ライフサイエンスコーパス: sarcoma

1 h tumor (MPNST) is an aggressive soft tissue sarcoma.

2 for most patients with advanced soft-tissue sarcoma.

3 transcriptional programs underlying Ewing's sarcoma.

4 the clinic for the benefit of patients with sarcoma.

5 and MEK inhibitor in patients with advanced sarcoma.

6 lic complications, frequently develop Kaposi sarcoma.

7 aluation of epigenetic pathway inhibitors in sarcoma.

8 tment for advanced or metastatic soft-tissue sarcoma.

9 cts, depending on the developmental stage of sarcoma.

10 ts with advanced soft-tissue sarcoma or bone sarcoma.

11 lignancies, including lymphomas and Kaposi's sarcoma.

12 erve sheath tumor, an aggressive soft-tissue sarcoma.

13 and one (10%) of ten patients with synovial sarcoma.

14 , meningioma, chondrosarcoma and fibromyxoid sarcoma.

15 carcinoma, and 13% for secondary soft-tissue sarcoma.

16 r and drug target for the treatment of Ewing sarcoma.

17 ential shift in the treatment of soft-tissue sarcoma.

18 's disease, as well as its namesake Kaposi's sarcoma.

19 l tumor (GIST) is the most common subtype of sarcoma.

20 treatment strategy for childhood soft tissue sarcoma.

21 d bone sarcoma, and 26 (59%) had soft tissue sarcoma.

22 ed with the endothelial-derived tumor Kaposi sarcoma.

23 arcoma is the most common subtype of uterine sarcoma.

24 nsplant period, one of whom developed Kaposi sarcoma.

25 r locally advanced or metastatic soft-tissue sarcoma.

26 primary nonmetastatic extremity soft tissue sarcomas.

27 more active compared with other soft tissue sarcomas.

28 est increases for haematological tumours and sarcomas.

29 sarcoma, Ewing sarcoma, and other round cell sarcomas.

30 nosed and refractory or recurrent round cell sarcomas.

31 de exposure increases the risk of subsequent sarcomas.

32 first-line therapy for advanced soft-tissue sarcomas.

33 linical outcomes in patients with round cell sarcomas.

34 ced perturbation of the PI3K/mTOR pathway in sarcomas.

35 ed for the treatment of advanced soft tissue sarcomas.

36 formation to high-grade radiation-associated sarcomas.

37 s (2 lung adenocarcinomas, 1 osteosarcoma, 1 sarcoma, 1 astrocytoma, 1 low-grade glioma, and 2 preinv

38 e breast cancer (5 patients) and soft-tissue sarcoma (2 patients).

39 ratio [95% CI], 3.5 [1.7-7.1]); soft-tissue sarcoma (2.8 [2.1-3.9]); breast carcinoma (2.1 [1.8-2.4]

40 1.67-1.72), AIDS-defining cancers (Kaposi's sarcoma [498.11, 477.82-519.03], non-Hodgkin lymphoma [1

41 centres in the USA that were members of the Sarcoma Alliance for Research through Collaboration (SAR

42 is method to Illumina-sequenced 10x Genomics sarcoma and breast cancer data sets.

43 This effect occurs in metastatic human sarcoma and carcinoma cells- but not in normal or non-me

44 f previous regimens for advanced soft-tissue sarcoma and in blocks of six.

45 ciency of acid-dependent fusion of the avian sarcoma and leukosis virus (ASLV), with endosomes.

46 s except for specific tumors, such as Kaposi sarcoma and mantle cell lymphoma.

47 associated with the development of Kaposi's sarcoma and multicentric Castleman's disease, as well as

48 the Haitian Group for the Study of Kaposi's Sarcoma and Opportunistic infections (GHESKIO) Clinic in

49 cancer models, as well as clinical data from sarcoma and prostate cancer patients.

50 However, patients without bone sarcoma and those able to tolerate therapy for more than

51 tumors than in normal tissues and longer in sarcomas and gliomas than in other cancers.

