ライフサイエンスコーパス: bone disease

1 eful targets for the treatment of MM-induced bone disease.

2 dent risk factor for cystic fibrosis-related bone disease.

3 no evidence for the development of adynamic bone disease.

4 ogressive chest deformity or have persistent bone disease.

5 tions including cytopenias, organomegaly and bone disease.

6 lytic damage in the murine 5TGM1 model of MM bone disease.

7 d suppression of osteoblasts, leads to lytic bone disease.

8 efore represents a therapeutic target for MM bone disease.

9 azard as it may lead to fluorosis, a serious bone disease.

10 mor growth within bone marrow and osteolytic bone disease.

11 mouse model of multiple myeloma (MM) and MM bone disease.

12 e myeloma growth and survival and osteolytic bone disease.

13 articularly in the development of osteolytic bone disease.

14 ologies, including cancer, inflammation, and bone disease.

15 he treatment of MM and associated osteolytic bone disease.

16 the treatment of myeloma and the associated bone disease.

17 nal surveillance and management of metabolic bone disease.

18 related illnesses such as cardiovascular and bone disease.

19 and provide a new therapeutic target for MM bone disease.

20 myeloma-bearing mice, and prevented myeloma bone disease.

21 ing embryonic bone development and postnatal bone disease.

22 in our understanding of pediatric metabolic bone disease.

23 tion by EphB4-Fc inhibits myeloma growth and bone disease.

24 s associated with prostate cancer metastatic bone disease.

25 levated serum immunoglobulin, and osteolytic bone disease.

26 l for myeloma patients suffering from severe bone disease.

27 ing the treatment of patients with metabolic bone disease.

28 or growth in bone and development of myeloma bone disease.

29 critical role in the pathogenesis of myeloma bone disease.

30 yeloma counteracts development of osteolytic bone disease.

31 ial implications for the pathogenesis of NF1 bone disease.

32 h potential applications in the treatment of bone disease.

33 nd suggest new therapeutics for treatment of bone disease.

34 he design of drugs that can be used to treat bone disease.

35 tion of survival in patients with metastatic bone disease.

36 atients who underwent surgery for metastatic bone disease.

37 ration to increase linear growth and prevent bone disease.

38 hat effect this therapeutic trend has had on bone disease.

39 at MIP-1alpha is an important mediator of MM bone disease.

40 ated in patients with MM and correlated with bone disease.

41 eutic targets for ameliorating MM-associated bone disease.

42 eful therapeutic agents for inflammation and bone disease.

43 turnover and increased incidence of adynamic bone disease.

44 of secondary hyperparathyroidism and uremic bone disease.

45 efit to multiple myeloma patients with lytic bone disease.

46 eating and managing patients with metastatic bone disease.

47 by the radioresistant compartment to promote bone disease.

48 steoblasts and are causative agents of human bone disease.

49 (RANKL), factors also implicated in myeloma bone disease.

50 yeloma progression and associated osteolytic bone disease.

51 to correctly predict the presence of active bone disease.

52 for controlling mineralization in metabolic bone disease.

53 eliorates some aspects of cardiovascular and bone disease.

54 lopment to treat osteoporosis and metastatic bone disease.

55 ibiting NF-kappaB in vivo in mouse models of bone disease.

56 tanding of the role the vasculature plays in bone disease.

57 o rescue Pstpip2(cmo) mice from inflammatory bone disease.

58 ospects for molecular therapy for metastatic bone disease.

59 ronment to the development of cancer-induced bone disease.

60 mor growth and development of the associated bone disease.

61 havbeta3 was required for CCN1 prevention of bone disease.

62 x were dispensable for Pstpip2(cmo)-mediated bone disease.

63 CYR61 should be investigated for treating MM bone disease.

64 cts on bone and management of ADT-associated bone disease.

65 management of multiple myeloma (MM) -related bone disease.

