ライフサイエンスコーパス: metastasis

1 pression efficiently blocked TMPRSS2-induced metastasis.

2 alously reactivated during tumorigenesis and metastasis.

3 eutic potential in AKT overactivation-driven metastasis.

4 ing tumor cells (CTCs) to suppress TNBC lung metastasis.

5 ng PCa cells and subsequently reduce distant metastasis.

6 As occur and CAAs predicting tissue-specific metastasis.

7 lls with a senolytic BCL-2 inhibitor impairs metastasis.

8 ute to the reduced tumor cell activities and metastasis.

9 C), which has poor prognosis due to frequent metastasis.

10 ssion profile of genes implicated in EMT and metastasis.

11 where decreased expression led to increased metastasis.

12 nced primary tumor and SW620 from lymph-node metastasis.

13 quamous cell carcinoma (CSCC) recurrence and metastasis.

14 ytokine secretion that may contribute to CRC metastasis.

15 h cancer cell heterogeneity, plasticity, and metastasis.

16 respectively), and prevented liver satellite metastasis.

17 and in patients with breast cancer with lung metastasis.

18 ng both local tumor growth and distant tumor metastasis.

19 al transition (EMT), a process that promotes metastasis.

20 ary tumor growth, angiogenesis, invasion and metastasis.

21 to mesenchymal, migration and invasion, and metastasis.

22 c plasticity is a pivotal factor that drives metastasis.

23 astrocyte reactivity, specifically, in brain metastasis.

24 re well known to be related to breast cancer metastasis.

25 energy reservoir to fuel breast cancer lung metastasis.

26 cells, which promotes tumor progression and metastasis.

27 referred to as dormancy, and progression and metastasis.

28 rexpression increased the incidence of brain metastasis.

29 ellular features altered during invasion and metastasis.

30 olon cancer may increase the risk of further metastasis.

31 ependent drivers of lung cancer invasion and metastasis.

32 on is essential for wound healing and cancer metastasis.

33 oenvironment interactions, tumor growth, and metastasis.

34 ion in a preclinical model of ovarian cancer metastasis.

35 c Wnt5A knockdown also led to decreased lung metastasis.

36 nomic plasticity, phenotypic plasticity, and metastasis.

37 ally synergistic drivers associated with CRC metastasis.

38 lar subtypes cooperate to drive invasion and metastasis.

39 s activated and functionally required during metastasis.

40 of therapeutic agents for controlling cancer metastasis.

41 east cancer cell dedifferentiation, EMT, and metastasis.

42 ty is associated with high-grade disease and metastasis.

43 ation events mediate PDHc function in cancer metastasis.

44 d is thought to play a role in breast cancer metastasis.

45 l state associated with an increased risk of metastasis.

46 and Il17ra-/- mice altered tumor growth and metastasis.

47 ng growth of invasive cancers and lymph node metastasis.

48 mour size, enhanced blood vessel density and metastasis.

49 raft tumors to chemotherapeutics and reduces metastasis.

50 promising therapeutic strategies to suppress metastasis.

51 ecific metabolic targeting of ovarian cancer metastasis.

52 tight selective bottleneck preceding distant metastasis.

53 n primary tumor initiation, progression, and metastasis.

54 nd functions of EMT plasticity during cancer metastasis.

55 sseminating is an important cause of distant metastasis.

56 mmunotherapy and reduce tumor recurrence and metastasis.

57 resses epithelial-mesenchymal transition and metastasis.

58 e metal-based nanomedicines to reduce cancer metastasis.

59 caused reduced primary tumor burden and lung metastasis.

60 CNN may have the potential to predict liver metastasis.

61 osphorylation of this site in EGFR regulates metastasis.

62 istant metastasis but not regional lymphatic metastasis.

63 nchymal transition of tumor cells, promoting metastasis.

64 pEMT, and plasticity in the context of tumor metastasis.

65 s under certain conditions) and in vivo lung metastasis.

66 ene, KDELR3, whose loss impairs experimental metastasis.

67 that tend to develop therapy resistance and metastasis.

68 f this isoform during cancer progression and metastasis.

69 tumour microenvironment in terms of distant metastasis.

70 gnant cells and thus affect tumor growth and metastasis.

71 olled cell proliferation, tumorigenesis, and metastasis.

72 year recurrence rates, and increased risk of metastasis.

73 5, and CXCL5 signaling in the early steps of metastasis.

74 gnalling as a driver for primary bone cancer metastasis.

75 ited a significantly high incidence of brain metastasis.

76 JAK3 as a potential suppressor for melanoma metastasis.

77 d tumor growth and weight and inhibited lung metastasis.

78 s are one of the main sites of breast cancer metastasis.

79 n lung cancer control versus progression and metastasis.