52 dian GARD values were lowest for gliomas and sarcomas and highest for cervical cancer and oropharynge

53 implicated in unexpected cancers, including sarcomas and lung tumors.

54 ential existence of EMT-related processes in sarcomas and propose that sarcomas can reside in a metas

55 ced, unresectable, or metastatic soft-tissue sarcomas and so this combination cannot be recommended i

56 rials, 27 (61%) were male; 18 (41%) had bone sarcoma, and 26 (59%) had soft tissue sarcoma.

57 onal and alveolar rhabdomyosarcoma, synovial sarcoma, and adult soft tissue sarcomas diagnosed in ado

58 reatment-associated risks for breast cancer, sarcoma, and all solid cancers.

59 (MCAM) as a novel KDM3A target gene in Ewing Sarcoma, and an important effector of KDM3A pro-metastat

60 ymphoma, acute myeloid leukemia, soft-tissue sarcoma, and central nervous system cancer.

61 ren, particularly in rhabdomyosarcoma, Ewing sarcoma, and other round cell sarcomas.

62 Nonmelanoma skin cancer, Kaposi sarcoma, and posttransplant lymphoproliferative disease

63 Sarcomas, and the mesenchymal precursor cells from which

64 Conclusion Survivors of Ewing sarcoma apparently returned to a normal life with minor

65 Although a subset of sarcomas appears inflamed and responsive to immune check

66 n fact, although the existence of the EMT in sarcomas appears paradoxical because these cancers are,

67 epithelioid hemangioendothelioma, and Kaposi sarcoma are classified according to the line of differen

68 Sarcomas are a broad family of mesenchymal malignancies

69 Soft tissue and bone sarcomas are malignancies of mesenchymal origin, and mor

70 gnancies, these sarcomas (excepting synovial sarcoma) are characterized predominantly by copy-number

71 One consequence of their rarity among sarcomas, as well as their biologic and clinical heterog

72 rpes virus 8 (HHV-8), also known as Kaposi's sarcoma associated herpesvirus (KSHV), is an oncogenic v

73 Kaposi's sarcoma-associated herpes virus (KSHV) polyadenylated nu

74 osi sarcoma is caused by infection of Kaposi sarcoma-associated herpesvirus (KSHV) and is characteriz

75 ng domains (DBDs), LANA homologs from Kaposi sarcoma-associated herpesvirus (KSHV) and MHV68 exhibit

76 t is transferable to MHV68.IMPORTANCE Kaposi sarcoma-associated herpesvirus (KSHV) and murine gammahe

77 DNA tumor viruses such as Kaposi's sarcoma-associated herpesvirus (KSHV) are known to inter

78 sing the dimeric protease (Pr) from Kaposi's sarcoma-associated herpesvirus (KSHV) as a model system,

79 s of the KSHV life cycle.IMPORTANCE Kaposi's sarcoma-associated herpesvirus (KSHV) causes AIDS-relate

80 Kaposi's sarcoma-associated herpesvirus (KSHV) encodes 12 pre-mic

81 viruses Epstein-Barr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV) establish persiste

82 cription across the entirety of the Kaposi's sarcoma-associated herpesvirus (KSHV) genome and postula

83 hat most transcripts encoded by the Kaposi's sarcoma-associated herpesvirus (KSHV) genome undergo m(6

84 ssembly of RNA polymerase II around Kaposi's sarcoma-associated herpesvirus (KSHV) genomes in the hos

85 ls.IMPORTANCE B cells infected with Kaposi's sarcoma-associated herpesvirus (KSHV) harbor multiple co

86 Oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV) has latent and lyt

87 t an innovative approach to culture Kaposi's sarcoma-associated herpesvirus (KSHV) infected human B c

88 ymphogenic disorder associated with Kaposi's sarcoma-associated herpesvirus (KSHV) infection.

