ライフサイエンスコーパス: liposarcoma

1 ancreas (focal fatty infiltration, teratoma, liposarcoma).

2 in Fus/TLS (fused in sarcoma/translocated in liposarcoma).

3 y have therapeutic value in dedifferentiated liposarcoma.

4 stratification for individual patients with liposarcoma.

5 ream targets might lead to novel therapy for liposarcoma.

6 that ZIC1 contributes to the pathogenesis of liposarcoma.

7 y resected locally recurrent retroperitoneal liposarcoma.

8 expression dataset for new drug discovery in liposarcoma.

9 inoma, and breast carcinoma, and 1 recurrent liposarcoma.

10 in patients with high-risk primary extremity liposarcoma.

11 stic for survival in primary retroperitoneal liposarcoma.

12 ies of patients with primary retroperitoneal liposarcoma.

13 stic factors for survival in retroperitoneal liposarcoma.

14 l three are directly targeted by miR-193b in liposarcoma.

15 raditionally ascribed to well-differentiated liposarcoma.

16 S patients with a single histopathology, ie, liposarcoma.

17 comparable to that observed in human myxoid liposarcoma.

18 each of the major histologic types of human liposarcoma.

19 eful therapeutic agents for the treatment of liposarcoma.

20 lastoma, breast cancer, prostate cancer, and liposarcoma.

21 ies of six patients with primary mediastinal liposarcoma.

22 uveal melanoma, synovial sarcoma, and myxoid liposarcoma.

23 he tumor suppressive function of miR-193b in liposarcoma.

24 ated pleomorphic sarcoma or dedifferentiated liposarcoma.

25 etus for further study of HDM2 inhibitors in liposarcoma.

26 f 44%, higher than previously reported in DD liposarcoma.

27 15 evaluable patients with dedifferentiated liposarcoma.

28 ted pleomorphic sarcoma and dedifferentiated liposarcoma.

29 m surgically resected human dedifferentiated liposarcoma.

30 ted in about 75% of FRS2-positive high-grade liposarcomas.

31 aracterize pathologic features of high-grade liposarcomas.

32 ase (hTERT) repression in ALT cell lines and liposarcomas.

33 , which falls in a region amplified in human liposarcomas.

34 a as a protein involved in the generation of liposarcomas.

35 mas, rhabdomyosarcomas, chondrosarcomas, and liposarcomas.

36 id tumors, lipomas, uterine leiomyomata, and liposarcomas.

37 25.6%) were reclassified as dedifferentiated liposarcomas.

38 romosomes from well- and/or dedifferentiated liposarcomas.

39 ome 12q13-15 that is frequently amplified in liposarcomas.

40 (4 of 14, 29%) and sarcomas (2 of 14, 14%; 1 liposarcoma, 1 unspecified type) were the most common no

41 s initially diagnosed as well-differentiated liposarcomas, 44 (25.6%) were reclassified as dedifferen

42 ary RPS, the most prevalent histologies were liposarcoma (50%), leiomyosarcoma (26%), and malignant f

43 Here we show that TLS (translocated in liposarcoma), a protein originally identified as the pro

44 Liposarcoma, a rare disease, is classified into five his

45 with postbaseline scans, three patients with liposarcoma achieved a partial response (at 250, 400, an

46 d susceptibility in moderately VSV-resistant liposarcoma and bladder carcinoma.

47 In xenograft models of liposarcoma and chondrosarcoma, DOX-loaded meshes (DoM)

48 rrant transcriptional programs that underpin liposarcoma and Ewing's sarcoma, respectively.

49 in patients with primary well-differentiated liposarcoma and G1-2 DDLPS.

