ライフサイエンスコーパス: metastatic

1 d disease status (recurrent or persistent vs metastatic).

2 Ac-T3 suggesting the inhibitor might be anti-metastatic.

3 7 was silenced in breast cancer cells, their metastatic ability was inhibited.

4 in therapeutic planning to avoid postsurgery metastatic acceleration.

5 y expressed in breast cell lines with strong metastatic activities to the lung and co-expressed in a

6 metastases and display higher levels in the metastatic ALDH(high) sub-population of PC-3M-Pro4Luc2 P

7 f PC-3M-Pro4Luc2 PCa cells compared with non-metastatic ALDH(low).

8 tudy group, there were 32 (37%) and 54 (67%) metastatic and non-metastatic lymph nodes, respectively.

9 Disease control has been proven in the metastatic and, to a limited extent, the adjuvant settin

10 a samples, and this is especially drastic in metastatic and/or high Gleason score tumor samples.

11 ws malignant cells with greater tumorigenic, metastatic, and drug-resistant capacity.

12 In January 2016, the Metastatic Breast Cancer Alliance (the Alliance) convene

13 r whether bone regions typically targeted by metastatic breast cancer feature distinct HA materials p

14 onal study of 102 postmenopausal, HR + HER2- metastatic breast cancer patients treated with everolimu

15 one metastases occur in approximately 70% of metastatic breast cancer patients, often leading to skel

16 the treatment of patients with HER2-positive metastatic breast cancer previously treated with trastuz

17 n, intratumor vascularization, and local and metastatic breast cancer progression.

18 n of outcomes in patients with HER2-positive metastatic breast cancer randomized to an antibody-based

19 Metastatic breast cancer remains challenging to treat, a

20 Six patients with HER2-positive metastatic breast cancer were enrolled and administered

21 positive, HER2-negative, locally advanced or metastatic breast cancer, who had relapsed on or after e

22 sured immunohistochemically in patients with metastatic breast cancer.

23 crine-refractory, estrogen receptor-positive metastatic breast cancer.

24 es in clinical and translational research in metastatic breast cancer.

25 t PLD2 as a potential therapeutic target for metastatic breast cancer.

26 s from 170 patients with locally relapsed or metastatic breast cancer.

27 tcome in patients with ERBB2 (HER2)-positive metastatic breast cancer; a clinically effective biosimi

28 orubicin (CREKA-Lipo-Dox) for the therapy of metastatic breast tumor.

29 g the choice of the method used to determine metastatic burden and statistical analysis of the result

30 ng tumor cells in the blood and enhanced the metastatic burden at the lung.

31 t and pro-metastatic protein expression) and metastatic burden, accompanied with TAM polarization awa

32 toring Trp consumption and Kyn production in metastatic (Calu-6, NCI-H1299, and HT29) and nonmetastat

33 most prevalent genes somatically altered in metastatic cancer included TP53, CDKN2A, PTEN, PIK3CA, a

34 that regulate the transition from primary to metastatic cancer is a fundamental challenge.

35 rom hepatocellular carcinoma (HCC), a highly metastatic cancer, undergo epithelial to amoeboid transi

36 eiving MEK inhibitors for treatment of their metastatic cancer, who had evidence of serous retinal de

37 ng explored as a treatment for patients with metastatic cancer.

38 tructive uropathy, urothelial carcinoma, and metastatic cancer.

39 A defining hallmark of primary and metastatic cancers is the migration and invasion of mali

40 Further capturing of CTCs from metastatic cancers patients revealed a positive capture

41 Metastatic cancers produce exosomes that condition pre-m

42 has demonstrated efficacy in treating human metastatic cancers, but therapeutic resistance is a prac

43 alysis is available from clinically acquired metastatic cancers.

44 cept for their candidacy as targets to treat metastatic cancers.

45 tively, our findings show how RB loss drives metastatic capacity and highlight RHAMM as a candidate t

46 rcinoma cells with high tumor initiating and metastatic capacity, termed cancer stem cells (CSCs).

47 increased stem-like properties, and spawned metastatic capacity.

48 o the peripheral nervous system that elevate metastatic capacity.

49 spiration of a right axillary node confirmed metastatic carcinoma.