89 The K15P membrane protein of Kaposi's sarcoma-associated herpesvirus (KSHV) interacts with mul

90 Kaposi's sarcoma-associated herpesvirus (KSHV) is a gammaherpesvi

91 Kaposi's sarcoma-associated herpesvirus (KSHV) is etiologically a

92 Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative a

93 Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative a

94 Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic a

95 Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic a

96 ases.IMPORTANCE The K15P protein of Kaposi's sarcoma-associated herpesvirus (KSHV) is thought to play

97 Specific regions of Kaposi's sarcoma-associated herpesvirus (KSHV) latent episomes ar

98 DNA, although detail concerning how Kaposi's sarcoma-associated herpesvirus (KSHV) modulates these ce

99 lectively isolating VLVs by using a Kaposi's sarcoma-associated herpesvirus (KSHV) mutant that is def

100 iated nuclear antigen (LANA) of the Kaposi's sarcoma-associated herpesvirus (KSHV) performs a variety

101 ted mechanism of viral replication: Kaposi's sarcoma-associated herpesvirus (KSHV) stably clusters it

102 E-like inhibitor protein (vFLIP) of Kaposi's sarcoma-associated herpesvirus (KSHV), against influenza

103 The human gammaherpesvirus, Kaposi's sarcoma-associated herpesvirus (KSHV), is tightly associ

104 1 promotes the aggressive growth of Kaposi's sarcoma-associated herpesvirus (KSHV)-related malignanci

105 The responsible agent, Kaposi's sarcoma-associated herpesvirus (KSHV; HHV8), expresses m

106 Kaposi's sarcoma-associated herpesvirus is a leading cause of can

107 one of oncogenic viruses infection, Kaposi's sarcoma-associated herpesvirus.

108 Effects of Ca-SP on Kaposi sarcoma-associated herpesvirus/human herpes virus 8 repl

109 he oncogenic human gammaherpesvirus Kaposi's sarcoma-associated herpesvirus/human herpesvirus 8 (KSHV

110 resultant tumors are either monophasic (pure sarcomas), biphasic (a combination or epithelioid and sa

111 type 1 (HIV-1) infection and risk for Kaposi sarcoma, but behaviors associated with HHV-8 transmissio

112 nd histologic overlap, accurate diagnosis of sarcomas can be challenging.

113 lated processes in sarcomas and propose that sarcomas can reside in a metastable state, enabling them

114 io, accumulating evidence suggests that many sarcomas can undergo EMT-related processes, which may be

115 -specific needs), national centralisation of sarcoma care, international consortia, and factors relat

116 Research has been hampered by limited human sarcoma cell line availability and the large number of S

117 Rescue of BAF47 in BAF47-deficient sarcoma cell lines results in increased genome-wide BAF

118 d but not wild-type bladder cancer and Ewing sarcoma cell lines.

119 short- and long-term rapamycin treatment in sarcoma cell lines.

120 th and migration across a series of synovial sarcoma cell lines.

121 We observed that hypoxic gradients guide sarcoma cell motility and matrix remodeling through hypo

122 lective cytotoxicity of EA in human synovial sarcoma cells (SW982 cells) and investigated the mechani

123 ediated silencing of USP14 or UCHL5 in Ewing sarcoma cells produced significant growth inhibition.

124 a potent cytotoxic effect on human synovial sarcoma cells which is mediated by heteromeric TRPC4/C1

125 formation leaves a single EWS allele in the sarcoma cells, and the contribution that the loss of EWS

126 lysis in MiaPaCa2 pancreatic cancer and A673 sarcoma cells.

127 t but did not activate apoptosis in p53(-/-) sarcoma cells.

128 rs and poor survival, in two different Ewing Sarcoma clinical cohorts.

129 years or older to enrol; patients with bone sarcoma could enrol if they were aged 12 years or older.

130 oma data from Columbia University with adult sarcoma data collected from TCGA, in order to see if one

131 In this note, we combined pediatric sarcoma data from Columbia University with adult sarcoma

132 anagement of these patients with soft tissue sarcomas: delays in diagnosis, trial availability and pa

133 Although these malignant vascular sarcomas demonstrate immunohistochemical and ultrastruct

134 LI regulates myriad genes required for Ewing sarcoma development.

135 oma, synovial sarcoma, and adult soft tissue sarcomas diagnosed in adolescents and young adults, and

136 proximately 30% of patients with soft-tissue sarcoma die from pulmonary metastases.