50 articular, patients with well-differentiated liposarcoma and G1-2 dedifferentiated liposarcoma (G1-2

51 al dacarbazine in patients who have advanced liposarcoma and leiomyosarcoma after they experience fai

52 chondrosarcoma and patient-derived xenograft liposarcoma and leiomyosarcoma in mice, improve median 9

53 Liposarcoma and leiomyosarcoma were associated with late

54 factors included the histologic variants of liposarcoma and malignant peripheral nerve tumors and pa

55 ure of oncogene-containing neochromosomes in liposarcoma and provide evidence that they are generated

56 of non-liposarcomas, use of chemotherapy in liposarcoma and radiotherapy in leiomyosarcoma, suggesti

57 light of the high mortality associated with liposarcoma and the lack of effective systemic therapy,

58 advanced tumors especially de-differentiated liposarcoma and uterine leiomyosarcoma remains unsatisfa

59 Activation of this receptor in liposarcomas and breast and colon cancer cells also indu

60 entiating between high- and low-grade myxoid liposarcomas and can help in clinical decision making.

61 in the neoplastic component of human myxoid liposarcomas and increases the tumorigenicity of cells i

62 the q3 weeks 24-hour trabectedin regimen in liposarcomas and leiomyosarcomas, although the qwk 3-hou

63 teins implicated in the development of human liposarcomas and leukemias.

64 rominent in dedifferentiated and pleomorphic liposarcomas and nearly all other high-grade sarcomas.

65 FUS/TLS (fused in sarcoma/translocated in liposarcoma) and TDP-43 are integrally involved in amyot

66 % of myxofibrosarcomas and 8% of pleomorphic liposarcomas) and PIK3CA (18% of myxoid/round-cell lipos

67 f normal adipose tissue, well-differentiated liposarcoma, and dedifferentiated liposarcoma by both de

68 fferent human tumor xenografts, melanoma and liposarcoma, and from two normal endothelial cell counte

69 differentiated liposarcoma, dedifferentiated liposarcoma, and leiomyosarcoma.

70 Histologic types other than leiomyosarcoma, liposarcoma, and myxofibrosarcoma were associated with w

71 phic sarcoma, two (20%) of ten patients with liposarcoma, and one (10%) of ten patients with synovial

72 vity in mantle-cell lymphoma, breast cancer, liposarcoma, and teratoma with reversible neutropenia as

73 ated liposarcomas, >90% of myxoid round cell liposarcomas, and >70% of pleomorphic liposarcomas, wher

74 Visceral sarcomas, well-differentiated liposarcomas, and angiosarcomas were excluded.

75 Liposarcomas are aggressive mesenchymal cancers with poo

76 g a novel gene expression strategy, in which liposarcomas are compared to their corresponding adipocy

77 for liposarcoma is surgical excision because liposarcomas are often resistant to traditional chemothe

78 Liposarcomas are rare malignant tumors of adipocytic dif

79 Liposarcomas are the most common type of soft tissue sar

80 etrial stromal sarcoma, and HMGIC fusions in liposarcoma, are discussed.

81 wed diagnosis of localized resectable myxoid liposarcoma arising from an extremity or the trunk wall.

82 btained from patients with de-differentiated liposarcoma being treated with an inhibitor of the HDM2-

83 plete resection of a primary retroperitoneal liposarcoma between July 1982 and December 2005.

84 not only functions as a tumor suppressor in liposarcoma but also promotes adipogenesis in ASC.

85 erentiated liposarcoma, and dedifferentiated liposarcoma by both deep sequencing of small RNA librari

86 controls cell growth and differentiation in liposarcoma by targeting multiple key components (PDGFRb

87 rial for treatment of patients with advanced liposarcoma by using the peroxisome proliferator-activat

88 Liposarcoma can be an aggressive, debilitating, and fata

89 and FUS/TLS (fused in sarcoma/translated in liposarcoma) cause a subset of ALS.

90 Liposarcoma cell differentiation is characterized by acc

91 In the human dedifferentiated liposarcoma cell line (LS141) and the p53 wild-type HCT1

92 long-term stimulation of adipogenesis in the liposarcoma cell line LiSa-2 restored perilipin 1 expres

93 ib inhibits growth and induces senescence in liposarcoma cell lines and xenografts.

