ライフサイエンスコーパス: osteosarcoma

1 ctivity against cancer cell models (ovarian, osteosarcoma).

2 l improvements in outcomes for patients with osteosarcoma.

3 k in osteoprogenitors results in accelerated osteosarcoma.

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

5 son for future phase II trials for recurrent osteosarcoma.

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

7 tion in future trials of IGF1R inhibitors in osteosarcoma.

8 ironment to assess the prognostic utility in osteosarcoma.

9 F dysfunction and altered gene expression in osteosarcoma.

10 directly to the sites of lung metastases of osteosarcoma.

11 expressed at primary and metastatic sites of osteosarcoma.

12 functionally validated as oncogenes in human osteosarcoma.

13 ively improved the survival of patients with osteosarcoma.

14 genetic landscape and biological behavior of osteosarcoma.

15 luence the final differentiation state of an osteosarcoma.

16 some were formerly unknown in the context of osteosarcoma.

17 relates with poor prognosis in patients with osteosarcoma.

18 unraveled essential molecular biomarkers in osteosarcoma.

19 lymphoma, acute lymphoblastic leukemia, and osteosarcoma.

20 ulnerability for therapeutic exploitation in osteosarcoma.

21 therapy is a promising approach to treating osteosarcoma.

22 ocytic leukemia, non-Hodgkin's lymphoma, and osteosarcoma.

23 limiting step in the formation of IR-induced osteosarcoma.

24 re the strongest risk factors for developing osteosarcoma.

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

26 ical mechanisms underlying susceptibility to osteosarcoma.

27 most common primary malignancy of bone after osteosarcoma.

28 ors with divergent differentiation including osteosarcoma.

29 nical translation in patients with high-risk osteosarcoma.

30 LFS and are frequently observed in sporadic osteosarcoma.

31 pairment in long-term survivors of childhood osteosarcoma.

32 timate their predictive value of survival in osteosarcoma.

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

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

35 signalling were observed in murine and human osteosarcomas.

36 n sharply reduces CSCs and tumorigenicity of osteosarcomas.

37 r Sox2 maintains cancer stem cells (CSCs) in osteosarcomas.

38 uppressive Hippo pathway to maintain CSCs in osteosarcomas.

39 n metastasis), was increased in p53(R172H/+) osteosarcomas.

40 ls had accelerated development of IR-induced osteosarcomas.

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

42 tial therapeutic vulnerability in p53 mutant osteosarcomas.

43 6.9%) individuals (2 lung adenocarcinomas, 1 osteosarcoma, 1 sarcoma, 1 astrocytoma, 1 low-grade glio

44 the LFS tumor spectrum was characterized by osteosarcomas, adrenocortical carcinomas (ACC), CNS tumo

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

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

47 yet also robustly associates with the lectin osteosarcoma amplified 9 (OS-9), a component involved in

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

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

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

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

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

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

54 hown to be within a tumor suppressor unit in osteosarcoma and to suppress tumor cell growth.

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

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

57 astoma, rhabdomyosarcoma, Ewing sarcoma, and osteosarcoma), and brain tumors (gliomas, ependymomas, a

58 These include 2 leukemias, 1 osteosarcoma, and 2 lymphomas.

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

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

61 tool for detection of high CXCR4-expressing osteosarcoma, and particularly for its metastatic lesion

62 uroblastoma, Wilms' tumour, Ewing's sarcoma, osteosarcoma, and rhabdomyosarcoma.

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

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

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

66 Osteosarcomas are aggressive bone tumours with a high de

67 Osteosarcomas are sarcomas of the bone, derived from ost

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

69 essful isolation of CSCs from primary canine osteosarcoma, as well as established cell lines.