137 Despite the name, synovial sarcoma does not typically arise from a synoviocyte but

138 Synovial sarcoma (SS) is a rare sarcoma driven by a translocation between SS18 and SSX 1

139 as9 to generate multiple subtypes of primary sarcomas efficiently in wild type and genetically engine

140 Moreover, in a large panel of human synovial sarcomas, enhanced PI3'-lipid signaling also correlated

141 irst time, the functions of PPP1R1A in Ewing sarcoma (ES) pathogenesis.

142 NG2/CSPG4 antibody immunotherapy in human sarcomas established as xenografts in mice similarly dec

143 Together, contemporary sarcoma evaluation involves combining the initial morpho

144 ) unlike most epithelial malignancies, these sarcomas (excepting synovial sarcoma) are characterized

145 Human herpesvirus 8, which causes Kaposi sarcoma, expresses the MARCH family ubiquitin ligase K5.

146 les from 1,215 pediatric tumors representing sarcomas, extracranial embryonal tumors, brain tumors, h

147 -FLI1 translocation, the hallmark of Ewing's sarcoma family tumors, exhibited increased sensitivity t

148 nerve sheath tumors (MPNSTs) are devastating sarcomas for which no effective medical therapies are av

149 Of the 23 sarcomas, four (17.4%) showed good histologic response (

150 ed patients with soft-tissue sarcoma or bone sarcoma from 12 academic centres in the USA that were me

151 s of aggregated RNA-binding protein fused in sarcoma (FUS) are hallmarks of ALS and frontotemporal de

152 Mutations in the fused in sarcoma (FUS) gene can cause both juvenile and late onse

153 clusions of the RNA-binding protein fused in sarcoma (FUS) represent one type of membraneless ribonuc

154 rils formed by the LC domain of the fused in sarcoma (FUS) RNA-binding protein.

155 ally disordered RGG/RG domains from Fused in Sarcoma (FUS), FMRP and hnRNPU.

156 d with CRISPR-Cas9 technology are similar to sarcomas generated with conventional modelling technique

157 Primary sarcomas generated with CRISPR-Cas9 and Cre recombinase

158 These results show that sarcomas generated with CRISPR-Cas9 technology are simil

159 ynovial sarcoma is an aggressive soft tissue sarcoma genetically defined by the fusion oncogene SS18-

160 rtial thromboplastin time in the soft-tissue sarcoma group (three [7%] each).

161 Nine (11%) patients (five [12%] in the bone sarcoma group and four [10%] in the soft-tissue sarcoma

162 ploratory study is based on the Scandinavian Sarcoma Group VIII/Arbeitsgemeinschaft Internistische On

163 coma group and four [10%] in the soft-tissue sarcoma group) had treatment-emergent serious adverse ev

164 ased platelet count (three [7%]) in the bone sarcoma group, and anaemia, decreased lymphocyte count,

165 h), Research Council of Norway, Scandinavian Sarcoma Group, Swiss Paediatric Oncology Group, Cancer R

166 Seven (18%) of 40 patients with soft-tissue sarcoma had an objective response, including four (40%)

167 Two (5%) of 40 patients with bone sarcoma had an objective response, including one (5%) of

168 None of the 13 patients with Ewing's sarcoma had an objective response.

169 Patients with soft-tissue sarcoma had to be aged 18 years or older to enrol; patie

170 or surgically unresectable locally advanced sarcoma, had received up to three previous lines of syst

171 r locally advanced or metastatic soft-tissue sarcoma has been doxorubicin.

