ライフサイエンスコーパス: metastatic tumor

1 cell lines SW480 (primary tumor) and SW620 (metastatic tumor).

2 diffuse immune cell infiltrate throughout a metastatic tumor.

3 r to migrating to the liver to establish the metastatic tumor.

4 novel paradigm for treatment of primary and metastatic tumors.

5 ed for efficient establishment and growth of metastatic tumors.

6 evels were increased in sera of mice bearing metastatic tumors.

7 ssion in a cohort of human PCa that included metastatic tumors.

8 nocompromised (CD-1 Nu) mice with orthotopic metastatic tumors.

9 clinical trials for treatment of advanced or metastatic tumors.

10 umor but rather by the formation of distinct metastatic tumors.

11 robiome stability between paired primary and metastatic tumors.

12 reatment of painful posterior vertebral body metastatic tumors.

13 c-PAMA-cobalamin in 10 patients with various metastatic tumors.

14 FL expression was increased significantly in metastatic tumors.

15 of the genetic changes found in invasive and metastatic tumors.

16 sed in human prostate cancers, especially in metastatic tumors.

17 nfused back into the individual to eliminate metastatic tumors.

18 rather than stromal cells within primary and metastatic tumors.

19 /ELF3 was overexpressed in human primary and metastatic tumors.

20 al stem cells were found in both primary and metastatic tumors.

21 orrelated with tumor grade and is highest in metastatic tumors.

22 ry tumors or with resistance to therapies in metastatic tumors.

23 but downregulated in a significant subset of metastatic tumors.

24 expression was significantly associated with metastatic tumors.

25 in primary GOF p53 SCCs and its retention in metastatic tumors.

26 ets against the breast cancer stem cells and metastatic tumors.

27 R2-positive primary tumors had HER2-negative metastatic tumors.

28 revalent pathogens as well as by primary and metastatic tumors.

29 agation of epithelial cells from primary and metastatic tumors.

30 astatic human HNSCC tumors compared with non-metastatic tumors.

31 titumor immune responses against primary and metastatic tumors.

32 ble for fascin overexpression in some of the metastatic tumors.

33 s, it is necessary to sequence recurrent and metastatic tumors.

34 fety and efficacy of miRNA targeting against metastatic tumors.

35 therapeutic strategies for a broad array of metastatic tumors.

36 ue in prolonging survival of animals bearing metastatic tumors.

37 l in the immune surveillance of residual and metastatic tumors.

38 carcinoma progression, including benign and metastatic tumors.

39 asis for testing similar strategies in human metastatic tumors.

40 ; resistance, however, invariably emerges in metastatic tumors.

41 hat favors the development of aggressive and metastatic tumors.

42 ramatic decrease in the numbers of secondary metastatic tumors.

43 ted and undifferentiated primary cancers and metastatic tumors.

44 otably cadherins, which are downregulated in metastatic tumors.

45 expression was significantly associated with metastatic tumors.

46 ignature, implicating a discrete lineage for metastatic tumors.

47 ite an overall increase in hnRNP-K levels in metastatic tumors.

48 nx2 is expressed in both adenocarcinomas and metastatic tumors.

49 bsequently gave rise to both the primary and metastatic tumors.

50 umors assayed, including primary and matched metastatic tumors.

51 pression of lymphocyte-homing signals in the metastatic tumors.

52 rimination between non-metastatic and highly metastatic tumors.

53 ignficantly diminished growth of primary and metastatic tumors.

54 mic profiles are not specific to H3K36me3 or metastatic tumors.

55 PPARA, PPARD, MLXIPL) genes were enriched in metastatic tumors.

56 nt also improved chemotherapy of primary and metastatic tumors.

57 ttractive strategy for treatment of advanced metastatic tumors.

58 laminin receptor 1 (LAMR1) known to mediate metastatic tumor adhesion.

59 ans, whereas inhibition of miR-105 in highly metastatic tumors alleviates these effects.

60 The response is usually transient, and metastatic tumors almost invariably eventually progress

61 clonality changes from patients' primary to metastatic tumor and dating somatic single nucleotide an

62 olled at a single academic center for paired metastatic tumor and normal tissue WES during a 19-month

63 e orthotopically generated primary and liver metastatic tumors and human CRC specimens.

