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1 ted dorsal root ganglia in a murine model of bone cancer.
2 behavior in mouse models of nerve injury and bone cancer.
3      Osteosarcoma is the most common type of bone cancer.
4    Other cytotoxics were not associated with bone cancer.
5  typical of the changes and heterogeneity in bone cancer.
6 s NGF blockade might confer in patients with bone cancer.
7 ith lipopolysaccharide (LPS) or in mice with bone cancer.
8 aracterized by bone dysplasia, myopathy, and bone cancer.
9 eosarcoma is the most common type of primary bone cancer.
10 eed of dogs that exhibit a high incidence of bone cancer.
11 ow support was conducted to treat metastatic bone cancer.
12 ks behaviors indicative of pain in mice with bone cancer.
13 ar to that found in patients with osteolytic bone cancer.
14 al growth factor receptor (EGFR) in chordoma bone cancers.
15 ght to drive a subset of pediatric brain and bone cancers.
16 ypes, and is present in approximately 25% of bone cancers.
17 tion as a cell-based gene delivery system to bone cancers.
18 e to alkylating agents increases the risk of bone cancer among survivors of childhood cancer, but the
19 ficant clinical utility in the management of bone cancer and bone cancer pain.
20 r plus single-cell RNA-sequencing in primary bone cancer and CTCs to perform weighted gene co-express
21 Osteosarcoma (OS) is the most common primary bone cancer and ranks amongst the leading causes of canc
22 mor that constitutes approximately 6% of all bone cancers and is the most frequently occurring adult
23 ) against breast, brain, skin, prostate, and bone cancers, and a section is devoted to other cancer t
24 l SCs combined and for soft tissue sarcomas, bone cancers, and melanoma were calculated.
25 F-353 administration onto the spinal cord of bone cancer animals.
26 g pain, and effective therapies for treating bone cancer are lacking.
27                       Primary and metastatic bone cancers are difficult to eradicate and novel approa
28 matrix can separate several major classes of bone cancer-associated diagnostic categories with an ave
29 tions of tumor-associated sensory neurons in bone cancers beyond pain sensation are unknown.
30 apy, and radiation therapy are used to treat bone cancer, but they often only shrink or slow tumor gr
31  siRNA can effectively treat pain induced by bone cancer by blocking the AKT-ERK signaling pathway.
32 very of pharmaceutical agents to the site of bone cancer by introduction of bone-targeting moieties,
33 oma, Wilms tumour, soft-tissue sarcomas, and bone cancer) by comparing both groups to siblings of the
34                  Whereas pain resulting from bone cancer can dramatically impact an individual's qual
35                             Nerve injury and bone cancer caused a rapid-onset and long-lasting expres
36 cules that provide targeting capabilities to bone cancer cells when conjugated with drug-carrying pol
37  essential role in tumour growth of the rare bone cancer chordoma and is implicated in other solid tu
38  as an exciting new drug target for the rare bone cancer chordoma.
39  signaling in normal bone development and in bone cancer could potentially lead to therapies modulati
40 le of BRCA1-NRF2 interplay in the context of bone cancer, demonstrating how Correlation AnalyzeR can
41          Ewing sarcoma (ES) is an aggressive bone cancer driven by the oncogenic fusion-protein EWSR1
42              Odds ratios (ORs) of developing bone cancer for different levels of cumulative radiation
43      Osteosarcoma(OS) is a highly aggressive bone cancer for which treatment has remained essentially
44                                           As bone cancer grows, osteoclasts, the principal bone-resor
45  Osteosarcoma is a highly metastatic form of bone cancer in adolescents and young adults that is resi
46        Osteosarcoma, the most common primary bone cancer in children and adolescents, presents signif
47 ma (OS) is the most common primary malignant bone cancer in children and adolescents.
48              Osteosarcoma is the most common bone cancer in children and adolescents.
49         Osteosarcoma (OS) is the most common bone cancer in children and young adults.
50      Ewing sarcoma is the second-most-common bone cancer in children.
51   Osteosarcoma (OS), the most common primary bone cancer in dogs, is commonly treated with adjuvant d
52 ropathic pain after sciatic nerve injury and bone cancer in rodents.
53 s in the diagnosis and therapy of metastatic bone cancer, in which radioactive metal ions including (
54 ration of STING agonists robustly attenuates bone cancer-induced pain and improves locomotor function
55                                              Bone cancer is common and severe.
56 onstrate-for the first time-that the risk of bone cancer is increased 5- to 10-fold after exposure of
57 ng sarcoma) and secondary (e.g., metastatic) bone cancers lead to significant health problems and dea
58    We demonstrated previously that rats with bone cancer learn to prefer a context paired with saphen
59  30, one to three months from a diagnosis of bone cancer, lymphoma or leukaemia.
60 nsional MAPK7/MMP9 signalling hub in primary bone cancer metastasis that is clinically actionable.
61 PK7/MMP9) signalling as a driver for primary bone cancer metastasis.
62 tment of chronic pain states associated with bone cancer metastasis.
63 helpful information in a rat mammary-derived bone cancer model.
64      Osteosarcoma is the most common primary bone cancer, occurring frequently in children and young
65               Ewing sarcoma is an aggressive bone cancer of children and young adults defined by the
66             Thus, even in advanced stages of bone cancer, ongoing osteoclast activity appears to be i
67  and some elevation in risk was apparent for bone cancer (OR = 1.92, 95% CI: 0.85, 4.34) with increas
68 um subarachnoidale of animals suffering from bone cancer pain and animals in the negative group.