172 ts into the molecular pathogenetic basis for sarcomas has dramatically (re)shaped contemporary diagno

173 proved survival rates in patients with Ewing sarcoma have raised interest in accessing the quality of

174 Patients with advanced sarcomas have a poor prognosis and few treatment options

175 ed 3 distinct HHV-8-related entities: Kaposi sarcoma, HHV-8-associated multicentric Castleman disease

176 0.23-0.93; P = .03) and those without a bone sarcoma (ie, neither primitive neuroectodermal tumor nor

177 Our understanding of the sarcoma immune microenvironment and heterogeneous mechan

178 e of the most common subtypes of soft tissue sarcoma in adults and can occur in almost any part of th

179 unt for approximately 13% of all soft tissue sarcoma in adults and cause substantial morbidity or mor

180 imaging features suggested a retroperitoneal sarcoma in the pelvic region with metastases to the live

181 ctin (F8-TNF), can be exploited to eradicate sarcomas in immunocompetent mice.

182 to generate multiple subtypes of soft tissue sarcomas in mice.

183 marizes the literature on malignant vascular sarcomas in the context of current models of angiogenesi

184 Primary retroperitoneal sarcomas in the pelvic region are extremely rare.

185 ons for patients with metastatic soft-tissue sarcomas in the United States, after a gap of more than

186 Sarcomas include diverse mesenchymal neoplasms with wide

187 leads to increased incidence of spindle cell sarcomas, including RMS.

188 HV-8, a DNA tumor virus that causes Kaposi's sarcoma, infects three types of dendritic cells: monocyt

189 UK, National Cancer Institute, Liddy Shriver Sarcoma Initiative.

190 ovel metastasis-promotional pathway in Ewing Sarcoma, involving the histone demethylase KDM3A, previo

191 or rarely variant, oncogenic fusions, Ewing Sarcoma is a biologically and clinically aggressive dise

192 Ewing sarcoma is a bone and soft-tissue tumor that depends on

193 Synovial sarcoma is an aggressive soft tissue sarcoma genetically

194 Kaposi sarcoma is caused by infection of Kaposi sarcoma-associa

195 Kaposi's sarcoma is one of the most common malignancies in HIV-in

196 Ewing Sarcoma is the second most common solid pediatric malign

197 hymal tissues, such as bone and soft-tissues sarcomas, is still largely unclear.

198 s 8 (HHV-8) is the causative agent of Kaposi sarcoma (KS) and multicentric Castleman disease (MCD), a

199 HV)-related malignancies, including Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL).

200 Kaposi's sarcoma (KS) as the most common AIDS-associated malignan

201 We compared Kaposi sarcoma (KS) risk in adults who started antiretroviral t

202 us (KSHV) is the etiologic agent of Kaposi's sarcoma (KS), a vascular tumor frequently found in immun

203 of 11 HIV-related, 7 non-HIV-related Kaposi sarcoma (KS), and 7 normal skin tissues (NSTs) of Dutch

204 irus (KSHV) is the causative agent of Kaposi sarcoma (KS), one of the leading cancers in human immuno

205 s an oncogenic virus that can cause Kaposi's sarcoma (KS).

206 us (KSHV) is the etiologic agent of Kaposi's sarcoma (KS).

207 ocompromised individuals, including Kaposi's sarcoma (KS).

208 d with human herpesvirus 8 (HHV-8) (Kaposi's sarcoma [KS]-associated herpesvirus) and have an importa

209 Deletion of Mdm2 in T-cell lymphomas or sarcomas lacking p53 induced apoptosis and G2 cell-cycle

210 nt and young adult patients with soft tissue sarcomas lag behind those of children diagnosed with his

211 infected spindle tumor cells in human Kaposi sarcoma lesions.

212 For most sarcomas, locally advanced or unresectable disease is st

213 ubicin in patients with advanced soft-tissue sarcoma met its predefined primary endpoint for progress

214 However, the mechanisms underpinning Ewing Sarcoma metastasis are currently not well understood.

215 Here, we report a mouse sarcoma model expressing SS18-SSX1, complementing our pr

216 Undifferentiated pleomorphic sarcomas, myxofibrosarcomas, and malignant peripheral ne

217 the spectrum of targeted drug development in sarcoma now spans many of the most active paradigms in c

218 The recognition of sarcomas occurring in cancer predisposition syndromes is

219 sarcoma (RMS) is the most common soft tissue sarcoma of skeletal muscle origin in children and adoles

220 ents after surgical resection of soft-tissue sarcoma of the extremities.