64 Metastatic tumors and malignant gliomas make up the majo

65 EB1, respectively, and their upregulation in metastatic tumors and mesenchymal cell lines is coordina

66 the use of AURKA inhibitors in treatment of metastatic tumors and predict the sensitivity of the pat

67 that PTPN1 and AR genes were coamplified in metastatic tumors and that PTPN1 amplification was assoc

68 Tau enrichment in metastatic tumors and the ability of tau to promote tumo

69 ate cancers derived from 16 different lethal metastatic tumors and three high-grade primary carcinoma

70 0 mutations were present in both primary and metastatic tumors, and 3 mutations were detected only in

71 arian and pancreatic carcinomas, enriched in metastatic tumors, and associated with reduced patient s

72 th in the orthotopic primary colon and liver metastatic tumors, and human CRC patient's specimen and

73 tochondrial mutational load, the presence of metastatic tumors, and normal aging.

74 Although both metastatic tumor antigen 1 (MTA1), a master chromatin mo

75 show that miR-661 inhibits the expression of metastatic tumor antigen 1 (MTA1), a widely up-regulated

76 g components as well as cytoplasmic level of metastatic tumor antigen 1 short form (MTA1s) are elevat

77 The MTA1 coregulator (metastatic tumor antigen 1), a component of the nucleoso

78 Here, we found for the first time that MTA1 (metastatic tumor antigen 1), a master chromatin modifier

79 h effects, associated with either primary or metastatic tumors, are generally poorly understood.

80 determine a pathway diagram that classifies metastatic tumors as "spreaders" or "sponges" and orders

81 on found in Li-Fraumeni syndrome and develop metastatic tumors at much higher frequency than p53(+/-)

82 single CTCs, which recapitulate primary and metastatic tumor biology, remains challenging because cu

83 ke signature in both tumor cell lines and in metastatic tumor biopsies.

84 e then generated and defined as the skeletal metastatic tumor burden by 2 parameters: total lesion fl

85 JP1201 with gemcitabine reduced primary and metastatic tumor burden in orthotopic xenograft and syng

86 115+ non-classical monocytes correlates with metastatic tumor burden in patients.

87 Treatment with cediranib decreased metastatic tumor burden in the brain and bone, decreased

88 on a "5 days on, 2 days off" regimen reduced metastatic tumor burden in the lung while not affecting

89 MTV-Neu) mice resulted in a 75% reduction in metastatic tumor burden in the lungs with a 3.6-fold dec

90 rst study to show a significant reduction in metastatic tumor burden with frequent eradication of met

91 SET domain) is overexpressed in a number of metastatic tumors, but its mechanism of action has not b

92 h can be defeated in the evolution of highly metastatic tumors by combined loss of both p66(Shc) and

93 tage of calcifications increased, whereas in metastatic tumors calcifications were observed only afte

94 nfirmed that loss of HER2-positive status in metastatic tumors can occur in patients with primary HER

95 Metastatic tumors can prepare a distant site for coloniz

96 developed a computational model of a nascent metastatic tumor capturing salient features of known tum

97 Here, we show that metastatic tumor cell attachment causes the induction of

98 cers of epithelial origin, and is crucial to metastatic tumor cell dissemination and drug resistance.

99 Metastatic tumor cell growth and survival in distant org

100 and proliferation, whereas reexpression in a metastatic tumor cell line inhibited migration, prolifer

101 d from colorectal cancer patients and from a metastatic tumor cell line.

102 east cancer cells from doxorubicin-resistant metastatic tumors (cell line 4T1-R).

103 tree, suggest a potential mechanism by which metastatic tumor cells access the lymphatic vasculature.

104 proteoglycan versican, which induces MET of metastatic tumor cells and accelerates metastases.

105 Metastatic tumor cells and basal-like tumor cells exert

106 e is implicated strongly in dissemination of metastatic tumor cells and cells of the immune system.

107 the mechanisms of PRC2 gene up-regulation in metastatic tumor cells and found up-regulation of E2F ge

108 ignature was the most significant feature of metastatic tumor cells and was also found in primary tum

109 ms by which these cells mediate outgrowth of metastatic tumor cells are not completely known.