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

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

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

73 s enhanced cell killing in a PAD4 expressing osteosarcoma bone marrow (U2OS) cell line and can also b

74 that the repurposing of chemotherapeutics in osteosarcoma by using an in vitro system may define nove

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

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

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

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

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

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

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

82 leted 143B TK- rho0 cells from an aggressive osteosarcoma cell line with mitochondria from benign bre

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

84 MMP-13 in UMR 106-01 cells, an osteoblastic osteosarcoma cell line.

85 In both human osteosarcoma cell lines and clinical osteosarcoma tissue

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

87 rial transplantation of cells from different osteosarcoma cell lines and primary osteosarcoma tissues

88 Osteosarcoma cell lines are responsive to pharmacologic

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

90 Overexpression of MTBP in human osteosarcoma cell lines lacking wild-type p53 did not al

91 thermore, experimental modulation of IRX1 in osteosarcoma cell lines profoundly altered metastatic ac

92 Here, we analyzed 2 syngeneic primary human osteosarcoma cell lines that exhibit disparate metastati

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

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

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

96 ession of mutant p53 in both mouse and human osteosarcoma cell lines, indicating that Pla2g16 is a do

97 herapeutics demonstrated IC50 values against osteosarcoma cell lines, known to metastasize to the lun

98 osteosarcoma cases and in highly metastatic osteosarcoma cell lines.

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

100 at clinically achievable concentrations in 5 osteosarcoma cell lines.

101 RNAs and AUF1 has been identified in various osteosarcoma cell lines.

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

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

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

105 The binding to representative osteosarcoma cells (F5M2 and F4 for high- and low- CXCR4

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

107 odomain inhibitor, reduces cell viability of osteosarcoma cells and inhibits osteoblastic differentia

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

109 e that AUF1 promotes mesenchymal features in osteosarcoma cells and that miR-141 and miR-146b-5p supp

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

111 rexpression of ezrin in low-ezrin-expressing osteosarcoma cells caused a notable increase in DDX3 pro

112 Silencing ICMT in human osteosarcoma cells decreased Notch1 signaling in respons

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

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

115 crease the oxidative phosphorylation rate in osteosarcoma cells grown under normoxic conditions.

116 ADC eliminated pulmonary lesions from human osteosarcoma cells in a lung-seeding tumor model in mice

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

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

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

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

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

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

123 ion/migration and proliferation abilities of osteosarcoma cells through inhibiting the AKT protein ki

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

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

126 vector pEGFP-ING4 and transfected the human osteosarcoma cells using this vector.

127 ed widely with the best response observed in osteosarcoma cells with MDM2 gene amplification.

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

129 The up-regulation of ING4 in the osteosarcoma cells, arising from the stable pEGFP-ING4 g

130 ERK2, and the effects are not restricted to osteosarcoma cells, as they can be extended to several o

131 2 cardiomyocytes and in DOXO-sensitive U-2OS osteosarcoma cells, as well as in related cell variants

132 esion of 3 different cell types (human Saos2 osteosarcoma cells, human synovial fibroblasts, and rat

133 ts and these were assessed in vitro in MG-63 osteosarcoma cells, leading to the identification of (R)

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

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

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

137 -sensitive mutant virus (Cts2 virus) in U2OS osteosarcoma cells.

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

139 proliferation, apoptosis and invasion of the osteosarcoma cells.

140 nd regulates cell cycle progression in human osteosarcoma cells.

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

142 osyltransferase GLT25D1 and GLT25D2 genes in osteosarcoma cells.

143 method to prepare stably IF1-silenced human osteosarcoma clones and explored the bioenergetics of IF

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

145 , suggesting that naturally occurring canine osteosarcoma could act as a preclinical model for the hu

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

147 lin C in a manner similar to MEF cells, U2OS osteosarcoma cultures display constitutively cytoplasmic

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

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

150 egulated mRNA transcripts genome-wide in the osteosarcoma-derived U2OS cell line.

