ライフサイエンスコーパス: osteosarcoma

1 itral valve disease, atrial fibrillation and osteosarcoma).

2 a (two [4%] for Ewing sarcoma, four [9%] for osteosarcoma).

3 r the treatment of drug resistant metastatic osteosarcoma.

4 pecific sarcoma subtypes, including advanced osteosarcoma.

5 mor suppressor activity for the treatment of osteosarcoma.

6 ors with divergent differentiation including osteosarcoma.

7 tion in future trials of IGF1R inhibitors in osteosarcoma.

8 relates with poor prognosis in patients with osteosarcoma.

9 unraveled essential molecular biomarkers in osteosarcoma.

10 inted to the AR as key to CDK11 signaling in osteosarcoma.

11 ion between community water fluoridation and osteosarcoma.

12 nical translation in patients with high-risk osteosarcoma.

13 LFS and are frequently observed in sporadic osteosarcoma.

14 pairment in long-term survivors of childhood osteosarcoma.

15 timate their predictive value of survival in osteosarcoma.

16 nt-free survival in patients with high-grade osteosarcoma.

17 have a role as a suppressor of metastases in osteosarcoma.

18 l improvements in outcomes for patients with osteosarcoma.

19 k in osteoprogenitors results in accelerated osteosarcoma.

20 ciation of community water fluoridation with osteosarcoma.

21 e potential role of the Slit-Robo pathway in osteosarcoma.

22 nd provide potential therapeutic targets for osteosarcoma.

23 son for future phase II trials for recurrent osteosarcoma.

24 e of the newest immune checkpoint, HHLA2, in osteosarcoma.

25 ironment to assess the prognostic utility in osteosarcoma.

26 F dysfunction and altered gene expression in osteosarcoma.

27 in patients with advanced Ewing sarcoma and osteosarcoma.

28 for anti-metastatic treatment strategies in osteosarcoma.

29 is not associated with an increased risk for osteosarcoma.

30 ncer, mesothelioma, melanoma, leukemias, and osteosarcoma.

31 l therapeutics for stratified application in osteosarcoma.

32 th high proportion of TIGIT(+) cells against osteosarcoma.

33 eral preclinical models of Ewing sarcoma and osteosarcoma.

34 preoperative metastatic disease, especially osteosarcoma.

35 option for patients with relapsed metastatic osteosarcoma.

36 nd 31.1 months (24.4-31.7) for patients with osteosarcoma.

37 enib in patients with progressive metastatic osteosarcoma.

38 t some similarities between canine and human osteosarcomas.

39 control of cyclin E1 is a general feature of osteosarcomas.

40 tial therapeutic vulnerability in p53 mutant osteosarcomas.

41 signalling were observed in murine and human osteosarcomas.

42 etic silencing of estrogen receptor in human osteosarcomas.

43 P is inactivated in a subset of ALT-positive osteosarcomas.

44 6.9%) individuals (2 lung adenocarcinomas, 1 osteosarcoma, 1 sarcoma, 1 astrocytoma, 1 low-grade glio

45 ors (54%), other soft tissue sarcomas (21%), osteosarcoma (11%), rhabdomyosarcoma (7%), and other (8%

46 was 7-fold higher in modestly GD2-expressing osteosarcomas (32% GD2-positive cells) than in a GD2-neg

47 1), distinguishing moderately GD2-expressing osteosarcomas (32%-69% GD2-positive cells) from high GD2

48 The most common cancers involved were osteosarcoma (53%), neuroblastoma (37%), prostate (17%)

49 ommon diagnoses were Ewing sarcoma (67%) and osteosarcoma (9%).

