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

3 diffuse immune cell infiltrate throughout a metastatic tumor.

4 tumors, including drug-resistant tumors and metastatic tumors.

5 robiome stability between paired primary and metastatic tumors.

6 agation of epithelial cells from primary and metastatic tumors.

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

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

9 umors assayed, including primary and matched metastatic tumors.

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

11 rimination between non-metastatic and highly metastatic tumors.

12 ignficantly diminished growth of primary and metastatic tumors.

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

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

15 nt also improved chemotherapy of primary and metastatic tumors.

16 ttractive strategy for treatment of advanced metastatic tumors.

17 novel paradigm for treatment of primary and metastatic tumors.

18 ed for efficient establishment and growth of metastatic tumors.

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

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

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

22 clinical trials for treatment of advanced or metastatic tumors.

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

24 reatment of painful posterior vertebral body metastatic tumors.

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

26 FL expression was increased significantly in metastatic tumors.

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

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

29 nfused back into the individual to eliminate metastatic tumors.

30 rather than stromal cells within primary and metastatic tumors.

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

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

33 d copy number variations between primary and metastatic tumors.

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

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

36 but downregulated in a significant subset of metastatic tumors.

37 expression was significantly associated with metastatic tumors.

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

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

40 cogene, which is correlated with high-grade, metastatic tumors.

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

42 ctivated in both tumor types and enriched in metastatic tumors.

43 ical pathway alterations between primary and metastatic tumors.

44 ated from purified epithelium of primary and metastatic tumors.

45 nd absence of observed clones in primary and metastatic tumors.

46 ogression, but failed to reverse established metastatic tumors.

47 and stromal compartments of both primary and metastatic tumors.

48 tified high expression of cytoplasmic p27 in metastatic tumors.

49 tency, resulting in the eradication of large metastatic tumors.

50 entified in primary tumors and replicated in metastatic tumors.

51 ify alterations associated with advanced and metastatic tumors.

52 urrence of triple-negative breast cancer and metastatic tumors.

53 to analyze nanoparticle-cell interactions in metastatic tumors.

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

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

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

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

58 reported, which enables visualization of the metastatic tumor and the tumor metastatic proximal LNs r

59 k on a molecular signature characteristic to metastatic tumors and associated with poor prognosis, MM

60 n H(+)-coupled symporter highly expressed in metastatic tumors and at inflammatory sites undergoing h

61 SST on multiple tumor models, including lung metastatic tumors and even multidrug-resistant tumors.

62 Here, we compared primary with metastatic tumors and found that the nuclei of tumor cel

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

64 protein that is frequently overexpressed in metastatic tumors and inhibits NMIIA activity by inducin

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

66 transcriptional/translational loss of RD3 in metastatic tumors and MSDACs.

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

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

69 0 mutations were present in both primary and metastatic tumors, and 3 mutations were detected only in

70 77% were transmitted from primary tumors to metastatic tumors, and 80% from primary to recurrent tum

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 Overexpression of metastatic tumor antigen 1 (MTA1) was correlated with po

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

76 mechanisms required for the establishment of metastatic tumors are not fully determined.

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

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

79 eumonectomy from 1990 to 2017 for primary or metastatic tumors at 12 institutions.

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

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

82 cing of cell free DNA (cfDNA) and of matched metastatic tumor biopsies from patients with metastatic

83 e diagnosis of CRPC-NE currently relies on a metastatic tumor biopsy, which is invasive for patients

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

85 gh-grade serous ovarian cancer cells reduced metastatic tumor burden in mice.

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

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

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

89 host WNT5A significantly reduced peritoneal metastatic tumor burden.