66 Wnt antagonists are promising new drugs for bone diseases.

67 surements of bone density and treatments for bone diseases.

68 n the pathogenesis of osteoporosis and other bone diseases.

69 bone quality in myeloma and other malignant bone diseases.

70 ogenesis of autoimmune-mediated inflammatory bone diseases.

71 that occurs in osteoporosis and inflammatory bone diseases.

72 n in the treatment of osteoporosis and other bone diseases.

73 and inflammation-induced bone loss in common bone diseases.

74 ltiple functions implicated for neuronal and bone diseases.

75 enhancing bone repair and treating metabolic bone diseases.

76 uld be further explored as a drug target for bone diseases.

77 rrant regulation are involved in a number of bone diseases.

78 Plain radiography is key in diagnosing bone diseases.

79 tially, the molecular rationale for treating bone diseases.

80 tial therapeutic target for the treatment of bone diseases.

81 ector immunomodulatory cells in inflammatory bone diseases.

82 utic approaches to combat various osteolytic bone diseases.

83 utic intervention for osteoporosis and other bone diseases.

84 at influence the progression of inflammatory bone diseases.

85 n the pathogenesis of osteoporosis and other bone diseases.

86 e in the treatment of osteoporosis and other bone diseases.

87 ccumulation in degenerative and inflammatory bone diseases.

88 ay provide insights into novel therapies for bone diseases.

89 ed to investigate bone metabolism and manage bone diseases.

90 ls with which to gain insight into metabolic bone diseases.

91 gesting FGF23 as a key factor of CKD related bone diseases.

92 imiting arthropathies and other degenerative bone diseases.

93 ral, and craniofacial manifestations of rare bone diseases.

94 activity might be a therapeutic strategy for bone diseases.

95 oquine, may limit bone destruction in common bone diseases.

96 nt inflammatory bone resorption and to treat bone diseases.

97 ROS are implicated in bone diseases.

98 ure (21 genes), breast cancer (16 genes) and bone diseases (11 genes).

99 te their use with other treatments for lytic bone disease, (3) how to evaluate their role in myeloma

100 were markedly protected against inflammatory bone disease and bone erosion.

101 ay influence the development of low-turnover bone disease and coronary artery calcification (CAC) in

102 Wnt signaling on the development of myeloma bone disease and demonstrate that, despite a direct effe

103 eoprotegerin, were protected from osteolytic bone disease and developed fewer soft-tissue tumors.

104 G/+) and Lmna(csmHG/csmHG) mice exhibited no bone disease and displayed entirely normal body weights

105 l tool for assessing patients with metabolic bone disease and evaluating novel drugs being developed

106 his study was to test the effect of Wnt3a on bone disease and growth of MM cells in vitro and in vivo

107 t disorder that is characterized by rachitic bone disease and hypophosphatemia due to renal phosphate

108 pendent production of IL-1beta in osteolytic bone disease and identify PSTPIP2 as a negative regulato

109 ting sclerostin would prevent development of bone disease and increase resistance to fracture in MM.

110 nment can prevent the development of myeloma bone disease and inhibit myeloma growth within bone in v

111 ease of bone (PDB) is the second most common bone disease and is characterized by focal bone lesions

112 Periodontitis is the most common lytic bone disease and one of the first clinical manifestation

113 ovide novel approaches to therapy of myeloma bone disease and osteoporosis.

114 ntiation characterizes multiple myeloma (MM) bone disease and persists even when patients are in long

115 usion, our results implicate IL-8 in myeloma bone disease and point to the potential utility of an an

116 y established in the treatment of metastatic bone disease and significantly reduce skeletal morbidity

117 newly diagnosed MM to evaluate their role in bone disease and survival.

118 We conclude that DKK1 is a key player in MM bone disease and that blocking DKK1 activity in myelomat

119 cells are critical to the genesis of myeloma bone disease and that immunologic manipulations shifting

120 ify phenotypes associated with human brittle bone disease and thyroid stimulating hormone receptor hy

121 for clinical evaluation of BHQ880 to improve bone disease and to inhibit MM growth.