50 onse within 6 months of treatment onset; for osteosarcoma, a dual primary endpoint of 6-month objecti

51 k of well validated prognostic biomarkers in osteosarcoma, a rare, recalcitrant disease for which tre

52 with newly diagnosed, resectable, high-grade osteosarcoma aged 40 years or younger were eligible for

53 Osteosarcomas also developed in 44% of Oc-Cre;Rb1(fl/fl)

54 Importantly, depletion of RB in osteosarcoma and breast cancer cell lines results in sen

55 tion induces MALT1 protease activity in both osteosarcoma and breast cancer cells, an activity that i

56 tion results in NF-kappaB activation in both osteosarcoma and breast cancer, which is suppressed by s

57 transgenic models of c-fos oncogene-induced osteosarcoma and chondrosarcoma in addition to c-Fos-ind

58 s with efficient cytotoxic activity in human osteosarcoma and colon carcinoma cells.

59 The adjusted OR for osteosarcoma and ever having lived in a fluoridated area

60 The EFS for 96 patients with osteosarcoma and measurable disease was 12% at 4 months

61 onal oncogenic role for SEMA4C in metastatic osteosarcoma and more importantly that SEMA4C has action

62 onse, including one (5%) of 22 patients with osteosarcoma and one (20%) of five patients with chondro

63 ight be a unique target for the treatment of osteosarcoma and other cancers.

64 to increase understanding of the biology of osteosarcoma and the use of preclinical models to test n

65 maging with PET to measure GD2 expression in osteosarcoma and thus maximize the clinical impact of an

66 in patients with advanced Ewing sarcoma and osteosarcoma and was generally well tolerated.

67 goes neoplastic transformation, resulting in osteosarcoma and, less frequently, in giant cell tumor o

68 d by multiple solid tumors, including 88% of osteosarcomas and 98% of neuroblastomas.

69 fer a mechanistic rationale for treatment of osteosarcomas and other cancers that exhibit dependencie

70 x (one [2%] for Ewing sarcoma, four [9%] for osteosarcoma), and neutropenia (two [4%] for Ewing sarco

71 artilage diseases, including osteoarthritis, osteosarcoma, and chondrosarcoma.

72 ases, cases included patients diagnosed with osteosarcoma, and controls were patients diagnosed with

73 r, skeletal abnormalities, increased risk of osteosarcoma, and decreased bone mass.

74 script levels in a subset of mouse and human osteosarcoma, and SRGAP2 protein expression is reduced o

75 Long-term survivors of osteosarcoma are at risk for neurocognitive impairment,

76 Further studies in osteosarcoma are needed to determine if targeting the PD

77 Osteosarcomas are characterized by highly disrupted geno

78 However, osteosarcomas are highly heterogeneous, with many tumors

79 Osteosarcomas are sarcomas of the bone, derived from ost

80 We identified OS9 (amplified in osteosarcomas) as a novel and specific binding partner o

81 five [11%] for Ewing sarcoma, three [7%] for osteosarcoma), aspartate aminotransferase increase (two

82 ated genes identified numerous known and new osteosarcoma-associated genes enriched in the ErbB, PI3K

83 nd others with promising preclinical data in osteosarcoma at clinically achievable concentrations in

84 DAC may be repurposed to treat patients with osteosarcoma based on its efficacy to decrease prolifera

85 motherapy in patients with poorly responding osteosarcoma because its administration was associated w

86 e performed microRNA sequencing in 74 frozen osteosarcoma biopsy samples, constituting the largest si

87 on cytotoxicity, HOS cell bioactivity (human osteosarcoma) by alkaline phosphatase (ALP) and fluoresc

88 in osteosarcoma, their role in regulation of osteosarcoma cancer stem cells (CSCs) remains unknown.

89 ocalized to the cytoplasm in the majority of osteosarcoma cases and in highly metastatic osteosarcoma

90 ognostic biomarker and therapeutic target in osteosarcoma cases exhibiting aberrant p27 subcellular l

91 This retrospective analysis of 162 osteosarcoma cases was performed to estimate their predi

92 inase 11 (CDK11) signaling was essential for osteosarcoma cell growth and survival.