221 irst posttransplant SCC, melanoma, or Kaposi sarcoma of the skin.

222 d locally advanced or metastatic soft-tissue sarcoma of Trojani grade 2 or 3, disease progression bef

223 nsformed breast cancer cells and soft tissue sarcomas of diverse histological subtypes.

224 anced unresectable or metastatic soft-tissue sarcoma, of intermediate or high grade, for which no sta

225 study, we enrolled patients with soft-tissue sarcoma or bone sarcoma from 12 academic centres in the

226 tivity in patients with advanced soft-tissue sarcoma or bone sarcoma.

227 n patients with undifferentiated pleomorphic sarcoma or dedifferentiated liposarcoma.

228 enrolment, and no previous chemotherapy for sarcoma or previous doxorubicin for any cancer.

229 ere over-represented among men with Kaposi's sarcoma (OR, 48.2; 95% CI, 22.0 to 105.6), anal (OR, 15.

230 Of high-grade sarcomas, OSs are among the most curable, with more than

231 Meta-analysis of human synovial sarcoma patient series identified two tumor-gentoype-phe

232 Of the 44 advanced sarcoma patients in these trials, 27 (61%) were male; 18

233 enic activities to HHV-8-associated Kaposi's sarcoma, primary effusion lymphoma (PEL), and multicentr

234 ation of the NR0B1 gene as well as for Ewing sarcoma proliferation and anchorage-independent growth.

235 The Ewing Sarcoma protein (EWS) is a multifaceted RNA binding prot

236 molecular landscape of 206 adult soft tissue sarcomas representing 6 major types.

237 profiles, providing a valuable resource for sarcoma research and cell line development.

238 tion, cyclophosphamide was found to increase sarcoma risk in a dose-dependent manner ( Ptrend = .01).

239 Retroperitoneal sarcomas (RPS) are rare tumors composed of several well

240 Indeed, mice sarcoma S37 cell line was treated in vitro with disulfid

241 Synovial sarcoma (SS) is a rare sarcoma driven by a translocation

242 Synovial sarcoma (SS) is an aggressive soft-tissue malignancy cha

243 Synovial sarcoma (SS) is an aggressive soft-tissue sarcoma that i

244 study of 18 canine patients with soft tissue sarcoma (STS), CIVO captured complex, patient-specific t

245 Human soft-tissue sarcomas (STS) are rare mesenchymal tumors with a 5-year

246 red autochthonous mouse model of soft-tissue sarcomas (STSs) to determine NG2/CSPG4's role in STS ini

247 In 2005, the European Pediatric Soft Tissue Sarcoma Study Group (EpSSG) proposed a conservative trea

248 nt treatment option for patients with LPS, a sarcoma subtype for which limited effective systemic tre

249 esses may be especially operative in certain sarcoma subtypes, such as carcinosarcomas displaying a b

250 ing undifferentiated phenotype in a p53-null sarcoma system revealed a critical role for interleukin

251 HER2, and MAPK/RAS/RAF gene alterations from sarcoma TCGA.

252 al sarcoma (SS) is an aggressive soft-tissue sarcoma that is often discovered during adolescence and

253 PNSTs) are aggressive, frequently metastatic sarcomas that are associated with neurofibromatosis type

254 n mice bearing T3 methylcholanthrene-induced sarcomas that are susceptible to checkpoint blockade imm

255 ANCE KSHV is the etiologic agent of Kaposi's sarcoma, the most common tumor of AIDS patients.

256 nd protein, providing insights into refining sarcoma therapy and relationships to other cancer types.

257 d from the RNA granule protein FUS (fused in sarcoma) to a multivalent poly-Src homology 3 (SH3) doma

258 Mutations in Fused in Sarcoma/Translocated in Liposarcoma (FUS) cause familial

259 Patients with advanced sarcoma treated on phase I clinical trials had a clinica

260 come of 618 survivors from consecutive Ewing sarcoma trials was assessed by the Toronto Extremity Sal

261 el approach to model the initiation of Ewing sarcoma tumorigenesis that exploits the developmental an

262 n the initiation and progression of Kaposi's sarcoma tumors.