110 However, how metastatic tumor cells become dormant and how and why tu

111 ated mesenchymal to epithelial transition of metastatic tumor cells by attenuating phospho-Smad2 leve

112 eparating the birth of benign, invasive, and metastatic tumor cells can be determined by analysis of

113 extracellular vesicles secreted from highly metastatic tumor cells can be internalized by weakly met

114 The metastatic tumor cells disturb the equilibrium in bone t

115 Specifically, we discovered that metastatic tumor cells do not express the inhibitor to N

116 urthermore, ectopic expression of Id2 in low metastatic tumor cells downregulated SEMA3F and, as a co

117 How invasive and metastatic tumor cells evade anoikis induction remains u

118 Metastatic tumor cells exhibit a phenotype that differs

119 Individual metastatic tumor cells exhibit two interconvertible mode

120 That metastatic tumor cells grow in selective non-native envi

121 de additional advantage for the outgrowth of metastatic tumor cells in lymph nodes.

122 -200 can confer metastatic ability to poorly metastatic tumor cells in some settings.

123 ibit the development and accumulation of 4T1 metastatic tumor cells in the lungs of treated mice.

124 derstanding the underlying mechanisms of how metastatic tumor cells induce bone destruction is critic

125 transformation of normal cells to malignant, metastatic tumor cells is a multistep process caused by

126 We review evidence that metastatic tumor cells must acquire the capability to au

127 C2) core subunits EED and EZH2 in lymph node metastatic tumor cells over primary tumor cells which we

128 Thus, high metastatic tumor cells overexpress c-myc, leading to upr

129 ughput method for quantifying the ability of metastatic tumor cells to colonize a secondary organ.

130 fibrosarcomas and decreases the delivery of metastatic tumor cells to the draining lymph nodes.

131 It is delivered to primary and lymph node metastatic tumor cells using an imaging-capable nanodrug

132 Compared with primary tumor cells, metastatic tumor cells were highly sensitive to TLR3-med

133 of Cdk5, and Cdk5 activity were increased in metastatic tumor cells, and that Cdk5 kinase activity is

134 17A also induced IL6 and CCL20 production in metastatic tumor cells, favoring the recruitment and dif

135 ascular cell adhesion molecule 1 (VCAM-1)(+) metastatic tumor cells, thereby promoting lymph node met

136 ('anoikis') is a defining characteristic of metastatic tumor cells.

137 ent upregulation of GAD1 expression in brain metastatic tumor cells.

138 djuvant therapy intended to kill the cryptic metastatic tumor cells.

139 opodial maturation and matrix degradation in metastatic tumor cells.

140 in the presence of either metastatic TCM or metastatic tumor cells.

141 lity and survival are important hallmarks of metastatic tumor cells.

142 clasts and also serve to attract and support metastatic tumor cells.

143 did not provide an invasive advantage to the metastatic tumor cells.

144 in selective accumulation of the nanodrug in metastatic tumor cells.

145 itional blocker for E-cadherin expression in metastatic tumor cells.

146 images showed discrete uptake in individual metastatic tumor colonies; autoradiographic data demonst

147 1 expression was higher in human primary and metastatic tumors compared with noncancerous tissue.

148 e in the SRC-2-driven metabolic signature in metastatic tumors compared with that seen in localized t

149 er and was effective in both the primary and metastatic tumor compartments.

150 ofile (GEP) testing on a series of choroidal metastatic tumors confirmed by cytopathology so that cli

151 where nodes are anatomical locations where a metastatic tumor could develop, and edge weightings are

152 in ERCC5 discovered in both the primary and metastatic tumors could also have contributed to the mut

153 iltrating T lymphocytes (TIL) in primary and metastatic tumors could improve active and adoptive T-ce

154 ully and reliably induce abscopal effects in metastatic tumors could meet many unmet clinical needs.

155 mors without metastasis compared with larger metastatic tumors derived from control MDA-MB-231 cells

156 Invasive/metastatic tumors developed in both models closely recap

157 ration of TAMs than locoregional tumors, and metastatic tumors diagnosed in patients at age >/= 18 mo

158 y associated with 12 common cancers based on metastatic tumor distribution autopsy data.