93 nly partially impaired in cells of the human osteosarcoma cell line Saos-2.

94 red in most cells, except cells of the human osteosarcoma cell line U2OS, and it is only partially im

95 By using an U2OS osteosarcoma cell line with high metastatic potential, p

96 chondrosarcoma cell line, in a CRISPR-edited osteosarcoma cell line, and in chondrocytes derived from

97 ivate hIL-10 receptors in an engineered U2OS osteosarcoma cell line, and increase cellular phospho-ST

98 Here we characterize an osteosarcoma cell line, G292, with wild-type ATRX but a

99 n solution or in situ by the ALP produced by osteosarcoma cell line, SaOs2.

100 , we studied biomineralization in the Soas-2 osteosarcoma cell line.

101 AR protein was highly expressed in various osteosarcoma cell lines and patient tumor tissues.

102 and conditional overexpression in the murine osteosarcoma cell lines K12 and K7M2.

103 demonstrate that JAB1-knockdown in malignant osteosarcoma cell lines significantly reduced their onco

104 We found that the two human osteosarcoma cell lines that supported the growth of the

105 RGAP2 in metastases-associated properties of osteosarcoma cell lines through Srgap2 knockout via the

106 e for growth in most cells, except the human osteosarcoma cell lines U2OS and Saos-2.

107 Xenograft mouse models, using human osteosarcoma cell lines, also demonstrated that LKB1 def

108 With that aim, we used two paired osteosarcoma cell lines, with each one comprising a pare

109 sed transcriptional activation of AR gene in osteosarcoma cell lines.

110 osteosarcoma cases and in highly metastatic osteosarcoma cell lines.

111 at clinically achievable concentrations in 5 osteosarcoma cell lines.

112 pecifically up-regulated in human metastatic osteosarcoma cell lines; engagement of this autocrine lo

113 ecirculated through the microchamber over an osteosarcoma cell monolayer.

114 The proteome needed to support an aggressive osteosarcoma cell phenotype remains largely undefined.

115 plete loss of collagen glycosylation impairs osteosarcoma cell proliferation and viability.

116 ubiquitination level of p21(Cip1), inhibited osteosarcoma cell proliferation, led to cell cycle arres

117 molecule inhibitor of JAB1, CSN5i-3, reduces osteosarcoma cell viability, and has specific effects on

118 id decreased cell viability and migration of osteosarcoma cells (SAOS-2) and preosteoblasts (MC3T3-E1

119 We discovered that osteosarcoma cells (SJSA) are naturally depleted of CDK8

120 A levels of UNC5B by approximately 3-fold in osteosarcoma cells (U2OS) and also stabilizes UNC5B at t

121 ntify on average 829 proteins with 1000 U2OS osteosarcoma cells (~100 ng) with 75-min LC/MS/MS runs,

122 entify its roles in tumors, we employed 143B osteosarcoma cells and HCC1806 triple-negative breast ca

123 y in regulating the stem cell-like traits of osteosarcoma cells and provide a potential target for os

124 ide quantitative volumetric imaging of human osteosarcoma cells at various stages through cell divisi

125 thotopic injection in vivo of FGFR1-silenced osteosarcoma cells caused a marked twofold to fivefold d

126 al overexpression of miR-26a in ZOS and 143B osteosarcoma cells decreases the expression of stem cell

127 Our results reveal that the low metastatic osteosarcoma cells display larger spreading sizes and ge

128 La epithelial cervical cancer cells and 143B osteosarcoma cells express a set of glutamine transporte

129 blocked MAPK activation and colony growth of osteosarcoma cells in vitro.

130 omotes lung colonization by human metastatic osteosarcoma cells in vivo in an orthotopic mouse model.