94 onal genomics to classify a panel of diverse liposarcoma cell lines based on hierarchical clustering

95 liposarcoma compared with normal fat, and in liposarcoma cell lines compared with adipose-derived ste

96 RNAi-mediated knockdown of these genes in liposarcoma cell lines reduced proliferation and invasiv

97 leiomyosarcoma, dedifferentiated, and myxoid liposarcoma cell lines were used for in vitro studies.

98 is in dedifferentiated and myxoid/round cell liposarcoma cell lines, but not in either adipose-derive

99 rtant role in the growth of dedifferentiated liposarcoma cell lines.

100 osarcoma samples of all five subtypes and in liposarcoma cell lines.

101 expressed and functional in three high-grade liposarcoma cell lines: FU-DDLS-1, LiSa-2, and SW872.

102 7/8-dependent manner, which in turn promoted liposarcoma cell proliferation, invasion, and metastasis

103 methionine sulfoxide reductase A to modulate liposarcoma cell survival and ASC differentiation state.

104 Inhibition of PDGFRbeta reduces liposarcoma cell viability and increases adipogenesis.

105 sfection of HT1080 (fibrosarcoma) and SW872 (liposarcoma) cell lines and their conditioned media resu

106 ntroduction of miR-193b induced apoptosis in liposarcoma cells and promoted adipogenesis in human adi

107 ogression, identifying communication between liposarcoma cells and their microenvironment as a proces

108 Moreover, primary human liposarcoma cells can be induced to undergo terminal dif

109 ptosis and growth arrest in dedifferentiated liposarcoma cells compared with normal adipocytes.

110 rentiation of normal preadipocytes and human liposarcoma cells in vitro.

111 lular vesicles derived from dedifferentiated liposarcoma cells induce oncogenic properties in preadip

112 oring miR-143 expression in dedifferentiated liposarcoma cells inhibited proliferation, induced apopt

113 hat miR-25-3p and miR-92a-3p are secreted by liposarcoma cells through extracellular vesicles and may

114 Expression of miR-193b in liposarcoma cells was downregulated by promoter methylat

115 erodimer, and that simultaneous treatment of liposarcoma cells with both PPAR gamma- and RXR-specific

116 r (ICG-001) had potent inhibitory effects on liposarcoma cells, suggesting their potential applicatio

117 nduced G(2)-M growth arrest and apoptosis in liposarcoma cells.

118 e of all three iPLA2 isoforms in human SW872 liposarcoma cells.

119 d one each of infantile fibrosarcoma, myxoid liposarcoma, cellular congenital mesoblastic nephroma) a

120 omatous samples and shows the feasibility of liposarcoma classification based entirely on gene expres

121 ght to develop a more systematic approach to liposarcoma classification based on gene expression anal

122 Synovial sarcomas, round-cell/myxoid liposarcomas, clear-cell sarcomas and gastrointestinal s

123 in conjunction with histologic features for liposarcoma clinical characterization and lay the ground

124 nt, is overexpressed in all five subtypes of liposarcoma compared with normal fat, and in liposarcoma

125 ctable synovial sarcoma or myxoid round cell liposarcoma (confirmed by cytogenetics) expressing MAGE-

126 otein, found in the majority of human myxoid liposarcomas, consists of a fusion between the transcrip

127 se I study of patients with dedifferentiated liposarcoma (DD-LPS) was observed with selinexor.

128 Dedifferentiated liposarcoma (DDLPS) is a highly malignant subtype of hum

129 Dedifferentiated liposarcoma (DDLPS) is frequently diagnosed late, and pa

130 and of the closely related dedifferentiated liposarcoma (DDLPS) subtype, revealed immunohistochemica

131 recover the leiomyosarcoma, dedifferentiated liposarcoma (DDLPS), and synovial sarcoma histological s

132 FRS2 with CDK4 and MDM2 in dedifferentiated liposarcoma (DDLS) and undifferentiated high-grade pleom

133 ated liposarcoma (WDLS) and dedifferentiated liposarcoma (DDLS), both characterized by chromosome 12q

134 l-differentiated (WDLS) and dedifferentiated liposarcomas (DDLS).