151 nodules identified 232 sites associated with osteosarcoma development and 43 sites associated with me

152 To identify the genes driving osteosarcoma development and metastasis, we performed a

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

154 rmalities have been demonstrated to underlie osteosarcoma development; however, the epigenetic mechan

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

156 Human bone osteosarcoma epithelial cell line U2OS was transfected w

157 Systemic therapy has improved osteosarcoma event-free and overall survival, but 30-50%

158 athways drive chromosomal instability during osteosarcoma evolution and result in the acquisition of

159 However, >80% of osteosarcomas exhibit a specific combination of single-b

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

161 as from p53(R172H/+) mice with metastasis to osteosarcomas from p53(+/-) mice lacking metastasis.

162 we used expression arrays to compare primary osteosarcomas from p53(R172H/+) mice with metastasis to

163 downstream signalling pathways that regulate osteosarcoma growth and metastasis.

164 Osteosarcoma has a complex karyotype, with loss of p53 i

165 Both canine and human osteosarcoma has been shown to contain a sub-population

166 The differentiation state of osteosarcomas has therefore become a topic of interest a

167 The genetic drivers of osteosarcoma have been difficult to identify because of

168 DeltaN-IkappaBalpha allows cells of a human osteosarcoma (HOS) cell line to be chronically infected

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

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

171 Mouse LM8 osteosarcoma, human 143B, and Caprin-1 stably overexpres

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

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

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

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

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

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

178 Osteosarcoma is a common malignant bone tumor with a pro

179 Osteosarcoma is a highly metastatic form of bone cancer

180 Osteosarcoma is a primary malignancy of bone that affect

181 Osteosarcoma is associated with massive genomic instabil

182 Osteosarcoma is the bone tumor that most commonly affect

183 Osteosarcoma is the most common bone cancer in children

184 Osteosarcoma is the most common primary bone malignancy

185 Osteosarcoma is the most common primary bone tumor, with

186 Osteosarcoma is the most common primary bone tumor, yet

187 Osteosarcoma is the most common primary bone tumour of b

188 Osteosarcoma is the most common primary malignancy of th

189 metastasectomies in patients with metastatic osteosarcoma is well substantiated.

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

191 ent in prognosis for patients with localized osteosarcoma; long-term survival rates of less than 20%

192 f(+) subpopulation composing the bulk of the osteosarcoma mass.

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

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

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

196 activation may be beneficial for controlling osteosarcoma metastasis.

197 suggest a mechanistic role for DeltaNp63 in osteosarcoma metastasis.

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

199 nificantly inhibited the growth of the human osteosarcoma MNNG/HOS xenograft in nude mice.

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

201 ues showed higher activity especially in the osteosarcoma model.

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

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

204 Osteosarcoma occurs predominantly in children and young

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

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

207 ted by the transcriptional activation of FBJ osteosarcoma oncogene (Fos) and fos-like antigen 1 (Fosl

208 g the recruitment of the AP-1 components FBJ osteosarcoma oncogene (FOS) and jun proto-oncogene (JUN)

209 gulation of oxytocin receptor (Oxtr) and FBJ osteosarcoma oncogene (Fos), the promoters of which also

210 ed 19 patients with HER2-positive tumors (16 osteosarcomas, one Ewing sarcoma, one primitive neuroect

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

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

213 Osteosarcoma (OS) is a primary bone tumor that is most p

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

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

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

217 Osteosarcoma (OS) is the most frequent pediatric maligna

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

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

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

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

222 the role of mutant p53 in the development of osteosarcoma (OS).

223 p.D104N affects the risk and progression of osteosarcoma (OS).

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

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

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

227 Osteosarcoma patient survival has remained stagnant for

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

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

230 lung metastasis and poor overall survival of osteosarcoma patients.