131 thotopic murine osteosarcoma model and human osteosarcoma cells in which the MT1-MMP gene was knocked

132 lantation of DeltaNp63alpha-expressing human osteosarcoma cells into athymic mice resulted in larger

133 te regulation allows selective inhibition of osteosarcoma cells over hepatocytes, which promises to t

134 showed selective inhibition of SETD8 in U2OS osteosarcoma cells that reflect its selectivity against

135 e complex (CRL4B), is overexpressed in human osteosarcoma cells through an unknown mechanism.

136 Similar results were found in osteosarcoma cells treated with AR inhibitor.

137 l hYVH1-associating proteins from human U2OS osteosarcoma cells using affinity chromatography coupled

138 Here we show that treatment of 143B osteosarcoma cells with decitabine (DAC, 5-Aza-2'-deoxyc

139 ectively image mitochondria in live or fixed osteosarcoma cells with subcellular resolution at 1 nM,

140 mbers is seen to increase DNA breaks in U2OS osteosarcoma cells without affecting migration and with

141 2 cardiomyocytes and in DOXO-sensitive U-2OS osteosarcoma cells, as well as in related cell variants

142 one to screen the envelope libraries on 143B osteosarcoma cells, three novel and unique retargeted en

143 ine and the Wee1 kinase inhibitor AZD1775 in osteosarcoma cells, was dependent on drug sequencing tha

144 asmic p27 promoted migration and invasion of osteosarcoma cells, whereas shRNA-mediated gene silencin

145 posited by cancer-associated fibroblasts and osteosarcoma cells.

146 ophysical properties and force generation of osteosarcoma cells.

147 actomyosin bundles from their precursors in osteosarcoma cells.

148 ted for miR-874 and CCNE1 interdependence in osteosarcoma cells.

149 DDB1 and CUL4 associated factor 11) in human osteosarcoma cells.

150 nd regulates cell cycle progression in human osteosarcoma cells.

151 ormed between CDK11 knock down and wild type osteosarcoma cells.

152 osyltransferase GLT25D1 and GLT25D2 genes in osteosarcoma cells.

153 bilization and the invasion and migration of osteosarcoma cells.

154 rgest single center translationally analyzed osteosarcoma cohort to date, and we separately analyzed

155 s with sarcoma and report the results of the osteosarcoma cohort.

156 cellular internalization studies with mouse osteosarcoma confirm the selectivity of nanomedicine whe

157 emonstrated that miR-26a is downregulated in osteosarcoma CSCs when derived by either sarcosphere gen

158 nosine triphosphate (ATP) synthesis rates of osteosarcoma cybrid cells were measured before and after

159 In an orthotopic model of osteosarcoma, DAC inhibited tumor growth and metastasis

160 row-derived mesenchymal stem cells and human osteosarcoma-derived cells.

161 phenotype of mutant p53 but had no effect on osteosarcoma development, which remained 100% penetrant.

162 the role of MT1-MMP during various stages of osteosarcoma development.

163 The tumor cells in human osteosarcoma display a strong expression of MT1-MMP, but

164 estrogen receptor alpha (ERalpha); however, osteosarcomas do not express ERalpha due to promoter DNA

165 ngoing at >/= 19 months), and a patient with osteosarcoma (duration, 4 months).

166 his system by imaging S1P(1)-eGFP-Human bone osteosarcoma epithelial (U2OS) cells.

167 ed to a test sample consisting of human bone osteosarcoma epithelial cells, with plasma membrane tran

168 ial responses) by 6 months; in patients with osteosarcoma, five (12%; 4-26) of 42 patients had an obj

169 roblastoma, but its application to recurrent osteosarcomas, for which no effective therapies exist, h

170 ortant role in osteoblast transformation and osteosarcoma formation and regulates the development of

171 cient miRNAs were remarkably preserved in an osteosarcoma from a skeleton with extensive disease, wit

172 downstream signalling pathways that regulate osteosarcoma growth and metastasis.

173 igated the role of semaphorin 4C (SEMA4C) in osteosarcoma growth, progression, and metastasis.