135 ominant histologies were well-differentiated liposarcoma, dedifferentiated liposarcoma, and leiomyosa

136 Both lipoma and liposarcoma demonstrated thin septa and regions of incre

137 s subtype that accounts for less than 10% of liposarcoma diagnoses.

138 ction of Preoperative Radiotherapy in Myxoid Liposarcomas (DOREMY) trial is a prospective, single-gro

139 ts with large, high-grade, primary extremity liposarcoma; DOX is not associated with improved DSS and

140 malignant lesions consisted of scrotal wall liposarcoma, epididymal leiomyosarcoma, and recurrent sp

141 e clinical behavior of myxoid and round-cell liposarcomas, even in neoplasms with few or no round-cel

142 We further show that while angiogenic liposarcomas expand rapidly after inoculation of tumor c

143 All patients who were treated for liposarcoma from July 1, 1982, through July 1, 1998, wer

144 The expression profiles discriminated liposarcoma from normal adipose tissue and well differen

145 ing marker for the differential diagnosis of liposarcomas from other soft tissue sarcomas, whereas pe

146 utations in Fused in Sarcoma/Translocated in Liposarcoma (FUS) cause familial forms of amyotrophic la

147 ing protein fused in sarcoma/translocated in liposarcoma (FUS) is a novel component of the DNA damage

148 t robustly, fused in sarcoma/translocated in liposarcoma (FUS/TLS or FUS).

149 Fused in sarcoma/translated in liposarcoma (FUS/TLS) and TAR DNA-binding protein (TDP)-

150 TDP-43) and fused in sarcoma/translocated in liposarcoma (FUS/TLS) as causative of ALS and FTLD, comb

151 ations in the fused in sarcoma/translated in liposarcoma (FUS/TLS) gene on chromosome 16 that were sp

152 TDP-43 and fused in sarcoma/translocated in liposarcoma (FUS/TLS), and massive accumulation of mitoc

153 DP-43) and fused in sarcoma/translocation in liposarcoma (FUS/TLS), cause an inherited form of ALS th

154 tiated liposarcoma and G1-2 dedifferentiated liposarcoma (G1-2 DDLPS, n=266) treated with RT+S had be

155 ir gene expression profiles, indicating that liposarcoma gene expression profiles and histologic clas

156 ally expressed genes that may be involved in liposarcoma genesis/progression and serve as potential t

157 as a dose-fractionation approach for myxoid liposarcoma, given that phase 3 trials are logistically

158 In dedifferentiated liposarcomas, grade concordance was 59.7% (weighted kapp

159 reatment with idasanutlin and carfilzomib on liposarcoma growth in vivo.

160 in all studied cases of well-differentiated liposarcomas, >90% of myxoid round cell liposarcomas, an

161 In total, 27 patients with liposarcoma had a median progression-free survival of 23

162 ell-differentiated/de-differentiated (WD/DD) liposarcomas has been reported to be minimal, however tr

163 tor in the spectrum of myxoid and round-cell liposarcomas has not been examined.

164 ctivity with milademetan in dedifferentiated liposarcomas has prompted a randomized phase III trial (

165 oneal sarcoma and suggest that patients with liposarcoma have a 3-fold higher risk of local recurrenc

166 rates of self renewal, including melanomas, liposarcomas, hepatocellular carcinomas, urothelial carc

167 the biological and clinical heterogeneity of liposarcoma, here, we confirmed the under-expression of

168 five histologic subtypes: high-grade myxoid liposarcoma (HG-MLPS); leiomyosarcoma (LMS), synovial sa

169 nhancer landscape and 3D genome structure in liposarcoma identifies extensive enhancer-oncogene coamp

170 ment of combined modality treatments against liposarcoma in recent years, a significant proportion of

171 aluated the functions of miRNA (miR-193b) in liposarcoma in vitro and in vivo Deep RNA sequencing on