50 of the three sentinel lymph nodes contained metastatic carcinoma.

51 t gained into the events that constitute the metastatic cascade and the paucity of therapeutic option

52 EMT/MET) and phenotypically recapitulate the metastatic cascade.

53 cess promises to aid in efforts to block the metastatic cascade.

54 n Index [BSI]) in patients who have advanced metastatic castration-resistant prostate cancer (mCRPC)

55 Purpose In patients with metastatic castration-resistant prostate cancer (mCRPC),

56 one metastases to treatment in patients with metastatic castration-resistant prostate cancer (mCRPC).

57 ningful and occur early are an unmet need in metastatic castration-resistant prostate cancer clinical

58 trial-ENTHUSE M1-in which 266 patients with metastatic castration-resistant prostate cancer were tre

59 ON: We noted no survival benefit in men with metastatic castration-resistant prostate cancer with the

60 symptomatic patients with chemotherapy-naive metastatic castration-resistant prostate cancer without

61 ilimumab did not improve OS in patients with metastatic castration-resistant prostate cancer.

62 e to taxanes in men with chemotherapy-naive, metastatic, castration-resistant prostate cancer.

63 ds Eligible patients had locally advanced or metastatic ccRCC that had progressed during one or more

64 ne expression profiling revealed primary and metastatic cells as two distinct cell populations define

65 Reducing GAD1 in metastatic cells by primary glia cell coculture abolishe

66 Metastatic cells cultured on osteo-mimetic surfaces coat

67 (ER) to Golgi trafficking gene signature in metastatic cells enhances transport kinetics, which prom

68 rced expression of DUSP4 drove conversion of metastatic cells to nonmetastatic cells.

69 lia cell coculture abolished the capacity of metastatic cells to utilize extracellular glutamine, lea

70 a(2+)-mediated focal adhesion disassembly in metastatic cells, rather than changes in integrin expres

71 a-derived proteins secreted from highly lung metastatic cells.

72 is uniformly absent in the AR-positive (AR+) metastatic cells.

73 ifacients may be good for safe and effective metastatic chemoprevention targeting circulating tumor c

74 01 patients with treatment-naive progressive metastatic clear cell renal cell carcinoma were enrolled

75 is required for the survival of primary and metastatic colon cancers and that oncogenic K-RAS activa

76 ntify novel microenvironmental regulators of metastatic colonization.

77 opied neutrophil depletion by reducing liver metastatic colony growth, vascular density, and branchin

78 Chemotherapy-naive patients with metastatic colorectal cancer (WHO performance status 0 o

79 IRT) in third-line or subsequent therapy for metastatic colorectal cancer has clinical benefit in pat

80 ) with histologically confirmed recurrent or metastatic colorectal cancer locally assessed as dMMR/MS

81 trol in pre-treated patients with dMMR/MSI-H metastatic colorectal cancer, and could be a new treatme

82 patients with KRAS wt untreated advanced or metastatic colorectal cancer, there was no significant d

83 n and reduced survival time of patients with metastatic colorectal cancer.

84 testinal mucosa and universally expressed by metastatic colorectal cancer.

85 tors was 10-fold higher in primary tumors of metastatic colorectal than in nonmetastatic cases and pr

86 occur in approximately 2.2% of patients with metastatic CRC and define a clinically distinct subtype

87 KRAS in CRC, we engineered a mouse model of metastatic CRC that harbors an inducible oncogenic Kras

88 reated with Trametinib and Dabrafenib due to metastatic cutaneous melanoma stage IV.

89 in BrM could identify clinically actionable metastatic dependencies.

90 as significantly increased for patients with metastatic disease (adjusted hazard ratio [AHR], 2.3; 95

91 00 ng/mL; and the PRETEXT annotation factors metastatic disease (M), macrovascular involvement of all

92 lopment, local tumor recurrence, presence of metastatic disease after surgery, and sufficiency of the

93 hildren, frequently presents with aggressive metastatic disease and for these children the 5-year sur

94 ET/CT enables discrimination of local versus metastatic disease and thus might have a crucial impact

95 ccessful sentinel-lymph-node mapping who had metastatic disease correctly identified in the sentinel

96 squamous cell carcinoma of the anus without metastatic disease from 59 centres in the UK.