122 lly making it possible to diagnose metabolic bone disease and track the impact of treatments more eff

123 ion may suggest novel treatments for genetic bone diseases and bone injuries.

124 owledge gained in the treatment of metabolic bone diseases and in periodontal clinical trials are dis

125 his may lead to new targets for treatment of bone diseases and injuries.

126 ect role that the Wnt pathway plays in human bone diseases and malignancies, our findings may support

127 signaling in osteoblasts, inhibited myeloma bone disease, and decreased tumor burden in bone, but in

128 ith decreased bone mineral density, adynamic bone disease, and fractures.

129 s of hypertension, hyperlipidemia, diabetes, bone disease, and hematologic and serum chemistry indica

130 versed osteoblast inhibition, ameliorated MM bone disease, and inhibited tumor growth in an in vivo h

131 for inflammatory bowel disorders, metabolic bone disease, and malignancy is paramount when managing

132 function, biochemical parameters of mineral bone disease, and measures of renal function.

133 tudy patients had visceral metastases, lytic bone disease, and relatively low serum prostate-specific

134 disease is important in the genesis of renal bone disease, and several new treatments could help achi

135 , improved nutrition, treatment of metabolic bone disease, and the use of recombinant human growth ho

136 f skeletal events in patients with malignant bone disease, and zoledronic acid has shown potential an

137 the physiologic roles of MPCs in arthritis, bone diseases, and joint regeneration.

138 s a central role in the pathogenesis of many bone diseases, and osteoclast inhibitors are the most wi

139 d OPG expression is also altered in numerous bone diseases, and these changes can reflect disease eti

140 nge of strategies directed at ADT-associated bone disease are available, including antiresorptive age

141 related illnesses such as cardiovascular and bone disease are becoming more prevalent in this populat

142 Neurologic disease and bone disease are intriguing complications of celiac dise

143 olved in the pathogenesis of myeloma-induced bone disease are not fully understood.

144 Bone diseases are often a result of increased numbers of

145 immune and skeletal systems in inflammatory bone diseases are well appreciated, but the underlying m

146 vere disease with renal stones and metabolic bone disease arises less frequently now than it did 20-3

147 Wwox(-/-) mice develop metabolic bone disease, as a consequence of reduced serum calcium,

148 BPs offer any advantage in patients with no bone disease assessed by magnetic resonance imaging or p

149 e-related peptide (PTHrP), namely osteolytic bone disease associated with breast cancer and humoral h

150 discovery of genes responsible for monogenic bone diseases associated with abnormal bone mass; the id

151 it may be a therapeutic target for treating bone diseases associated with increased OCL activity.

152 and comprehensively evaluated for metabolic bone disease at a median of 16 days (range 9-33) posttra

153 PXR can also induce vitamin D deficiency and bone disease because of its ability to cross-talk with t

154 perpetrator-admitted child abuse, metabolic bone disease, birth trauma, or injury caused by vehicula

155 nsplant and posttransplant lipid metabolism, bone disease (bone mineral density and fracturing), and

156 that vitamin D deficiency not only promotes bone diseases but also type I sensitization.

157 have potential efficacy in cancer-associated bone disease, but further studies are warranted and ongo

158 oprotection and a new therapeutic target for bone diseases, but also elucidate a previously unrecogni

159 progression and treating myeloma-associated bone disease by inhibiting DKK1 expression.

160 myeloma (MM) cells contributes to osteolytic bone disease by inhibiting the differentiation of osteob

161 bility to make an accurate assessment of the bone disease by noninvasive means.

162 a therapeutic approach to prevent metastatic bone disease by this route.

