microenvironment.
5 with spatial relevance in a preserved native bone microenvironment.
6 of the cytokine interleukin-6 (IL-6) in the bone microenvironment.
7 tion of ameloblastoma with its native tumour bone microenvironment.
8 skeletal CAFs and conditions the surrounding bone microenvironment.
9 on breast cancer cells in bone by the local bone microenvironment.
10 ored tumor growth, lesion phenotype, and the bone microenvironment.
11 the dormancy of prostate cancer cells in the bone microenvironment.
12 ous multicellular interactions in the cancer-bone microenvironment.
13 medicine hold promises in delivering drug to bone microenvironment.
14 rom the primary tumour site and colonize the bone microenvironment.
15 one cell/cancer cell interactions within the bone microenvironment.
16 e matrix homeostasis and the prostate cancer-bone microenvironment.
17 stem cell development are independent of the bone microenvironment.
18 activator of NF-kappaB (RANK)-ligand in the bone microenvironment.
19 in the communication between tumors and the bone microenvironment.
20 regulating local response to changes in the bone microenvironment.
21 ht to act through the osteoclast by changing bone microenvironment.
22 ells blocked their ability to survive in the bone microenvironment.
23 umor cells and resident stromal cells in the bone microenvironment.
24 uppression of canonical Wnt signaling in the bone microenvironment.
25 clasts, and proinflammatory cells within the bone microenvironment.
26 en I and by cleavage of other factors in the bone microenvironment.
27 ng are likely mediated by alterations in the bone microenvironment.
28 ow, suggesting a potential alteration of the bone microenvironment.
29 ranching morphogenesis and metastasis to the bone microenvironment.
30 henotypes with a growth advantage within the bone microenvironment.
31 Bone metastases interact with the bone microenvironment.
32 be functionally suppressed by factors in the bone microenvironment.
33 es of cancer cells and their activity in the bone microenvironment.
34 argeting both the cancer cell as well as the bone microenvironment.
35 s, osteoblasts, and endothelial cells of the bone microenvironment.
36 -feedback loops between tumour cells and the bone microenvironment.
37 ession and inhibition of OCL activity in the bone microenvironment.
38 y of the prostate cancer cells to invade the bone microenvironment.
39 e in modulating RANKL gene expression in the bone microenvironment.
40 esumably, both pathways are activated in the bone microenvironment.
41 f tumor cells to colonize and survive in the bone microenvironment.
42 timuli modulate RANKL gene expression in the bone microenvironment.
43 bition of prostate cancer cell growth in the bone microenvironment.
44 cytoplasm and nucleus of cancer cells in the bone microenvironment.
45 and cells of osteoblastic lineage within the bone microenvironment.
46 genesis and by enhancing osteogenesis in the bone microenvironment.
47 ve growth factor (NGF) by the tumour-bearing bone microenvironment, alongside other known pain-relate
48 mib, as a pretreatment regimen, modified the bone microenvironment and enhanced bone strength and vol
49 pivotal in the maintenance of a homeostatic bone microenvironment and for proper osteoblast-osteocla