263 n patients with undifferentiated pleomorphic sarcoma, two (20%) of ten patients with liposarcoma, and

264 significantly across 1996-2012 for Kaposi's sarcoma, two subtypes of non-Hodgkin lymphoma, and cance

265 le analysis reveals previously unappreciated sarcoma-type-specific changes in copy number, methylatio

266 rearrangements are diagnostic of particular sarcoma types, certain fusion partners, most notably EWS

267 tly mutated across sarcoma types; (2) within sarcoma types, genomic and regulomic diversity of driver

268 ovel insights into the biology of individual sarcoma types, we report three overarching (1) unlike mo

269 ATRX, RB1) highly recurrently mutated across sarcoma types; (2) within sarcoma types, genomic and reg

270 Medical Research Council, Cancer Australia, Sarcoma UK, National Cancer Institute, Liddy Shriver Sar

271 Ewing sarcoma usually expresses the EWS/FLI fusion transcripti

272 ldhood cancers (leukemia, CNS, and non-Ewing sarcoma) versus survivors of other cancers ( Pdifference

273 growth factor receptor (EGFR) or Kristen rat sarcoma viral (KRAS) mutations, respectively.

274 regulation of v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog (KIT) receptor tyrosine k

275 advantage, especially within the Kirsten rat sarcoma viral oncogene homolog (KRAS) mutant subgroup.

276 We additionally compared Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations in pancr

277 h factor receptor (EGFR), mutant Kirsten rat sarcoma viral oncogene homolog (Kras), or overexpression

278 To examine whether the Kirsten rat sarcoma viral oncogene homolog (KRAS)-variant, a germlin

279 he V600E mutation in the kinase v-RAF murine sarcoma viral oncogene homolog B (BRAF(V600E)), oncogeni

280 tivating mutations in the BRAF (V-raf murine sarcoma viral oncogene homolog B1) oncogene with a combi

281 K-Ras (Kirsten-rat sarcoma viral oncogene homolog) is a prominent oncogene

282 te NMR (ssNMR) resonance assignments of Rous sarcoma virus (RSV) CA, assembled into hexamer tubes tha

283 tial steps in understanding the chicken Rous sarcoma virus (RSV) genome association with a nonpermiss

284 We produced kinetically stabilized Rous sarcoma virus (RSV) intasomes with human immunodeficienc

285 ation of HIV-1 Gag, as well as purified Rous sarcoma virus (RSV) MA and Gag, depends strongly on the

286 In some orthoretroviruses, including Rous Sarcoma Virus (RSV), CA carries a short and hydrophobic

287 well-established retroviral model-avian Rous sarcoma virus (RSV)-we analyzed changes in an RSV varian

288 eliminary evidence of anticancer activity in sarcoma was demonstrated.

289 ntral role in regulating glycolysis in human sarcomas was evaluated by short- and long-term rapamycin

290 In Ewing sarcoma, we find that the BAF complex is recruited by th

291 Biomarkers predicting rapalog responses in sarcomas where PI3K and mTOR are often hyperactivated co

292 transdifferentiation in prostate cancer, and sarcomas, which are fixed in a mesenchymal state owing t

293 examinations in 23 patients with soft-tissue sarcomas who had undergone neoadjuvant therapy were revi

294 ap between adolescents and young adults with sarcomas will help drive new initiatives to improve fina

295 Angiosarcoma is an aggressive vascular sarcoma with an extremely poor prognosis.

296 reatment of a xenograft mouse model of Ewing sarcoma with VLX1570, a benzyl-4-piperidone compound der

297 ve sheath tumors (MPNSTs) are a type of rare sarcomas with a poor prognosis due to its highly invasiv

298 For those sarcomas with complex cytogenetic changes that lack spec

299 mic features with gynecologic carcinomas and sarcomas with intermediate EMT features.

300 a new metastasis-promoting pathway in Ewing Sarcoma, with therapeutically targetable components.

301 ically associated with all forms of Kaposi's sarcoma worldwide.