80 y acids accelerate tumor growth and increase metastasis.

81 ry factor that impedes EMT and breast cancer metastasis.

82 _positive are direct risk factors for 5 year metastasis.

83 environment that promotes tumourigenesis and metastasis.

84 lasticity and immune-mediated pruning during metastasis.

85 ve primary status, and size of largest liver metastasis.

86 were alive and 34 (79%) had died of systemic metastasis.

87 alone successfully distinguishes cases with metastasis.

88 associated with invasive disease and distant metastasis.

89 nchymal transition (EMT), cell invasion, and metastasis.

90 ell lines decreased primary tumor growth and metastasis.

91 lone for predicting as well as understanding metastasis.

92 sted their therapeutic efficacy against TNBC metastasis.

93 misleads 18F-FDG-PET/CT for detecting nodal metastasis.

94 dels reduced angiogenesis, tumor growth, and metastasis.

95 te the immune response to promote lung tumor metastasis.

96 nt a valid therapeutic target for inhibiting metastasis.

97 ation, wound healing, tumor growth, and lung metastasis.

98 oncogenic transformation, proliferation, and metastasis.

99 ypes by tumor epithelial cells contribute to metastasis?

100 ZNF367 promoted tumor metastasis accompanied with increase of CTC numbers.

101 , and a full EMT is not always necessary for metastasis; also, positive roles for E-cadherin expressi

102 CSC-like cells play crucial roles in cancer metastasis and are exceptionally tolerant with genetic l

103 onships between malignant transformation and metastasis and cellular adhesion processes, several area

104 ell-recruited neutrophils result in enhanced metastasis and chemotherapy resistance.

105 erlying embryogenesis, wound healing, cancer metastasis and drug resistance.

106 ct cancer prognosis, shape tumour evolution, metastasis and drug response, and may advance precision

107 We consider evidence for genomic drivers of metastasis and explore studies investigating modes of me

108 amined 281 lung cancer patients with distant metastasis and found that smokers exhibited a significan

109 iogenesis, extracellular matrix remodelling, metastasis and immunosuppression.

110 in mouse models of spontaneous breast cancer metastasis and in patients with breast cancer with lung

111 tumor growth, reduced the incidence of lung metastasis and increased overall survival of mice when i

112 nd may lead to decreased survival, increased metastasis and invasion.

113 ectly phosphorylates EGFR at T654 to promote metastasis and is the first study to show that the phosp

114 We have shown previously that oral cancer metastasis and pain are controlled by the endothelin axi

115 e drug to effectively treat both oral cancer metastasis and pain in a preclinical model.

116 However, concurrently visualizing metastasis and performing imaging-guided lymph node surg

117 of Zic1 was correlated with more lymph node metastasis and poor outcome of GC patients.

118 giopoietin-2 in vascular remodeling and lung metastasis and provides new insights into mechanisms und

119 omes overlapping with previous hepatobiliary metastasis and stemness, unique stromal properties, and

120 e neuroglial cells in cancer progression and metastasis and the response to therapy.

121 of anesthetics used during surgery in cancer metastasis and the underlying mechanism remains largely

122 sticity of cancer cells more specifically in metastasis and therapy-resistance.

123 65.2% had 1 site of distant metastasis, and 42.9% had bone-only metastases.

124 TME, where they are implicated in invasion, metastasis, and angiogenesis.

125 molecular underpinnings, show high rates of metastasis, and display limited responsiveness to curren

126 TIMP1 deletion allows senescence to promote metastasis, and elimination of senescent cells with a se

127 RSS2 overexpression promoted prostate cancer metastasis, and HAI-2 overexpression efficiently blocked

128 sion, resistance to apoptosis, angiogenesis, metastasis, and invasion to secondary sites.

129 d paracrine means by which EMT cells enhance metastasis, and provides potential targets for therapeut

130 igens, inhibition of the progression of lung metastasis, and significantly extended animal survival a

131 racellular vesicles accelerate breast cancer metastasis, and targeted inhibition of tumor-derived ves

132 including tumor initiation, local expansion, metastasis, and therapeutic resistance-involve complex i

133 r heterogeneity, the tumor microenvironment, metastasis, and therapeutic resistance.

134 Given that rate-limiting steps of metastasis are known to occur while tumor cells enter, t

135 erged as key regulators of tumour growth and metastasis as well as response to chemotherapy, targeted

136 e IKK2/NF-kappaB signaling pathway modulates metastasis-associated protein 2 (MTA2), a component of t

137 of 10 patients with metastatic CRC to assess metastasis avidity.

138 Plus, brain metastasis (BMs) is a major mortality cause for NSCLC; t

139 Dissemination is an essential early step in metastasis but its molecular basis remains incompletely

140 risk of metastasis is mainly due to distant metastasis but not regional lymphatic metastasis.