163 y described osteolytic effects in metastatic bone disease, can also be an important mediator of joint

164 s-related diabetes, renal disease, metabolic bone disease, cancers, drug allergies and toxic effects,

165 ll survival and iron deficiency; and mineral bone disease caused by disturbed vitamin D, calcium, and

166 Classical osteogenesis imperfecta (OI) is a bone disease caused by type I collagen mutations and cha

167 ts in the development of spontaneous chronic bone disease characterized by bone deformity and inflamm

168 Osteopetrosis is a genetic bone disease characterized by increased bone density and

169 of value in the prevention and treatment of bone diseases characterized by increased bone loss such

170 dentified from patients with either blood or bone disease demonstrates that the primary defect in the

171 ibility of developing novel therapeutics for bone diseases designed to target specific aspects of thi

172 panel of clinical experts on MM and myeloma bone disease developed recommendations based on publishe

173 A low incidence of focal bone disease distinguished one and increased expression

174 ) coupled with clues from patients with rare bone diseases (eg, romosozumab, odanacatib).

175 ies such as chromosome 13 deletion, advanced bone disease, extramedullary involvement, and patients w

176 Pycnodysostosis is a genetic bone disease featuring the unique bone homeostasis disor

177 significant differences in the prevalence of bone disease, frequency at relapse, and progression to e

178 outinely used in the treatment of metastatic bone disease from breast cancer to reduce pain and bone

179 Conclusion Metastatic bone disease from mCRPC can be evaluated and quantified

180 ses excludes patients with breast cancer and bone disease from participating in clinical trials of ne

181 Osteogenesis imperfecta or 'brittle bone disease' has mainly been considered a bone disorder

182 tilage-associated protein) causing recessive bone disease have been reported.

183 s that impact our understanding of metabolic bone disease have evolved dramatically.

184 notypes, and many genes that cause monogenic bone diseases have been identified by use of this approa

185 Linkage studies in rare Mendelian bone diseases have identified several previously unknown

186 yperparathyroidism have been associated with bone disease, hypertension, and in some studies, cardiov

187 have investigated the impact of response on bone disease in 1111 transplant-eligible patients.

188 Bone histology revealed low turnover bone disease in 50% of the patients at baseline.

189 issue in 13 (22%) of 59 patients, stabilised bone disease in 61 (56%) of 109 patients, and conversion

190 f progression, and independent predictors of bone disease in a large number of patients with all stag

191 nstitutes a potential approach to mitigating bone disease in affected patients.

192 resemble the clinical features reported for bone disease in HGPS patients, was associated with an ab

193 han (99m)Tc-BS and enhances detection of new bone disease in high-risk patients.

194 the screening, diagnosis, and monitoring of bone disease in HIV-infected patients.

195 bility to promote myeloma and the associated bone disease in mice.

196 itical role in the development of osteolytic bone disease in multiple myeloma and that targeting this

197 sphonates in the prevention and treatment of bone disease in multiple myeloma.

198 l1beta, but not Il1alpha, rescued osteolytic bone disease in mutant mice.

199 Lytic bone disease in myeloma is characterized by an increase

200 notype tightly correlated with the extent of bone disease in myeloma.

201 Bone disease in patients who have had bariatric surgery

202 r the long-term prevention and management of bone disease in patients with CF.

203 erapeutic strategy to prevent or correct the bone disease in patients with CF.

204 ear factor-kappaB is able to prevent myeloma bone disease in pre-clinical models.

205 teoimmunological underpinnings of osteolytic bone disease in Pstpip2(cmo) mice.

206 on of the prevalence and extent of metabolic bone disease in RTS.