172 s that were dysregulated in dedifferentiated liposarcomas in both the sequencing and the microarray a

173 ree patients with intermediate to high-grade liposarcomas in whom troglitazone administration induced

174 ed therapeutics have had limited efficacy in liposarcomas, in part because of inadequate knowledge of

175 ant imaging features favoring a diagnosis of liposarcoma included lesion larger than 10 cm (P <.001),

176 several genes amplified in dedifferentiated liposarcoma, including CDK4 and YEATS4, decreased cell p

177 Classification of liposarcoma into subtypes, based on morphologic features

178 Classification of liposarcoma into three biological types encompassing fiv

179 The classification of liposarcomas into four principal subtypes reflects the d

180 omplete resection of primary retroperitoneal liposarcoma is a common clinical problem that frequently

181 ncogenic fusion protein, whereas pleomorphic liposarcoma is a karyotypically complex and especially p

182 Liposarcoma is a type of soft tissue sarcoma that exhibi

183 Myxoid liposarcoma is characterized by a pathognomonic chromoso

184 Myxoid liposarcoma is classified in the group of sarcomas with

185 However, myxoid liposarcoma is not a homogeneous entity, because the beh

186 However, myxoid liposarcoma is not a homogeneous entity, because the beh

187 Because the differentiation status of liposarcoma is predictive of clinical outcomes, modulati

188 Currently, the mainstay of therapy for liposarcoma is surgical excision because liposarcomas ar

189 Liposarcoma is the most common soft tissue sarcoma.

190 Well-differentiated liposarcoma is the most common subtype and is associated

191 Liposarcoma is the most commonly occurring soft-tissue s

192 nce of FRS2 and FGFR signaling in high-grade liposarcomas is unknown.

193 enrolled in disease subtype-specific groups (liposarcoma, leiomyosarcoma, angiosarcoma, undifferentia

194 he following histopathologies: fibrosarcoma, liposarcoma, leiomyosarcoma, malignant fibrous histiocyt

195 eiomyomas, Wilms' tumors, rhabdomyosarcomas, liposarcomas, leiomyosarcomas, and adrenal cortical carc

196 In well-differentiated liposarcomas, lipomas, or normal adipose tissue, perilip

197 Liposarcoma (LPS) can be divided into 4 different subtyp

198 n with dacarbazine in patients with advanced liposarcoma (LPS) or leiomyosarcoma showed a significant

199 DLPS) is a highly malignant subtype of human liposarcoma (LPS), whose genomic profile is characterize

200 of histologic subtype for extremity/truncal liposarcoma (LPS).

201 ociated with worse outcomes in patients with liposarcoma (LPS).

202 Liposarcomas (LPSs) are a group of malignant mesenchymal

203 Liposarcomas (LPSs) are the most common soft-tissue canc

204 In contrast to extremity liposarcoma, LR without distant metastasis often results

205 rentiation; has tumor suppressor activity in liposarcoma, lung, and prostate cancers; and suppresses

206 to be up-regulated in early growth of human liposarcoma, mammary adenocarcinoma, and osteosarcoma.

207 :DDIT3 fusion oncoprotein hallmark to myxoid liposarcoma (MLPS) inhibits BAF complex-mediated remodel

208 ated/dedifferentiated/pleomorphic and myxoid liposarcomas (MLS).

209 Here, we use a liposarcoma model system to assay telomere maintenance m

210 Myxoid round cell liposarcoma (MRCLS) is a common liposarcoma subtype char

211 ynovial sarcoma (n=44) and myxoid round cell liposarcoma (n=8) were enrolled and received afami-cel i

212 n = 12), six leiomyosarcomas (n = 29), seven liposarcomas (n = 31), three malignant fibrous histiocyt

213 associated with better ARFS in patients with liposarcoma [N=321, hazard ratio (HR), 0.61; 95% confide

214 ated genes included TP53 (17% of pleomorphic liposarcomas), NF1 (10.5% of myxofibrosarcomas and 8% of

215 sarcoma and pleomorphic or dedifferentiated liposarcoma of the extremity, which establishes a promis

216 Of 177 patients with primary retroperitoneal liposarcoma operated on for curative intent, 99 (56%) pr

217 the RNA/DNA-binding protein translocated in liposarcoma or fused in sarcoma (TLS/FUS or FUS).