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

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

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

93 genomic sequencing of a sufficient number of metastatic tumors can reveal previously unknown metastat

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

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

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

97 Metastatic tumor cell growth and survival in distant org

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

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

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

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

102 The nanoparticles preferentially target metastatic tumor cells and aHSCs within the metastatic l

103 Metastatic tumor cells and basal-like tumor cells exert

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

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

106 es is determined by both intrinsic traits of metastatic tumor cells and properties appertaining to th

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

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

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

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

111 The metastatic tumor cells disturb the equilibrium in bone t

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

113 Metastatic tumor cells exhibit a phenotype that differs

114 entifying and sorting highly tumorigenic and metastatic tumor cells from a heterogeneous cell populat

115 For example, in cancer, invasive and metastatic tumor cells have often been reported to be so

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

117 -200 can confer metastatic ability to poorly metastatic tumor cells in some settings.

118 mising strategy to counter the "castling" of metastatic tumor cells in the peritoneal immunoprivilege

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

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

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

122 tored in lung neutrophils are transported to metastatic tumor cells through a macropinocytosis-lysoso

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

124 d protein (PTHrP), which is produced by bone metastatic tumor cells to promote osteoclast-mediated bo

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

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

127 an actionable signaling pathway utilized by metastatic tumor cells whereby the transcriptional regul

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

129 17A also induced IL6 and CCL20 production in metastatic tumor cells, favoring the recruitment and dif

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

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

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

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

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

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

136 GFP switch of this model in reporting EMT of metastatic tumor cells.

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

138 opodial maturation and matrix degradation in metastatic tumor cells.

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

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

141 tes and mediates epigenetic reprogramming of metastatic tumor cells.

142 is a unique marker of highly tumorigenic and metastatic tumor cells.

143 aling pathway required for survival by brain-metastatic tumor cells.

144 invasion, and migration (AIM) properties of metastatic tumor cells.

145 1 expression was higher in human primary and metastatic tumors compared with noncancerous tissue.

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

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

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

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

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

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

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

153 Invasive/metastatic tumors developed in both models closely recap

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

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

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

157 the real-time visualization of the potential metastatic tumor-draining lymph node(s) for their needed

158 esulted in smaller, differentiated, and less metastatic tumors, due, in part, to decreased canonical

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

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

161 iple seeding events among tumor sites during metastatic tumor evolution, and extensive intermixture o

162 Simulated metastatic tumors exhibited decreased growth compared to

163 Many primary and metastatic tumors express high levels of DeltaNp63, whil

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 Integration of BKPyV in both primary and metastatic tumors followed the mechanism of microhomolog

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

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

170 astatic tumors from 60 patients and multiple metastatic tumors from 39 patients whose primary tumors

171 We analyzed paired primary and metastatic tumors from 60 patients and multiple metastat

172 ng (WES) of germline DNA and 157 primary and metastatic tumors from 80 UC patients.

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

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

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

176 inuous process occurring in both primary and metastatic tumors, generating heterogenous tumor cell po

177 enable immune checkpoint blockade to inhibit metastatic tumor growth and prevent tumor relapse by act

178 sing nanoparticles could offer a way to stop metastatic tumor growth before it causes excessive patie

179 senting cells (APC), and abrogates local and metastatic tumor growth by a T-cell-related effect.

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

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

182 dependent manner, and suppresses primary and metastatic tumor growth in vivo We conclude that exploit

183 treatment significantly delayed residual and metastatic tumor growth in vivo.

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

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

186 ation and invasion, and inhibits primary and metastatic tumor growth, in vivo.

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

188 tasis, whereas LOXL2 overexpression promoted metastatic tumor growth.

189 enesis and significantly decreased local and metastatic tumor growth.

190 promoting cyclin proteins, without enhancing metastatic tumor growth.

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

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

193 ntal metastases, without limiting primary or metastatic tumor growth.

194 mature myeloid cells blocks angiogenesis and metastatic tumor growth.

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

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

197 des an angiogenic prosperous environment for metastatic tumor growth.

198 the polarity of M2 microglia, which enhances metastatic tumor growth.