97 locoregional lymph nodes in 39%, and distant metastatic disease in 16%.

98 fluoride (NaF PET) for assessment of osseous metastatic disease led to changes in intended management

99 e entire cohort and 7.56% of the subset with metastatic disease to any site.

100 fluoride (NaF PET) for assessment of osseous metastatic disease was associated with substantial chang

101 To evaluate outcome in patients with limited metastatic disease who receive chemotherapy first and pr

102 tors: PRETEXT I/II, PRETEXT III, PRETEXT IV, metastatic disease, and AFP concentration of 100 ng/mL o

103 ould prove useful in determining the risk of metastatic disease, and its manipulation might offer a n

104 f the sentinel-lymph-node-based detection of metastatic disease, was defined as the proportion of pat

105 hment of a cancer cell to the development of metastatic disease, which is dependent on immune evasion

106 etion of first-line/initial chemotherapy for metastatic disease.

107 nonmetastatic disease and 0.31 in those with metastatic disease.

108 cted survival of neuroblastoma patients with metastatic disease.

109 with the liver being the most common site of metastatic disease.

110 of alterations associated with recurrent and metastatic disease.

111 nd more than 50% of patients presenting with metastatic disease.

112 ating intrahepatic HCC even in patients with metastatic disease.

113 n cancer types with no effective therapy for metastatic disease.

114 cer-related deaths, primarily due to distant metastatic disease.

115 eria in Solid Tumors (RECIST) for measurable metastatic disease.

116 tial for the development of solid tumors and metastatic disease.

117 Thus, we posit that, during metastatic dissemination (when cancer cells are exposed

118 hemical blockades of JNK and MMP1 suppressed metastatic dissemination associated with S100A4 elevatio

119 localization sequence resulted in increased metastatic dissemination in xenograft or syngeneic tumor

120 athways which promote therapy resistance and metastatic dissemination is the key to successful treatm

121 efine S100A4 effector functions that mediate metastatic dissemination of mutant Ras-induced tumors in

122 a more active role in solid tumor growth and metastatic dissemination than simply providing the physi

123 conserved pathways used by S100A4 to promote metastatic dissemination, with potential prognostic and

124 ese neutrophils were responsible for the pro-metastatic effect of MSCs since inhibition of this chemo

125 Also, 'anti-metastatic' effects of ectopic miR-383 expression were o

126 BB2/HER2 amplification and the other showing metastatic enrichment of the activating V777L ERBB2/HER2

127 ify the ability of tumour cells to establish metastatic foci, with 19 of these genes not previously d

128 tatic disease and increased formation of new metastatic foci.

129 MEM45B whose expression values discriminated metastatic from primary melanoma (87% classification acc

130 specifically mediate PERK's pro-invasive and metastatic functions.

131 c cancer (unresectable, locally advanced, or metastatic gastric cancer, including adenocarcinoma of t

132 years) with unresectable locally advanced or metastatic gastric or gastro-oesophageal junction adenoc

133 udy demonstrates that patients with relapsed metastatic GCT are curable by HDCT plus PBSCT even when

134 Array analysis of human metastatic genes identified the scaffolding protein meta

135 Conclusion Children with metastatic HB have a poor prognosis.

136 the pattern of lung nodules in children with metastatic hepatoblastoma (HB) correlates with outcome.

137 ad histologically or cytologically confirmed metastatic hormone receptor-positive, HER2-negative brea

138 In response to poly(I:C) addition, the metastatic IECs also induced the chemokine CXCL10 in a T

139 tastatic intestinal epithelial cells (IECs), metastatic IECs express TLR3 and that TLR3 promotes inva

140 pendent for growth in vitro, as well as more metastatic in vivo.

141 Metastatic infection is an important complication of Sta

142 Early diagnosis of metastatic infection is crucial, because specific treatm

143 a valuable technique for early detection of metastatic infectious foci, often leading to treatment m

144 immediately relegates all patients with non-metastatic inflammatory breast cancer to stage 3, regard

145 Here we report that, unlike non-metastatic intestinal epithelial cells (IECs), metastati

146 y explain in part the heterogeneous fates of metastatic lesions often observed in the clinic post-the

147 opus model of conversion of melanocytes to a metastatic-like phenotype only previously observed in an

148 hyperpermeability than exosomes from the non metastatic line (SW480Exos).