174 Patients with Ewing sarcoma or osteosarcoma have a median overall survival of less than

175 echanism of isolated mitochondria into human osteosarcoma (HOS) cells.

176 neither primitive neuroectodermal tumor nor osteosarcoma) (HR for PFS, 0.39; 95% CI, 0.18-0.81; P =

177 l sarcoma, neuroblastoma, Ewing sarcoma, and osteosarcoma) identified expression signatures associate

178 new tools to quantify tumor heterogeneity in osteosarcoma, identifying potentially useful prognostic

179 ondria-targeted cell imaging, in vivo NIR-II osteosarcoma imaging and excellent photothermal efficien

180 anism that contributes to the development of osteosarcoma in children and adults alike.

181 erentiated osteosarcomas that resemble human osteosarcoma in histology, location, metastatic behavior

182 poor for children with recurrent/refractory osteosarcoma in these single-arm phase II trials.

183 (pp. 1847-1857) develop a new mouse model of osteosarcoma in which a GOF mutant p53 allele is express

184 Strikingly, the development of osteosarcomas in these mice was greatly accelerated comp

185 ng squamous cell carcinoma, brain tumor, and osteosarcoma, in addition to several normal tissues, inc

186 Osteosarcoma is a highly metastatic form of bone cancer

187 Osteosarcoma is a malignant tumor in the bone, which ori

188 Osteosarcoma is a primary malignancy of bone that affect

189 Osteosarcoma is the most common bone cancer in children

190 Osteosarcoma is the most common primary bone tumor, with

191 Osteosarcoma is the most common primary malignancy of th

192 Osteosarcoma is the most common type of primary bone can

193 Osteosarcoma is the most frequent primary bone tumor wit

194 Osteosarcoma is the most frequent primary tumor of bone

195 ithelial (A549) and highly metastatic murine osteosarcoma (K7M2) cells lines.

196 Although osteosarcomas lack common fusions, we find evidence of m

197 rivation and that miR-874 down-regulation in osteosarcomas leads to CCNE1 up-regulation and more aggr

198 hondroblastic, recurrent and lung metastatic osteosarcoma lesions compared to primary osteoblastic os

199 primary, 2 recurrent, and 2 lung metastatic osteosarcoma lesions, 11 major cell clusters are identif

200 s infiltration is noticed in lung metastatic osteosarcoma lesions.

201 oma lesions compared to primary osteoblastic osteosarcoma lesions.

202 tomic properties, regulators and dynamics of osteosarcoma malignant cells together with their tumor m

203 Eighty survivors of osteosarcoma (mean [SD] age, 38.9 [7.6] years; time sinc

204 usly identified potential genetic drivers of osteosarcoma metastasis, including Slit-Robo GTPase-Acti

205 axon guidance proteins likely play a role in osteosarcoma metastasis, with loss of SRGAP2 potentially

206 activation may be beneficial for controlling osteosarcoma metastasis.

207 on in primary osteoblasts, but in aggressive osteosarcomas, miR-874 is down-regulated, leading to ele

208 We utilized an optimized orthotopic murine osteosarcoma model and human osteosarcoma cells in which

209 Deltaosx1) double knockout establishes a new osteosarcoma model with significant advancement over exi

210 ionality and in vitro and in vivo studies in osteosarcoma models showed no significant effect on B7H3

211 metastasis, we developed a traceable somatic osteosarcoma mouse model that is initiated with either a

212 The most frequent histologies were osteosarcoma (n = 6), inflammatory myofibroblastic tumor

213 se cohorts: rhabdomyosarcoma, Ewing sarcoma, osteosarcoma, neuroblastoma, Hodgkin lymphoma, non-Hodgk

214 in preclinical models of primary intratibial osteosarcomas, observing marked inhibition of both tumor

215 Osteosarcoma occurs predominantly in children and young

216 and magnetic resonance imaging (MRI) of the osteosarcoma of human patients.