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

200 Patients whose metastatic tumors harbor EGFR mutations are expected to

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

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

203 Metastatic tumors have been shown to establish microenvi

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

205 (D-A-D) dye, IR-FD, is screened for primary/metastatic tumor imaging in the NIR-IIa (1100-1300 nm) w

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

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

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

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

210 and metabolomics analyses of primary and LN-metastatic tumors in mice, we found that LN metastasis r

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

212 (mTiD) cultures resemble the architecture of metastatic tumors in the lung, including angiogenesis.

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

214 Residual metastatic tumors in the third and fourth ventricles and

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

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

217 The metastatic tumor-in-a-dish (mTiD) cultures resemble the

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

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

220 of whole-exome DNA sequencing of primary and metastatic tumors indicated that this mutation was prese

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

222 e evolution of transformed cancer cells into metastatic tumors is, in part, driven by altered intrace

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

224 protein (YAP) is selectively activated in LN-metastatic tumors, leading to the up-regulation of genes

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

226 itope in human pancreatic cancer primary and metastatic tumor lesions.

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

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

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

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

231 s uncover a tumor-stromal interaction in the metastatic tumor microenvironment and an intimate signal

232 ch has a pivotal role in the creation of the metastatic tumor microenvironment in the intraperitoneal

233 rious cancer-associated stromal cells in the metastatic tumor microenvironment with regard to the ome

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

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

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

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

238 e intracranially implanted glioma and breast metastatic tumor models.

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

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

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

242 1 and KRT6B are consistently up-regulated in metastatic tumors of both MB49 sub-clones.

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

244 argeting, imaging and therapy of primary and metastatic tumors of the brain.

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

246 Metastatic tumors of the retina are rare, simulate retin

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

248 evented P-body clearance and MET, inhibiting metastatic tumor outgrowth.

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

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

251 Our data reveal that metastatic tumors preferentially disseminate in specific

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

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

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

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

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

257 patient method for small to medium choroidal metastatic tumors, providing tumor control in 78% of eye

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

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

260 Metastatic tumors retained abnormal SHH signaling like t

261 of cells cultured from S2 and S4 primary and metastatic tumors revealed that a panel of genes with ba

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

263 fter a patient's passing to procure multiple metastatic tumor samples for genomic studies through nex

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

265 Analysis of matched primary and metastatic tumor samples supports a unidirectional, line

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

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

268 Moreover, lung metastatic tumors show a higher-level expression of KS c

269 ograft-based drug tests using 31 primary and metastatic tumors show personalized responses, which cou

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

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

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

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

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

275 Metastatic tumors that have become resistant to androgen

276 2 (HER2) -positive primary breast tumors had metastatic tumors that were HER2 positive (concordant) o

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

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

279 are frequently the only source for obtaining metastatic tumor tissue.

280 clinical outcomes based on primary, but not metastatic, tumor tissue.

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

282 Matched primary and metastatic tumor tissues were collected for 3 patients,

283 Metastatic tumor tissues were found to display a biodyna

284 on (68)Ga-FAPI PET/CT of various primary and metastatic tumors to identify the most promising indicat

285 g investigated as a new modality of advanced/metastatic tumors treatment and enhancement of virothera

286 Consistently, highly metastatic tumors upregulated multiple pyrimidine biosyn

287 umented increased PI4KIIIalpha expression in metastatic tumors vs. the primary tumor counterparts, fu

288 Metastatic tumors were enriched for proliferation-relate

289 n spectra, and signatures in matched primary-metastatic tumors were extremely similar, suggesting tra

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

291 ion virome capture sequencing of primary and metastatic tumors were performed in three patients with

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

293 and non-irradiated distant tumors, including metastatic tumors, when adrenergic stress or signaling t

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

295 us integration sites between the primary and metastatic tumors, which affected LINC01924, eIF3c, and

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

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

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

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

300 lonization using patient-derived primary and metastatic tumor xenografts (PDX).