149 Moreover, exosomes from the metastatic line (SW620Exos) exhibited higher ability to

150 le-cell DNA sequencing approach to trace the metastatic lineages of two CRC patients with matched liv

151 efective liver stem cells (LSCs) into highly metastatic liver cancer cells in premalignant liver tiss

152 , in which two independent clones seeded the metastatic liver tumor after having diverged at differen

153 More robust incorporation of numerical metastatic LN burden may augment staging and better info

154 Metastatic lung cancer cells can undergo an epithelial-t

155 contrast in detection and identification of metastatic lymph nodes was distinct and could be used fo

156 ls were present within tumors and invaded or metastatic lymph nodes, but were barely detectable withi

157 ere 32 (37%) and 54 (67%) metastatic and non-metastatic lymph nodes, respectively.

158 t to their tumor status in order to identify metastatic lymph nodes.

159 to identify ICAM-1 as a potential target for metastatic melanoma (MM).

160 rapies in the clinical armamentarium against metastatic melanoma (MMel).

161 chanistically, overexpression of miR-200a in metastatic melanoma cells induces cell cycle arrest by t

162 argeting epigenetic modulators against human metastatic melanoma cells.

163 ve trials in MMel.The clinical management of metastatic melanoma requires predictors of the response

164 c and histone epigenetic analysis of patient metastatic melanoma tumors taken prior to checkpoint blo

165 tudy reported the cases of two patients with metastatic melanoma who developed fatal myocarditis duri

166 zumab provides durable antitumor activity in metastatic melanoma, including complete response (CR) in

167 ls of immune checkpoint blockade therapy for metastatic melanoma, we found that tumor aneuploidy inve

168 ) represent promising therapeutic agents for metastatic melanoma, yet their mechanism of action remai

169 s major impact on the tumorigenic program of metastatic melanoma.

170 atic modules in monocytes and DCs from human metastatic melanoma.

171 n long-term survival of patients with widely metastatic melanoma.

172 t promise in a variety of cancers, including metastatic melanoma.

173 udy, we seek to identify a gene signature of metastatic melanoma.

174 roved the clinical outcomes of patients with metastatic melanoma.

175 to have a superior capacity to establish pre-metastatic microenvironment in distant organs is unclear

176 (C3) was upregulated in four leptomeningeal metastatic models and proved necessary for cancer growth

177 findings were validated in both primary and metastatic models of pancreatic cancer.

178 of site of unknown primary in patients with metastatic NET (4 papers, yield was 44%); impact on subs

179 Forty patients with metastatic NET and unknown primary site underwent (68)Ga

180 own primary in NET patients who present with metastatic NET, but no known primary tumor.

181 lization of unknown primary in patients with metastatic NET.

182 apeutics that could improve the treatment of metastatic neuroblastoma.

183 h emerging functions in establishing the pre-metastatic niche and other aspects of metastasis.

184 logical inhibition of CYP4A reduced lung pre-metastatic niche formation (evidenced by a decrease in v

185 CYP4A10(high) macrophages promoted lung pre-metastatic niche formation and metastasis.

186 s positively associated with metastasis, pre-metastatic niche formation and poor prognosis in breast

187 rcinomas and melanoma, and in ECs of the pre-metastatic niche in mice.

188 cancers produce exosomes that condition pre-metastatic niches in remote microenvironments to favor m

189 mouse models for live imaging of distal pre-metastatic niches.

190 lated continuously with increasing number of metastatic nodes without plateau, with the effect most p

191 gically confirmed, advanced (unresectable or metastatic), non-functional, well-differentiated (grade

192 y untreated patients with BRAF(V600E)-mutant metastatic NSCLC.

193 d >/=16 years) with histologically confirmed metastatic ocular melanoma were enrolled.

194 ctory ALK-positive ALCL and 14 patients with metastatic or inoperable ALK-positive IMT received crizo

195 rs grow despite suppression of NFS1, whereas metastatic or primary lung tumours do not.