218 versus dacarbazine in patients with advanced liposarcoma or leiomyosarcoma after prior therapy with a

219 th intermediate-grade or high-grade advanced liposarcoma or leiomyosarcoma who had received at least

220 rs previously labeled as well differentiated liposarcomas or atypical lipomas.

221 rcomas) and PIK3CA (18% of myxoid/round-cell liposarcomas, or MRCs).

222 ion (P = 0.01), low-grade tumors (P = 0.02), liposarcomas (P = 0.003), and no disease recurrence (P =

223 analysis of signaling pathways important to liposarcoma pathogenesis and progression in the well-dif

224 correlated with disease-specific survival of liposarcoma patients.

225 novel and previously unreported insight into liposarcoma progression, identifying communication betwe

226 ironment as a process critically involved in liposarcoma progression.

227 Translocation liposarcoma protein (TLS)-associated serine-arginine (TA

228 The translocation liposarcoma protein TLS has recently been shown to funct

229 ways in well-differentiated/dedifferentiated liposarcoma provides several possible novel therapeutic

230 f tumor cells in mice, nonangiogenic dormant liposarcomas remain microscopic up to one-third of the n

231 Liposarcoma remains the most common mesenchymal cancer,

232 Dedifferentiated liposarcoma represents focal progression of well-differe

233 These human xenograft models may facilitate liposarcoma research and accelerate the generation of re

234 d with neural differentiation and round cell liposarcoma, respectively.

235 A 120-day follow-up study of liposarcoma revealed a sustained 2-fold or higher increa

236 and beta-catenin signaling in progression of liposarcoma, revealing mechanistic vulnerabilities that

237 expression of miR-193b in additional patient liposarcoma samples and cell lines.

238 and CHEK1, were found to be overexpressed in liposarcoma samples of all five subtypes and in liposarc

239 ndertook expression profiling of 140 primary liposarcoma samples, which were randomly split into trai

240 but only cells from the nonangiogenic human liposarcoma secrete relatively high levels of the angiog

241 nes, including MYC, as potentially affecting liposarcoma signaling networks and cancer outcome.

242 osine kinase and DNA methylation pathways in liposarcoma, some with immediate implications for therap

243 vel pharmaceutical agents that aim to target liposarcoma-specific biology are under active investigat

244 nografts, and throughout the 120 days of the liposarcoma study.

245 d round cell liposarcoma (MRCLS) is a common liposarcoma subtype characterized by a translocation tha

246 Differentially expressed genes for each liposarcoma subtype compared with normal fat were used t

247 ariate analysis showed that dedifferentiated liposarcoma subtype was associated with a 6-fold increas

248 Several histologically defined liposarcoma subtypes exist, yet little is known about th

249 f a clinical trial with MDM2 antagonists for liposarcoma subtypes which overexpress MDM2 and show the

250 on profiling was able to distinguish between liposarcoma subtypes, lipoma, and normal fat samples.

251 trongly correlates to each of the four major liposarcoma subtypes.

252 lls, including fibrosarcoma, leiomyosarcoma, liposarcoma, synovial sarcoma, and neurofibrosarcoma cel

253 ts with >5 cm, high-grade, primary extremity liposarcoma that underwent surgical treatment of cure fr

254 and a distinct set of genes overexpressed in liposarcomas that are not found in the corresponding sta

255 Of the 23 myxoid liposarcomas that contained no fat, 16 (69.6%) were high

256 identified a group of genes overexpressed in liposarcomas that indicate the stage of differentiation

257 In liposarcoma, the median rate of CR was 64%, with wide va

258 In the subgroup with dedifferentiated liposarcomas, the disease control rate and median progre

259 tional role in the development of high-grade liposarcomas, therefore, serve as a potential therapeuti