217 oup database with primary central high-grade osteosarcoma of the extremities, treated between 1980 an

218 of patients with primary central high-grade osteosarcoma of the extremities.

219 3) in a 34% GD2-positive model of metastatic osteosarcoma of the lung.

220 the expression of the signaling proteins FBJ osteosarcoma oncogene (c-FOS, encoded by Fos) and dual-s

221 d mRNAs that are differentially regulated in osteosarcoma (OS) cell lines, we report that miR-449a an

222 as a factor that suppresses this ability in osteosarcoma (OS) cells, mainly by inhibiting NF-kappaB

223 Overall survival of patients with osteosarcoma (OS) has improved little in the past three

224 erapy, outcomes for patients with metastatic osteosarcoma (OS) have not improved in thirty years.

225 Osteosarcoma (OS) is the most common bone cancer in chil

226 Osteosarcoma (OS) is the most common bone tumor characte

227 Osteosarcoma (OS) is the most common cancer of bone and

228 Osteosarcoma (OS) is the most common primary bone cancer

229 Osteosarcoma (OS) is the most common primary malignant b

230 Osteosarcoma (OS) is the most common primary pediatric m

231 Limited clinical activity has been seen in osteosarcoma (OS) patients treated with immune checkpoin

232 Doxo-NPs) significantly attenuated localized osteosarcoma (OS) progression compared with nontargeted

233 Osteosarcoma (OS) represents 3.4% of all childhood cance

234 Osteosarcoma (OS), chondrosarcoma, and chordoma are char

235 complete loss of P53 is a frequent event in osteosarcoma (OS), the most common cancer of bone.

236 Osteosarcoma (OS), the most common primary bone cancer i

237 l in pediatric and young adult patients with osteosarcoma (OS).

238 tral valve disease, atrial fibrillation, and osteosarcoma (P < 0.05) after adjusting for multiple com

239 abdomyosarcomas (p<0.0001 in all cases), and osteosarcomas (p=0.011).

240 ia (poor general health, 9.5% and 13.9%) and osteosarcoma (pain, 23.9% and 36.6%).

241 (two [4%] for Ewing sarcoma, three [7%] for osteosarcoma), palmar-plantar syndrome (three [7%] for E

242 Osteosarcoma patient survival has remained stagnant for

243 ession and localization of SEMA4C in primary osteosarcoma patient tissues and its tumorigenic functio

244 Using a large cohort of serum samples from osteosarcoma patients (n = 233), we validated that a hig

245 All IMT patients survived while all osteosarcoma patients died during follow-up.

246 In serum from osteosarcoma patients, the presence of IRX1 hypomethylat

247 lung metastasis and poor overall survival of osteosarcoma patients.

248 CDKN1B) were elevated in plasma of high-risk osteosarcoma patients.

249 re top risk factors associated with death of osteosarcoma patients.

250 (three [7%] for Ewing sarcoma, two [4%] for osteosarcoma), pneumothorax (one [2%] for Ewing sarcoma,

251 ssion of MT1-MMP, but the role of MT1-MMP in osteosarcoma progression is currently unknown.

252 sed MT1-MMP is dispensable for all stages of osteosarcoma progression.

253 l in patients with advanced Ewing sarcoma or osteosarcoma recruited from ten centres in the French Sa

254 Survivors of osteosarcoma recruited from the St Jude Lifetime Cohort

255 Osteosarcoma resection is challenging due to the variabl

256 esign patient-specific guiding templates for osteosarcoma resection on the basis of the computer tomo

257 To overcome the challenge in precise osteosarcoma resection, computer-aided design (CAD) was

258 sr39tk CAR T cells in an orthotopic model of osteosarcoma revealed tumor homing and systemic immune e

259 l immune cell types examined were present in osteosarcoma samples, only infiltration by dendritic cel

260 ificantly decreased in calcifying human bone osteosarcoma (SaOs-2) cells.