196 care (SOC) was hormone therapy continuously (metastatic) or for >/= 2 years (nonmetastatic); prostate

197 programs that underlie the dissemination and metastatic outgrowth of cancer cells are beginning to co

198 motes survival and ultimately contributes to metastatic outgrowth.

199 pplications for the treatment of advanced or metastatic pancreatic adenocarcinoma and advanced epithe

200 ptember 2012 and May 2014, 137 patients with metastatic pancreatic adenocarcinoma for whom gemcitabin

201 on with modified FOLFIRINOX in patients with metastatic pancreatic cancer.

202 Purpose Metastatic pancreatic ductal adenocarcinoma is character

203 c sunitinib prescribed by her oncologist for metastatic pancreatic neuroendocrine and kidney tumors.

204 nt to find biomarkers and targets to improve metastatic PCa diagnosis and treatment.

205 vely palliate symptoms and prolong life, the metastatic PCa remains incurable.

206 were investigated in a patient with advanced metastatic PCa via sequential planar whole-body SPECT im

207 In skeletal lesions from patients with metastatic PCa, histological and molecular analyses reve

208 s for CADM1, SPHK1, and YAP/TAZ in mediating metastatic phenotypes in vitro and in vivo Notably, phar

209 t richness in community diversity, while the metastatic populations were most closely related to one

210 xed with TNBC cells-could increase TNBC cell metastatic potency.

211 signatures, and their depletion impairs the metastatic potential of breast cancer cells.

212 tumor might serve as a prognostic marker for metastatic potential.

213 tiation, transformation, tumorigenicity, and metastatic potential.

214 as a regulator in the myeloid cell-assisted metastatic process and establish lipid-sensing nuclear r

215 A deeper understanding of the metastatic process is required for the development of ne

216 ancer cell dissemination are specific to the metastatic process, as opposed to representing natural p

217 mutations involved in the colorectal cancer metastatic process, we performed deep mutational analysi

218 Cs has provided significant insight into the metastatic process.

219 r and tumor microenvironment, to inhibit the metastatic process.

220 latelets to avoid anoikis and succeed in the metastatic process.Platelets have been associated with i

221 ection of some of the mechanisms of the bone metastatic processes in prostate and breast cancer.

222 e T-driven tumors showed altered primary and metastatic profiles in previous studies, depending upon

223 oenvironment promotes invasive migration and metastatic progression by employing integrin alpha9beta1

224 ivity effectively interrupted osteolysis and metastatic progression in preclinical models, suggesting

225 gulatory protein kindlin-2 (FERMT2) promotes metastatic progression of breast cancer through the recr

226 phosphatases (PTPs), play a critical role in metastatic progression of cancers.

227 In this issue of Cell, Roe et al. show that metastatic progression of pancreatic cancer involves lar

228 h by selecting for drug resistance can drive metastatic progression, this study characterized the pla

229 tor Nkx2-1, a well-established suppressor of metastatic progression.

230 oenvironment promotes invasive migration and metastatic progression.Significance: These results illum

231 Eligible patients had metastatic prostate cancer and a PSA level higher than 4

232 planning (223)RaCl2 therapy of patients with metastatic prostate cancer and its impact on the therape

233 etected in circulating EV from the plasma of metastatic prostate cancer patients and was LO specific.

234 ther agents can improve outcomes in men with metastatic prostate cancer resistant to traditional horm

235 uits men with high-risk, locally advanced or metastatic prostate cancer who were initiating long-term

236 nthesis inhibitor, in the early treatment of metastatic prostate cancer.

237 Purpose Systemic Therapy for Advanced or Metastatic Prostate Cancer: Evaluation of Drug Efficacy

238 to 1439 blood samples from 520 patients with metastatic prostate or breast cancers.

239 (VEGFR1(+)) myeloid cell recruitment and pro-metastatic protein expression) and metastatic burden, ac

240 nd the 5-year survival rate of patients with metastatic RCC is 5-10%.

241 disease > 3 months, including a patient with metastatic RCC with progression-free survival of > 3.9 y

242 e Sunitinib is a standard initial therapy in metastatic renal cell carcinoma (mRCC), but chronic dosi

243 ivolumab plus a tyrosine kinase inhibitor in metastatic renal cell carcinoma (mRCC).