159 le-exome sequencing of 14 matched normal and metastatic tumor DNAs.

160 A better understanding of local and metastatic tumor dormancy could lead to novel cancer the

161 ficacy of chemotherapy in advanced solid and metastatic tumors, especially when exploiting cell-based

162 een Akt2 overexpression and PTEN mutation in metastatic tumor establishment and growth.

163 as amplified and overexpressed in 37% of the metastatic tumors evaluated.

164 Both primary and metastatic tumors express high levels of glucagon; furth

165 The second, a 47-year-old, patient's metastatic tumor extract given intravenously in dogs, pr

166 ature, which seed the scaffold, initiating a metastatic tumor focus.

167 shown huA33 can target and be retained in a metastatic tumor for 6 wk but eliminated from normal col

168 s), suggest tissue-specific proclivities for metastatic tumor formation.

169 Here we profile primary and metastatic tumors from an index patient and demonstrate

170 r, have failed to identify BRAF mutations in metastatic tumors from patients with BRAFmutant primary

171 nalysis of more than 140 matched primary and metastatic tumors from patients, we found that acetylati

172 ns were highly prevalent in ATC (44%) and in metastatic tumors from RAIR PTC patients (95%).

173 double-edged sword by inhibiting primary and metastatic tumor growth and modulating matrix metallopro

174 d angiogenesis and inhibition of primary and metastatic tumor growth in a variety of solid and hemato

175 target to strengthen bone mass and diminish metastatic tumor growth in bone.

176 FABP4 deficiency substantially impaired metastatic tumor growth in mice, indicating that FABP4 h

177 itor of iPLA(2), significantly inhibited EOC metastatic tumor growth in mouse xenograft models using

178 y reduce orthotopic tumor growth, as well as metastatic tumor growth in the lung of severe combined i

179 However, the impact of efferocytosis in metastatic tumor growth is unknown.

180 DSCs) are emerging as potential promoters of metastatic tumor growth, and there is interest in target

181 ) family have been implicated in primary and metastatic tumor growth, angiogenesis, and pathological

182 ased tumor cell proliferation and suppressed metastatic tumor growth, respectively.

183 mature myeloid cells blocks angiogenesis and metastatic tumor growth.

184 lungs and, unexpectedly, enhanced pulmonary metastatic tumor growth.

185 tro and in vivo at the levels of primary and metastatic tumor growth.

186 des an angiogenic prosperous environment for metastatic tumor growth.

187 red less important in established primary or metastatic tumor growth.

188 oxybenzoate (EDHB) on liver regeneration and metastatic tumor growth.

189 enesis and significantly decreased local and metastatic tumor growth.

190 promoting cyclin proteins, without enhancing metastatic tumor growth.

191 promoting cyclin proteins, without enhancing metastatic tumor growth.

192 tasis, whereas LOXL2 overexpression promoted metastatic tumor growth.

193 oxybenzoate (EDHB) on liver regeneration and metastatic tumor growth.

194 sor cells and macrophages, thereby promoting metastatic tumor growth.

195 e SETD2 and H3K36me3 dysregulation occurs in metastatic tumors, H3K36me3, SETD2 copy number (CN) or S

196 Patients whose metastatic tumors harbor EGFR mutations are expected to

197 ic BCCs, but refractory disease in distantly metastatic tumors has not been documented in this high-r

198 s in CRC and the changes between primary and metastatic tumors has yet to be developed.

199 Metastatic tumors have been shown to establish microenvi

200 oarray analysis of both localized tumors and metastatic tumors identified the downregulation of the n

201 rix stiffness or organization in primary and metastatic tumors, implying a function for LOXL2 indepen

202 rmed increased chromosomal loss of DIAPH3 in metastatic tumors in a different cohort of patients (P =

203 g showed CXCL12-CXCR7 binding in primary and metastatic tumors in a mouse model of breast cancer.

204 vent the spontaneous formation and growth of metastatic tumors in an orthotopic xenograft model of pr

205 eutic drug, on the development and growth of metastatic tumors in bone.