207 RH) and tested for its capacity to induce MM bone disease in SCID mice.

208 t, with the former showing no improvement of bone disease in the first year after transplantation and

209 has focused on its adverse effects, of which bone disease in the form of osteoporosis and fractures h

210 entation of WBDWI is feasible for metastatic bone disease in this pilot cohort of 11 patients, and co

211 To investigate the role of MIP-1alpha in MM bone disease in vivo, the human MM-derived cell line ARH

212 in osteoclast (OC) activation and osteolytic bone diseases in malignancies such as the plasma cell dy

213 p-regulating the vicious cycle of metastatic bone disease, in addition to Runx2 regulation of genes r

214 itamin D status, a modifiable risk factor in bone disease, in the renal transplant population in a no

215 Deregulation of Cbfa1 results in metabolic bone diseases including osteoporosis and osteopetrosis.

216 ha (MIP-1alpha) are reported in inflammatory bone diseases including periodontitis.

217 pathological feature of chronic inflammatory bone diseases including rheumatoid arthritis, in which C

218 and RANKL mediate bone destruction in common bone diseases, including osteoarthritis and RA.

219 lay a key role in various forms of metabolic bone diseases, including osteopenia and osteoporosis.

220 lidated mechanism for the treatment of lytic bone diseases, including osteoporosis and cancer related

221 reased osteoclastic resorption leads to many bone diseases, including osteoporosis and rheumatoid art

222 ent specific therapeutic targets for various bone diseases, including postmenopausal osteoporosis.

223 thermore, how IL-1beta provokes inflammatory bone disease inPstpip2(cmo)mice is not known.

224 Metabolic bone disease is a common complication of chronic kidney

225 Osteolytic bone disease is a major cause of morbidity in patients w

226 Bone disease is a significant problem for patients with

227 n the prevention of cancer treatment-induced bone disease is also defined.

228 l role for autophagy in bone remodelling and bone disease is beginning to emerge.

229 Myeloma bone disease is caused by uncoupling of osteoclastic bon

230 Metastatic bone disease is common in cancer patients and causes sub

231 Bone disease is common in the HIV population, and will l

232 rstanding the pathogenesis of cancer-related bone disease is crucial to the discovery of new therapie

233 Bisphosphonate control of bone disease is essential.

234 Progression of breast cancer to metastatic bone disease is linked to deregulated expression of the

235 The bone disease is mediated by increased osteoclastic bone

236 contribution to multiple myeloma growth and bone disease is unknown.

237 Osteogenesis imperfecta (OI or brittle bone disease) is a disorder of connective tissues caused

238 nesis imperfecta (OI), also known as brittle bone disease, is a clinically and genetically heterogene

239 Osteogenesis imperfecta (OI), or brittle bone disease, is most often caused by dominant mutations

240 mouse models of arthritis and RANKL-induced bone disease leads to an increase in the number of OCs,

241 um in bone formation, biomineralization, and bone diseases like osteoporosis.

242 osteonecrosis of the jaw (BONJ) is a morbid bone disease linked to long-term bisphosphonate use.

243 Four clinically important questions in bone disease management were identified, and recommendat

244 Preterm infants are at risk of metabolic bone disease (MBD) because of an inadequate mineral inta

245 steolytic bone lesions also known as myeloma bone disease (MBD).

246 ciated with the development of a devastating bone disease mediated by increased osteoclastic activity

247 ed tumor burden in a xenograft and syngeneic bone disease model of MM without exhibiting adverse side

248 n-related parameters were positively and low-bone-disease molecular subtype inversely correlated with

249 soft-tissue disease (nodes and/or viscera), bone disease (most common site of spread), and symptoms.

250 f paraneoplastic presentations of synovitis, bone disease, myositis, and vasculitis.

251 in the pathogenesis of MM-related osteolytic bone disease (OBD).

252 Osteopenic bone disease occurs frequently among patients with chron

253 This model both recapitulates the diffuse bone disease of human MM and allows for serial whole-bod

254 phosphonates for hypercalcemia or metastatic bone disease often present with a debilitating acute pha

255 Osteogenesis imperfecta (OI), or brittle bone disease, often results from missense mutation of on

256 erformance status 0-1, measurable disease or bone disease only, and disease relapse or progression af

257 e, most profoundly in patients with baseline bone disease or other SREs.