244 Streptococcus decreased in both primary and metastatic samples.

245 evious lines of therapy in the recurrent and metastatic setting and study site.

246 s platinum-based chemotherapy regimen in the metastatic setting.

247 stronger consensus in high-risk/advanced and metastatic setting.

248 ast cancer in the neoadjuvant, adjuvant, and metastatic settings; however, some patients remain at ri

249 ngs of increased lymph node invasion and new metastatic sites in 30% of sunitinib-treated patients an

250 umour-stroma interactions within primary and metastatic sites, including the lung.

251 terization of emerging subclones, which seed metastatic sites, might offer new therapeutic approaches

252 cells similarly regulate tumor cell fate at metastatic sites.

253 cells that are adapted to colonize different metastatic sites.

254 te cancer cells once they are established at metastatic sites.

255 s origin in the pancreas to colonize distant metastatic sites.

256 l carcinoma (cSCC) is one of the most common metastatic skin cancers with increasing incidence.

257 first-line treatment for locally advanced or metastatic soft-tissue sarcoma has been doxorubicin.

258 h a diagnosis of an advanced unresectable or metastatic soft-tissue sarcoma, of intermediate or high

259 first-line treatment for locally advanced or metastatic soft-tissue sarcoma.

260 ted to other organs where they contribute to metastatic spread of disease.

261 t of CXCR2 antagonists to inhibit or prevent metastatic spread of disease.

262 age in promoting both tumor angiogenesis and metastatic spread.

263 counteracting cancer cell proliferation and metastatic spread.

264 lly or cytologically confirmed recurrent and metastatic squamous cell carcinoma of the head and neck

265 phase 3 trial in patients with recurrent or metastatic squamous cell carcinoma of the head and neck

266 ality of life for patients with recurrent or metastatic squamous cell carcinoma of the head and neck,

267 el and placebo in patients with recurrent or metastatic squamous cell carcinoma of the head and neck.

268 gnment; and had to include patients with non-metastatic squamous cell carcinoma of the oral cavity, o

269 an breast cancer cell lines (fibrocystic and metastatic states) as well as normal and cancer cells in

270 asive p130Cas/ErbB2 cells and correlate with metastatic status in human breast cancer patients.

271 In the metastatic subpopulations, a gene signature was defined

272 egulatory mechanism to impact ovarian cancer metastatic success.

273 esponses in heavily pretreated patients with metastatic TNBC.

274 ieved through surgical resection of melanoma metastatic to the abdominal viscera in patients treated

275 alone are insufficient for cells to acquire metastatic traits.

276 This approach revealed that the metastatic transition is accompanied by massive and recu

277 als but worsening of accrual for neoadjuvant/metastatic trials.

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

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

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

281 tasis, whereas LOXL2 overexpression promoted metastatic tumor growth.

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

283 promoting cyclin proteins, without enhancing metastatic tumor growth.

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

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

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

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

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

289 cancer (PCa) may be identified by sequencing metastatic tumour genomes to identify molecular markers

290 ratified by histology of the primary tumour, metastatic tumour size, and number of metastases.

291 in melanoma with highest levels detected in metastatic tumours versus normal skin or benign skin les

292 ective review of MRI images of patients with metastatic UM to the liver at a single institution betwe

293 Patients (aged >/=18 years) with metastatic urothelial carcinoma who had progressed after

294 identified a treatment-naive patient who has metastatic uterine leiomyosarcoma and has experienced co

295 se initial results challenge the belief that metastatic uveal melanoma is immunotherapy resistant and

296 ial, a total of 21 consecutive patients with metastatic uveal melanoma were enrolled between June 7,

297 epresent the tumor subpopulation involved in metastatic virulence, and ongoing research seeks to char

298 ectively analyzed 352 patients with RAI-avid metastatic well-differentiated TC treated with (131)I by

299 ed >18 years) with advanced (unresectable or metastatic), well differentiated carcinoid tumours of th

300 ta2SP(+/-) LSCs) were highly tumorigenic and metastatic, whereas those derived from WT mice treated w