261 its potential role as a tumor suppressor in osteosarcoma.See related commentary by Roberts, p.

262 In situ assessment of all GD2-positive osteosarcoma sites with a novel PET radiotracer could si

263 OTA-hu14.18K322A to detect GD2 expression in osteosarcomas (six patient-derived xenografts and one ce

264 TILs were present in 75% of all osteosarcoma specimens.

265 ts registered in the Consecutive Cooperative Osteosarcoma Study Group database with primary central h

266 The previously unrecognized osteosarcoma subtypes with distinct clinical courses and

267 The guiding templates were used to guide the osteosarcoma surgery, leading to more precise resection

268 Thyroid Carcinoma (MTC) Surveillance Study, Osteosarcoma Surveillance Study, Prostate Cancer Outcome

269 deformities, photosensitivity, and increased osteosarcoma susceptibility.

270 n a murine xenograft model of advanced human osteosarcoma, tenascin-C and its receptor integrin alpha

271 nockout mice developed poorly differentiated osteosarcomas that resemble human osteosarcoma in histol

272 c progression is the major cause of death in osteosarcoma, the most common bone malignancy in childre

273 ble intervention point in murine p53/Rb-null osteosarcomas, the human counterpart of which lacks effe

274 hough several miRNAs have been implicated in osteosarcoma, their role in regulation of osteosarcoma c

275 oma cells and provide a potential target for osteosarcoma therapy.

276 lso play a role in bone-forming cancers like osteosarcoma, this idea has remained untested.

277 Using a human osteosarcoma tissue microarray we identified high expres

278 sequencing and immunohistochemistry of human osteosarcoma tissue samples were used to further evaluat

279 , we present the largest sequencing study of osteosarcoma to date, comprising 112 childhood and adult

280 prognostic marker and therapeutic target for osteosarcoma treatment.

281 esponse as the primary end point in phase II osteosarcoma trials may limit optimal detection of treat

282 or specimens and metastatic disease using an osteosarcoma tumor microarray (TMA) (n = 62).

283 novel immunosuppressive mechanism within the osteosarcoma tumor microenvironment.

284 n that HHLA2 is expressed in the majority of osteosarcoma tumors and its expression is associated wit

285 The 25% of primary osteosarcoma tumors that express PD-L1 were more likely

286 HHLA2 was expressed in 68% of osteosarcoma tumors.

287 Uninfected epithelial SLK and osteosarcoma U2OS cells transfected with KSHV luciferase

288 the SRSF3-regulated splicing events in human osteosarcoma U2OS cells, we found that SRSF3 regulates t

289 pecific manner in human B cell line Raji and osteosarcoma U2OS cells.

290 The results of this study of osteosarcomas underscores the numerous benefits associat

291 ine-3') sites close to the c-Fos (FBJ murine osteosarcoma viral oncogene homolog) transcriptional sta

292 PD-L1 expression in osteosarcoma was examined in two patient cohorts using i

293 However, the role of JAB1 in osteosarcoma was virtually unknown.

294 In this largest study to date with extremity osteosarcomas, we observed the occurrence of PF to corre

295 ith Ewing sarcoma and 42 (93%) patients with osteosarcoma were assessable for efficacy after histolog

296 Some of the osteocalcin-lineage-derived osteosarcomas were among the least osteoblastic.

297 , 90 patients (45 with Ewing sarcoma 45 with osteosarcoma) were recruited to the study.

298 a phase II study (AOST0221) of patients with osteosarcoma who were given inhaled granulocyte-macropha

299 udy confirmed that p53 mutant mice developed osteosarcomas with increased metastasis as compared with

300 itu hybridization (FISH) in an additional 87 osteosarcomas, with IGF1 receptor (IGF1R) amplification

301 se NIR fluorescence signals were detected in osteosarcoma xenografts, with signal/background ratio at