51 In this Review, we provide a summary of the bone microenvironment and its impact on bone metastasis.
52 nocarrier, which can sequentially target the bone microenvironment and myeloma cells to enhance the d
53 strategies for targeting the prostate cancer-bone microenvironment and several single- and multiagent
54 tudy of MM clonal evolution over time in the bone microenvironment and will be beneficial for optimiz
55 one marrow endothelium, extravasate into the bone microenvironment, and destroy bone tissue to allow
56 on the potential cell sources of TNF in the bone microenvironment, and on the mechanism of TNF actio
57 and MMP-13 are highly expressed in the tumor-bone microenvironment, and, of these, MMP-7 and MMP-9 we
58 he understanding of the biology of the tumor-bone microenvironment are leading to the development of
60 n tumor cells and myeloid progenitors in the bone microenvironment as a requirement for osteoclast di
63 actors secreted by primary tumors affect the bone microenvironment before the osteolytic phase of met
65 a serine protease, plays a vital role in the bone microenvironment by modulating tumor-stromal intera
66 t active KLK molecules are secreted into the bone microenvironment by PCa cells following stimulation
67 ignificance: Breast cancer cells remodel the bone microenvironment by promoting premature cellular se
68 provides tumor cell growth advantages in the bone microenvironment by stimulating interleukin-6 (IL6)
69 randomised study shows that targeting of the bone microenvironment can delay bone metastasis in men w
71 hich cellular interactions within the tumour-bone microenvironment contribute to disease, by promotin
72 hat osteosarcoma tumor-driven changes in the bone microenvironment contribute to the chemotherapy-res
74 o elucidate tumor-stroma interactions in the bone microenvironment contributing to invasion and proli
75 confirmed that MDSC isolated from the tumor-bone microenvironment differentiated into functional ost
76 ing barcode system, we demonstrated that the bone microenvironment facilitates breast and prostate ca
77 rrence of related diseases through targeting bone microenvironments for the treatment and early detec
79 drogel materials developed to optimize local bone microenvironment has made osteoporotic defect heali
80 biopharmaceuticals, reaching targets in the bone microenvironment has proved to be difficult due to
82 requirements of prostate cancer cells in the bone microenvironment, identifying the pentose phosphate
83 c plasticity of prostate cancer cells in the bone microenvironment, identifying the PPP and G6PD as m
84 abolish prostate cancer colonization in the bone microenvironment, implying this nuclear-mitochondri
85 e function, implicating a role for the tumor-bone microenvironment in cancer-associated muscle weakne
86 paracrine signaling cascade to modulate the bone microenvironment in favor of osteoclastogenesis and
87 all, we underscored the critical role of the bone microenvironment in influencing PCa progression, po
88 r work revealed an unappreciated role of the bone microenvironment in metastasis evolution and elucid
89 atite in vitro, and targeted delivery to the bone microenvironment in vivo following systemic adminis
91 al conditions affecting bone tissues and the bone microenvironment, including rheumatoid arthritis, o
92 ls: from systemic pathways to changes in the bone microenvironment, including the involvement of loca
95 breast cancer shows extreme tropism for the bone microenvironment, leading to the establishment of o
96 ined the role of proteases in modulating the bone microenvironment, little is currently known about t
97 ex temporal and cellular interactions in the bone microenvironment make drug development challenging.
98 e selective inhibition of MMP-7 in the tumor-bone microenvironment may be of benefit for the treatmen
101 t disease but that the protective effects of bone microenvironment mediated drug resistance (EMDR) si
103 ed novel experimental systems that model the bone microenvironment of the breast cancer metastatic ni
104 sting a link between primary cancers and the bone microenvironment prior to metastasis, and this link
108 mplex cross-talk between tumor cells and the bone microenvironment responsible for driving disease pr
109 ls increases tumor cell interaction with the bone microenvironment, resulting in greater formation of
110 In conclusion, deletion of grem1 in the bone microenvironment results in sensitization of BMP si
112 R-mediated interactions among cancer and the bone microenvironment stromal cells (osteoblasts and ost
113 lts support that FGFR inhibitors inhibit the bone microenvironment stromal cells including osteoblast
114 ctions between prostate cancer cells and the bone microenvironment that can explain the tendency of p
115 of osteoclast precursors migrating into the bone microenvironment that can subsequently differentiat
116 the interactions between tumor cells and the bone microenvironment that lead to osteolytic disease.
117 itamin D deficiency, contribute to a fertile bone microenvironment that might promote bone metastases
118 nd bone tissues promote changes in the tumor-bone microenvironments that are conducive to tumor growt
119 of host-derived MMP-7 and MMP-9 in the tumor-bone microenvironment, the tibias of MMP-7 and MMP-9 nul
120 lex interactions between tumor cells and the bone microenvironment to advance our understanding of th
121 cursors to rapidly respond to signals in the bone microenvironment to promote specifically osteoclast
122 tumor-generated pressure acts to modify the bone microenvironment to promote the growth of prostate
123 iogenic factors that are secreted within the bone microenvironment to regulate osteoporosis is lackin
126 alized synthetic matrix mimicking a CaP-rich bone microenvironment, we examine a molecular mechanism
127 However, the efficacy of FGFR TKIs in the bone microenvironment where breast cancer cells most fre
128 dence that senescent cells accumulate in the bone microenvironment with aging and that targeting thes
129 acted synergistically to modulate the tumor-bone microenvironment with encapsulation enhancing their
130 bone and the accompanying enrichment of the bone microenvironment with growth-promoting factors that