69  and suggest a potential target for treating bone cancer pain and improving analgesic effect of morph
70 pinal cord is critical to the development of bone cancer pain and morphine tolerance in treating bone
71 cal mechanism underlying the pathogenesis of bone cancer pain and suggest a potential target for trea
72 destruction is involved in the generation of bone cancer pain and that osteoprotegerin may provide an
73            This "neurochemical signature" of bone cancer pain appears unique when compared to changes
74 cking reagent EphB2-Fc prevents and reverses bone cancer pain behaviors and the associated induction
75 ighly significant prevention and reversal of bone cancer pain behaviour.
76  preventing bone destruction and alleviating bone cancer pain by suppressing osteoclastogenesis.
77                                     Treating bone cancer pain continues to be a clinical challenge an
78 nduced by the development of neuropathic and bone cancer pain in animal models.
79  used to attenuate nociception in a model of bone cancer pain in mice.
80 vity appears to have the potential to reduce bone cancer pain in patients with advanced tumor-induced
81 ptor reverses morphine tolerance in treating bone cancer pain in rats and defensive pain in mice.
82                                              Bone cancer pain is a major clinical problem and remains
83                                              Bone cancer pain is common among cancer patients and can
84 cer pain arises from metastases to bone, and bone cancer pain is one of the most difficult of all per
85 chief problem in designing new therapies for bone cancer pain is that it is unclear what mechanisms d
86                                              Bone cancer pain most commonly occurs when tumors origin
87 nical challenge and underlying mechanisms of bone cancer pain remain elusive.
88 e destruction, but how PD-1 blockade affects bone cancer pain remains unknown.
89          Data generated in a murine model of bone cancer pain suggest that a disturbance of local end
90 on provides unique advantages in controlling bone cancer pain through distinct and synergistic action
91 sibility that it is an important mediator of bone cancer pain via its capacity to detect osteoclast-
92 ine pain sensitivity, but the development of bone cancer pain was compromised in Pd1-/- mice.
93                             The rat model of bone cancer pain was induced by implanting rat mammary g
94 mouse femur and that, in an in vivo model of bone cancer pain, acute or chronic administration of a T
95        Using a well-established rat model of bone cancer pain, AF-353, a recently described potent an
96 uced bone destruction of the injected femur, bone cancer pain, and a stereotypic set of neurochemical
97 ical hyperalgesia developed in the rats with bone cancer pain, and these effects were accompanied by
98 ne the mechanisms that give rise to advanced bone cancer pain, osteolytic 2472 sarcoma cells or media
99 in to define the role COX-2 plays in driving bone cancer pain, we used an in vivo model where murine
100  attenuated both ongoing and movement-evoked bone cancer pain, whereas chronic inhibition of COX-2 si
101 icant reduction in both early and late stage bone cancer pain-related behaviors that was greater than
102 on, mice develop ongoing and movement-evoked bone cancer pain-related behaviors, extensive tumor-indu
103 ons, and CCR2 antagonism effectively reduced bone cancer pain.
104 mal and mechanical hyperalgesia in rats with bone cancer pain.
105 d growth factor (PDGF) was used to alleviate bone cancer pain.
106 echanical hypersensitivity in a rat model of bone cancer pain.
107 ssion level in the spinal cord is reduced in bone cancer pain.
108 educes pain hypersensitivity associated with bone cancer pain.
109 ach for treating neuropathic pain, including bone cancer pain.
110 ncer pain and morphine tolerance in treating bone cancer pain.
111 tributes to analgesic efficacy in a model of bone cancer pain.
112 fer a promising therapeutic tool in treating bone cancer pain.
113 s a promising strategy for the management of bone cancer pain.
114 life in patients with prostate tumor-induced bone cancer pain.
115 utility in the management of bone cancer and bone cancer pain.
116 whether ATP and P2X3 receptors contribute to bone-cancer pain in a mouse model, immunohistochemical t
117 avity tumor cell implantation (TCI) produces bone cancer-related thermal hyperalgesia, mechanical all
118 w environment that is useful for mechanistic bone cancer research and drug screening.
119 TGF)-beta1, a crucial molecule in metastatic bone cancer, stimulates collagenase-3 expression in the
120         Bone pain is a presenting feature of bone cancers such as osteosarcoma (OS), relayed by skele
121                 Ewing sarcoma is a pediatric bone cancer that expresses the chimeric protein EWSR1/FL
122                           Chordoma is a rare bone cancer that is aggressive, locally invasive, and ha
123 ility of fDM as a biomarker for detection of bone cancer treatment efficacy, thus warranting clinical
124                                              Bone cancer upregulated CCR2 in primary sensory neurons,
125         Here, using multiple mouse models of bone cancer, we report that agonists of the immune regul
126 body was administered in a prostate model of bone cancer where significant bone formation and bone de
127 e for the palliation of pain from metastatic bone cancer, whereas rhenium-186 and rhenium-188 are inv
128      Osteosarcoma is the most common primary bone cancer, whose standard treatment includes pre-opera
129    Skull-base chordoma is a rare, aggressive bone cancer with a high recurrence rate.
130 f selectively essential genes in chordoma, a bone cancer with few validated targets.
131                        Chordoma is a primary bone cancer with no approved therapy(1).
132 killing in vivo revealed dramatic killing of bone cancer with only a modest effect on osteoclast numb
133  sarcoma is the second most common pediatric bone cancer, with a 5-year survival rate for metastatic

 
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