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1 typical of the changes and heterogeneity in bone cancer.
2 s NGF blockade might confer in patients with bone cancer.
3 ith lipopolysaccharide (LPS) or in mice with bone cancer.
4 aracterized by bone dysplasia, myopathy, and bone cancer.
5 eed of dogs that exhibit a high incidence of bone cancer.
6 ow support was conducted to treat metastatic bone cancer.
7 ks behaviors indicative of pain in mice with bone cancer.
8 ar to that found in patients with osteolytic bone cancer.
9 ted dorsal root ganglia in a murine model of bone cancer.
10 ypes, and is present in approximately 25% of bone cancers.
11 tion as a cell-based gene delivery system to bone cancers.
12 ght to drive a subset of pediatric brain and bone cancers.
14 mor that constitutes approximately 6% of all bone cancers and is the most frequently occurring adult
19 siRNA can effectively treat pain induced by bone cancer by blocking the AKT-ERK signaling pathway.
22 signaling in normal bone development and in bone cancer could potentially lead to therapies modulati
24 Osteosarcoma is a highly metastatic form of bone cancer in adolescents and young adults that is resi
27 Osteosarcoma (OS), the most common primary bone cancer in dogs, is commonly treated with adjuvant d
29 s in the diagnosis and therapy of metastatic bone cancer, in which radioactive metal ions including (
30 We demonstrated previously that rats with bone cancer learn to prefer a context paired with saphen
35 and suggest a potential target for treating bone cancer pain and improving analgesic effect of morph
36 pinal cord is critical to the development of bone cancer pain and morphine tolerance in treating bone
37 cal mechanism underlying the pathogenesis of bone cancer pain and suggest a potential target for trea
38 destruction is involved in the generation of bone cancer pain and that osteoprotegerin may provide an
40 cking reagent EphB2-Fc prevents and reverses bone cancer pain behaviors and the associated induction
45 vity appears to have the potential to reduce bone cancer pain in patients with advanced tumor-induced
46 ptor reverses morphine tolerance in treating bone cancer pain in rats and defensive pain in mice.
49 cer pain arises from metastases to bone, and bone cancer pain is one of the most difficult of all per
50 chief problem in designing new therapies for bone cancer pain is that it is unclear what mechanisms d
54 sibility that it is an important mediator of bone cancer pain via its capacity to detect osteoclast-
56 mouse femur and that, in an in vivo model of bone cancer pain, acute or chronic administration of a T
58 uced bone destruction of the injected femur, bone cancer pain, and a stereotypic set of neurochemical
59 ical hyperalgesia developed in the rats with bone cancer pain, and these effects were accompanied by
60 ne the mechanisms that give rise to advanced bone cancer pain, osteolytic 2472 sarcoma cells or media
61 in to define the role COX-2 plays in driving bone cancer pain, we used an in vivo model where murine
62 attenuated both ongoing and movement-evoked bone cancer pain, whereas chronic inhibition of COX-2 si
63 icant reduction in both early and late stage bone cancer pain-related behaviors that was greater than
64 on, mice develop ongoing and movement-evoked bone cancer pain-related behaviors, extensive tumor-indu
77 whether ATP and P2X3 receptors contribute to bone-cancer pain in a mouse model, immunohistochemical t
78 avity tumor cell implantation (TCI) produces bone cancer-related thermal hyperalgesia, mechanical all
79 TGF)-beta1, a crucial molecule in metastatic bone cancer, stimulates collagenase-3 expression in the
81 ility of fDM as a biomarker for detection of bone cancer treatment efficacy, thus warranting clinical
82 body was administered in a prostate model of bone cancer where significant bone formation and bone de
83 e for the palliation of pain from metastatic bone cancer, whereas rhenium-186 and rhenium-188 are inv
84 killing in vivo revealed dramatic killing of bone cancer with only a modest effect on osteoclast numb
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