206 and mice developed larger and more invasive metastatic tumors in lymph nodes and died earlier than w

207 gression, we combined intra-vital imaging of metastatic tumors in mice, microfluidics-based artificia

208 ighly aggressive, angiogenic, and multiorgan metastatic tumors in nude mice.

209 mors enhanced the growth of both primary and metastatic tumors in response to estradiol.

210 ar carcinoma in one lesion, and a variety of metastatic tumors in the remaining 10 lesions.

211 Residual metastatic tumors in the third and fourth ventricles and

212 lonal evolution patterns between primary and metastatic tumors in the two cases.

213 gerated in unresectable, locally invasive or metastatic tumors, in which embryonal tumor cells are EG

214 ew recent comparative studies of primary and metastatic tumors, including data suggesting that macroe

215 d MSI have been associated with responses of metastatic tumors, including PDACs, to immune checkpoint

216 a cytokine that is often highly expressed in metastatic tumors, induces Ski degradation through the u

217 e cancer cells that are shed from primary or metastatic tumors into the peripheral blood circulation.

218 ity of the genomic profiles from primary and metastatic tumors is driven by the patient.

219 f the Kras(mut) subpopulation in primary and metastatic tumors, leading to apoptotic elimination of a

220 patient survival, normal expression in some metastatic tumors led us to wonder whether other mechani

221 t of purified oHSV alone, effectively tracks metastatic tumor lesions and significantly prolongs the

222 In vivo tumor modeling studies with a highly metastatic tumor line, PC-3ML cells, revealed that EGCG

223 ms to become smaller in patients with higher metastatic tumor load.

224 Notably, among metastatic tumors, low ATIP3 levels associate with decre

225 at several proteins characteristic of highly metastatic tumors (LTBP3, SNED1, EGLN1, and S100A2) play

226 (primary reseeding), and (iii) reseeding of metastatic tumors (metastasis reseeding).

227 static cancer cell phenotypes as well as the metastatic tumor microenvironment in different organs.

228 ssion of T cells and NK cells in primary and metastatic tumor microenvironments.

229 of mice in 2 of the subcutaneous and in the metastatic tumor model.

230 y to Los respectively in A549 orthotopic and metastatic tumor models (p<0.05) when given by inhalatio

231 the therapeutic window successfully treated metastatic tumor models, including B16OVA lung metastasi

232 e tumor metastasis to lung in multiple mouse metastatic tumor models.

233 two histologically distinct murine pulmonary metastatic tumor models.

234 e intracranially implanted glioma and breast metastatic tumor models.

235 Performance within the subgroup of metastatic tumors (n = 258) was found to be slightly low

236 rs and significant decrease in the number of metastatic tumor nodules, whereas treatment with untarge

237 ressor cells was increased in the lungs with metastatic tumors of Bcl11b(F/F)/CD4-Cre mice, their arg

238 sion, which was also elevated in primary and metastatic tumors of individuals with CRPC.

239 Instead, these mice develop highly metastatic tumors of neuroendocrine, not epithelial, ori

240 The goal of hepatectomy for primary or metastatic tumors of the liver is complete resection wit

241 ly advanced pancreatic cancer and primary or metastatic tumors of the liver.

242 Metastatic tumors of the retina are rare, simulate retin

243 romoting the angiogenic switch for growth of metastatic tumors or find no role at all for these circu

244 There were 374 uveal metastatic tumors originating from primary lung cancer i

245 ratory and tumorigenic property to establish metastatic tumors outside the primary microenvironment.

246 etion of the locus encoding DRF3 (DIAPH3) in metastatic tumors (P = 0.001) in comparison with organ-c

247 Primary and matched metastatic tumor pairs from 15 patients were analyzed by

248 Our data reveal that metastatic tumors preferentially disseminate in specific

249 This study thus demonstrates that pre-metastatic tumors produce exosomes, which elicit a broad

250 g as an effective strategy for inhibition of metastatic tumor progression in vivo.

251 s in the tumor microenvironment that promote metastatic tumor progression.

252 lted in significant determent of primary and metastatic tumor progression.

253 00A4-dependent link between inflammation and metastatic tumor progression.