260 ng this with the gene expression profiles of liposarcoma tissue samples, we refined this signature to

261 rmalin-fixed, paraffin-embedded human myxoid liposarcoma tissues, we demonstrate an 80% reduction of

262 The translocation liposarcoma (TLS) gene is fused to the ETS-related gene

263 sarcoma (FUS, also known as translocated in liposarcoma (TLS)) account for approximately 30% of clas

264 Translocated in liposarcoma (TLS), a member of the Ewing's sarcoma famil

265 Human translocation liposarcoma (TLS)-CCAAT/enhancer binding protein (C/EBP)

266 fetal liver cells expressing translocated in liposarcoma (TLS)-ERG, an activated form of ERG found in

267 We find that translocation in liposarcoma (TLS)/FUS, an RNA-binding nuclear protein th

268 ssociated with the differentiation status of liposarcoma to gain insight into the basis for its progr

269 olecular characterization of the response of liposarcoma to the MDM2 inhibitor nutlin-3.

270 xplains the remarkable sensitivity of myxoid liposarcomas to radiation therapy.

271 in patients with retroperitoneal (RP) WD/DD liposarcoma treated at The University of Texas MD Anders

272 fy 177 patients with primary retroperitoneal liposarcoma treated between July 1982 and June 2002.

273 s, suggesting their potential application in liposarcoma treatment.

274 We tested Meltos on multiple samples from a liposarcoma tumor and on a multi-sample breast cancer da

275 In liposarcoma, tumor location exerts as strong an influenc

276 t carcinoma, glioblastoma, osteosarcoma, and liposarcoma tumors.

277 ion was found in pre-operative biopsy of non-liposarcomas, use of chemotherapy in liposarcoma and rad

278 s stratified by histological subtype (myxoid liposarcoma vs others).

279 typical lipomatous tumor/well differentiated liposarcoma vs. other).

280 Retroperitoneal dedifferentiated liposarcoma was associated with an 83% local recurrence

281 ical trial including 46 patients with myxoid liposarcoma was conducted in 4 centers in Spain, 1 in It

282 considered the best predictor of outcome in liposarcoma, was 0.669.

283 % of well-differentiated or dedifferentiated liposarcomas (WD/DDLS) have CDK4 amplification.

284 Well-differentiated liposarcoma (WDLPS), one of the most common human sarcom

285 These include well differentiated liposarcoma (WDLS) and dedifferentiated liposarcoma (DDL

286 Well-differentiated and dedifferentiated liposarcomas (WDLS/DDLS) account for approximately 13% o

287 In myxofibrosarcomas and pleomorphic liposarcomas, we found both point mutations and genomic

288 Seven hundred twenty patients with liposarcoma were evaluated, and of these, 460 had comple

289 Forty-seven cases of myxoid and round-cell liposarcomas were examined.

290 METTL1-amplified liposarcomas were hypersensitive to actinomycin D, a cli

291 ifferentiated components of dedifferentiated liposarcomas were immunohistochemically positive for per

292 In our series, patients with myxoid liposarcomas were mainly young adults (median age, 43 ye

293 umors (35 lipomas and 25 well-differentiated liposarcomas) were retrospectively reviewed in 31 female

294 d cell liposarcomas, and >70% of pleomorphic liposarcomas, whereas only the differentiated components

295 Liposarcomas, which are malignant fatty tumors, are the

296 ubset of Ewing's family of tumors and myxoid liposarcomas, which lack one of the characteristic trans

297 he majority of patients with retroperitoneal liposarcoma will eventually have recurrence and die of d

298 ed pleomorphic sarcomas and dedifferentiated liposarcomas with low infiltrating CD3 + T-lymphocyte le

299 tutions influenced LR of well differentiated liposarcoma without impacting OS, whereas discrepancies

300 and FAK inhibitor (PF-562271) each inhibited liposarcoma xenograft growth.