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

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

233 Our work suggests that ING4 can suppress osteosarcoma progression through signaling pathways such

234 Survivors of osteosarcoma recruited from the St Jude Lifetime Cohort

235 Osteosarcomas remain an enigmatic group of malignancies

236 However, the function of ING4 in human osteosarcoma remains unclear.

237 Osteosarcoma resection is challenging due to the variabl

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

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

240 When tested in human osteosarcoma, rhabdomyosarcoma, and Ewing's sarcoma stem

241 hibition in mouse xenograft models of SJSA-1 osteosarcoma, RS4;11 acute leukemia, LNCaP prostate canc

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

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

244 ge reiterate the radiation susceptibility to osteosarcoma seen in patients with germline RB1 mutation

245 ron alfa-2b (IFN-alpha-2b) in patients whose osteosarcoma showed good histologic response (good respo

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

247 global gene expression profiles of isolated osteosarcoma stem cells and the daughter adherent cells.

248 ta from prospective neoadjuvant chemotherapy osteosarcoma studies and registries to examine the relat

249 itulated the corresponding behavior for each osteosarcoma subtype; thus, we used cell lines to valida

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

251 s to identify genomic events contributing to osteosarcoma survival.

252 deformities, photosensitivity, and increased osteosarcoma susceptibility.

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

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

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

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

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

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

259 dentified two distinct molecular subtypes of osteosarcoma through gene expression profiling.

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

261 ifferent osteosarcoma cell lines and primary osteosarcoma tissues progressively increased the CD49f(+

262 h human osteosarcoma cell lines and clinical osteosarcoma tissues, IRX1 overexpression was strongly a

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

264 prognostic marker and therapeutic target for osteosarcoma treatment.

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

266 ) and an experimental dataset of four canine osteosarcoma tumor cultures following application of 60

267 ross validation error of <10% for the canine osteosarcoma tumor cultures using a drug screen consisti

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

269 novel immunosuppressive mechanism within the osteosarcoma tumor microenvironment.

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

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

272 HHLA2 was expressed in 68% of osteosarcoma tumors.

273 spose to both sporadic and radiation-induced osteosarcoma, tumors characterized by high levels of gen

274 ucettine L41 triggers bona fide autophagy in osteosarcoma U-2 OS cells and immortalized mouse hippoca

275 of gp130 per se, as silencing ERK2 in human osteosarcoma U2OS cells inhibits the expression of gp130

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

277 Human osteosarcoma U2OS cells treated with anti-cancer drugs D

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

279 arkedly reduced in both XPD-suppressed human osteosarcoma (U2OS) cells and XPD-deficient human fibrob

280 ease in PtdIns5P in cells derived from human osteosarcoma, U2OS (5-fold); breast tumors, MDA-MB-468 (

281 examined in a mouse xenograft model of human osteosarcoma using NIR fluorescence microscopy and a Kod

282 ore binding factor 1 (CBFA1), and FBJ murine osteosarcoma viral oncogene homolog (c-Fos).

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

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

285 potential roles and mechanisms in inhibiting osteosarcoma, we constructed an expression vector pEGFP-

286 the pediatric solid tumors neuroblastoma and osteosarcoma, we find overexpression of DeltaNp63; howev

287 By using a second set of human osteosarcomas, we merged IHC and biochemical analyses to

288 age </= 40 years with resectable high-grade osteosarcoma were registered.

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

290 rable antitumor activity in a mouse model of osteosarcoma, whereas activated NK cells were ineffectiv

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

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

293 ibited accelerated development of IR-induced osteosarcoma, with a latency of 39 weeks.

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

295 n vivo antitumor activity in both the SJSA-1 osteosarcoma xenograft model (ED50 = 2.6 mg/kg QD) and t

296 and in vivo antitumor activity in the SJSA-1 osteosarcoma xenograft model (ED50 = 9.1 mg/kg).

297 s excellent antitumor activity in the SJSA-1 osteosarcoma xenograft model with an ED50 of 11 mg/kg.

298 s excellent antitumor activity in the SJSA-1 osteosarcoma xenograft model with an ED50 of 41 mg/kg.

299 Pulmonary metastases in mice bearing osteosarcoma xenografts were detected by micro CT, (18)F

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