258 d a history of trauma or infection, familial bone disease, or related abnormal laboratory findings.

259 A mouse model of the genetic brittle bone disease, osteogenesis imperfect, oim, is characteri

260 oporosis among adults and causes the painful bone disease osteomalacia.

261 Osteoporosis is a degenerative bone disease predominantly in postmenopausal women.

262 nates, drugs used widely in the treatment of bone diseases, prevent osteoblast and osteocyte apoptosi

263 s Imperfecta (OI), also known as the brittle bone disease, relates to the extent of conformational ch

264 omplications-including fatigue and metabolic bone disease-remain unavailable.

265 Osteoclast (OC)-mediated lytic bone disease remains a cause of major morbidity in multi

266 te ((99m)Tc-MDP) in metastatic and metabolic bone disease require the measurement of free tracer in p

267 Sickle bone disease (SBD) affects a large part of the SCD patie

268 of skeletal-related events, irrespective of bone disease status at baseline.

269 ar to those associated with human metastatic bone disease such as osteolytic bone destruction.

270 The model is also able to simulate metabolic bone diseases such as estrogen deficiency, vitamin D def

271 creased numbers of osteoclasts in osteolytic bone diseases such as osteolytic bone metastasis and inf

272 r the function of bone cells, exemplified by bone diseases such as osteopetrosis, which frequently re

273 so implicated in the pathogenesis of various bone diseases such as osteoporosis and bone loss in infl

274 is and evaluation of therapies for metabolic bone diseases such as osteoporosis and some cancers.

275 function is central to the understanding of bone diseases such as osteoporosis, rheumatoid arthritis

276 and possibly for the treatment of metabolic bone diseases such as osteoporosis.

277 These studies give insight into inflammatory bone diseases such as periodontal disease and arthritis

278 e central to the progression of inflammatory bone diseases such as periodontal disease.

279 Bone diseases such as postmenopausal osteoporosis are pr

280 at bacterial challenge of osteoblasts during bone diseases, such as osteomyelitis, induces cells to p

281 of infection and promote inflammation during bone diseases, such as osteomyelitis.

282 Bone diseases, such as osteoporosis, which are character

283 Notch signaling that enhances MM growth and bone disease, suggesting that targeting osteocyte-multip

284 ent with NB-DNJ markedly improved osteolytic bone disease symptoms.

285 nts have been shown to have a higher risk of bone disease than the general population.

286 Osteoporosis is a common and debilitating bone disease that is characterised by low bone mineral d

287 Osteoporosis is a common, age-related bone disease that results from an imbalance between the

288 ell-established therapeutic target for lytic bone diseases, the currently available bisphosphonate dr

289 the development or progression of metabolic bone disease; there is minimal risk, providing that low

290 portance of sRANKL/OPG in the development of bone disease, they also highlight the role of this pathw

291 breast cancer, neurodegenerative disorders, bone diseases, Type 1 and Type 2 diabetes).

292 ascade leading to hyperthyroidism, metabolic bone disease, vascular calcification, and cardiovascular

293 eatment and management of treatment of lytic bone disease was reviewed and compared with other forms

294 Increased tumor burden and bone disease were observed in myeloma-bearing adiponecti

295 ial screening or diagnostic tool for diverse bone diseases, where magnetic resonance imaging (MRI) ma

296 At 6 mo, all of PAM had adynamic bone disease, whereas 50% of CON continued to have or de

297 tion against IL-1beta-dependent inflammatory bone disease, whereas the deletion of either caspase alo

298 The management of metastatic bone disease with (223)RaCl2 is uniquely satisfying, as

299 Osteogenesis imperfecta (OI) is a heritable bone disease with dominant and recessive transmission.

300 nts with metabolic bone conditions and other bone diseases with near-normal MRI of the spine, in whom