254 Chromatin remodeling factor metastatic tumor protein 1 (MTA1), one of the most upreg

255 ients that ABCA1 was overexpressed in 41% of metastatic tumors, reducing time to metastasis by 9 year

256 The instability of metastatic tumors remains a leading obstacle to personal

257 Metastatic tumors retained abnormal SHH signaling like t

258 Analysis of patient matched blood and metastatic tumors revealed that ABCB5 and RANK subpopula

259 Analysis of patient-matched primary and metastatic tumors reveals that 52% possess tau expressio

260 n) and fatty acid uptake in >9000 primary or metastatic tumor samples from the multi-cancer TCGA data

261 r grade with the highest expression level in metastatic tumor samples, suggesting that RecQL4 may be

262 controls indicated downregulation of KLF4 in metastatic tumor samples.

263 n melanoma metastasis-derived cell lines and metastatic tumor samples.

264 rug vectors will need to consider primary vs metastatic tumor setting, or early vs late stage metasta

265 e therapeutic vulnerabilities of primary and metastatic tumors, shed light on the temporal patterns o

266 croenvironment of the primary as well as the metastatic tumor sites can determine the ability for a d

267 r effector T cells successfully migrate into metastatic tumor sites.

268 intra-tumor heterogeneity at the primary and metastatic tumor sites.

269 a model for a common clonal progenitor with metastatic tumor-specific divergence.

270 potential targets for new therapies to limit metastatic tumor spread.

271 ive component of cancer progression, namely, metastatic tumor spread.

272 Indeed, both CD133+ and CD133- metastatic tumor subpopulations formed colonospheres in

273 sponse assessment, by specifically assessing metastatic tumor subpopulations, likely responsible for

274 as reduced or absent in cells from a matched metastatic tumor, suggesting that changes occur in metas

275 o trace evolutionary lineages in primary and metastatic tumors suggests that employing a finite-sites

276 cantly enhanced efficacy against primary and metastatic tumors, supporting the therapeutic relevance

277 roduced smaller, less vascularized, and less metastatic tumors than TRAMP control tumors.

278 cord-stromal, or germ cell origin as well as metastatic tumors that frequently originate in the gastr

279 2 (HER2) -positive primary breast tumors had metastatic tumors that were HER2 positive (concordant) o

280 the mouse lung to promote aggressive, highly metastatic tumors, that are initially sensitive to chemo

281 Among these targets specific to metastatic tumors, there was an enrichment in those impl

282 ranscriptional profile and T cell markers in metastatic tumor tissue.

283 ess reveals increased collagen deposition in metastatic tumor tissues as a direct consequence of ampl

284 demonstrate that hepatic growth of melanoma metastatic tumors was strongly inhibited in mice with Cd

285 In this study, we show that the metastatic tumors we examined overexpress granulocyte-co

286 y, in one patient where multiple independent metastatic tumors were available, we show common and div

287 Metastatic tumors were enriched for proliferation-relate

288 udy population: Eighteen patients with uveal metastatic tumors were evaluated.

289 etastasis, we found that although late-stage metastatic tumors were indeed surrounded by osteoclasts,

290 The genetic profiles of recurrent and metastatic tumors were often distinct from primary tumor

291 normal tissues, PBMC, recurrent tumors, and metastatic tumors) were incorporated into YM500v2.

292 in cells with extra centrosomes can generate metastatic tumors when transplanted into the abdomens of

293 ntiate and reconstitute heterogeneity in the metastatic tumors whereas CD24(-)CD29(-) cells could not

294 ced prostate cancer can progress to systemic metastatic tumors, which are generally androgen insensit

295 nd demonstrate high concordance of cfDNA and metastatic tumor whole-exome sequencing.

296 Treatment of mice bearing orthotopic, metastatic tumors with anti-CD40 antibody resulted in on

297 establishment of a clinical trial for WES of metastatic tumors with prospective follow-up of patients

298 Half of the specimens were metastatic tumors, with the remainder being poorly diffe

299 in the formation of secondary (recurrent or metastatic) tumors, with potential implications for ther

300 hips between these events in the primary and metastatic tumors within an individual.