141 physiological adaptation is associated with metastasis , but we still have a superficial understandi

142 -beta (TGF-beta) promotes tumor invasion and metastasis by inducing epithelial-mesenchymal transition

143 velopment and has also been known to promote metastasis by inducing invasive phenotype and tumor-init

144 roach, we found that miR-671-5p reduces LUSC metastasis by inhibiting a circular RNA (circRNA), CDR1a

145 promotes cancer initiation, progression, and metastasis by regulating cell proliferation, migration,

146 mor suppressor in intestinal cancer and lung metastasis by triggering cancer cell death when netrin-1

147 ncovers a mechanism of chemotherapy-mediated metastasis by which drug-induced upregulation of sEV sec

148 Notably, a metastasis case was observed in the vehicle but not in t

149 Although systemic Akt1 deletion inhibits metastasis, cell-autonomous Akt1 deletion does not.

150 During development and metastasis, cells migrate large distances through comple

151 iated macrophages (TAMs) in colorectal liver metastasis (CLM) represents a correlate of functional di

152 Metastasis contributes to the vast majority of cancer-re

153 d gene co-expression networks and identified metastasis-correlated gene networks of immune-suppressio

154 s > 1 mm), IIIB, or IIIC (without in-transit metastasis) cutaneous melanoma were randomly assigned to

155 Using a novel model of spontaneous bone metastasis derived from human ER+ MCF7 cells, molecular

156 Metastasis-derived cell lines in vitro and metastases an

157 cation had a greater effect on the growth of metastasis-derived cells.

158 s of matched primary breast tumours and bone metastasis-derived patient-derived xenografts (PDX).

159 /neu to enhance breast cancer initiation and metastasis, despite having no effect on primary tumor gr

160 Regional node metastasis determined by sentinel node biopsy (SNB) is a

161 porary adjuvant therapies on the risk of CNS metastasis development.

162 In around 20% of men with prostate cancer, metastasis develops during the course of their disease.

163 be achieved with local cytoreductive and/or metastasis-directed therapies.

164 base for a cytoreductive strategy, including metastasis-directed therapy, in the current era of seque

165 ssive form of breast cancer characterized by metastasis, drug resistance and high rates of recurrence

166 ministration for the treatment of peritoneal metastasis due to their physical stability, tumor target

167 inefficient in colorectal cancer (CRC) liver metastasis following existing therapies due to abundant

168 duced signature also predicted site-specific metastasis for lung, liver, and brain, but not for bone

169 correlates with overall survival and distant metastasis free survival.

170 The child has remained disease- and metastasis-free at a 5-year follow-up since the last mel

171 amples on breast cancer-specific and distant metastasis-free survival (BCSS and DMFS, respectively).

172 Conditional metastasis-free survival (cMFS) and conditional overall

173 onal status of MIUC with metastatic pattern, metastasis-free survival (MFS), and overall survival (OS

174 ned prognostic score associated with distant metastasis-free survival (the time between randomisation

175 The 5-year distant metastasis-free survival of the low-risk, medium-risk, a

176 after surgical resection and results in 100% metastasis-free survival upon re-challenge.

177 The primary endpoint of bone metastasis-free survival was not significantly different

178 mary analysis of a phase 3 trial, the median metastasis-free survival was significantly longer with d

179 ncer has implications on metastatic pattern, metastasis-free survival, and overall survival.

180 be positively correlated with relapse-free, metastasis-free, or overall survival in breast cancer.

181 rapeutic agent for early stage bone and lung metastasis from triple-negative breast cancer that shoul

182 inib (SEL) had significantly inhibited liver metastasis growth (p = 0.013 and p = 0.035, respectively

183 AJCC-7), stage IIIA (at least one lymph node metastasis > 1 mm), IIIB, or IIIC (without in-transit me

184 ory effect of nanoparticles by themselves on metastasis has not been explored.

185 positive roles for E-cadherin expression in metastasis have been reported.

186 It was observed that cells after lung metastasis have the fastest migration and lowest stiffne

187 Platelets promote metastasis, however, their role in tumor growth remains

188 Cancer metastasis, i.e., the spreading of tumor cells from the

189 ustaining tumor proliferation and underlying metastasis in breast cancer and provide an initial frame

190 Despite extensive studies on metastasis in cancer cells from patients with detectable

191 Here we studied tumor growth and metastasis in Cyp2c44(-/-) mice crossed onto the polyoma

192 mal transition (EMT), and lung and lymphatic metastasis in GC cells.

193 ighly associated with lung tumorigenesis and metastasis in Gprc5a-ko mice.

194 in 1C, that contributes to the high rates of metastasis in melanoma.

195 rafish, and niclosamide drastically impaired metastasis in mice.

196 ients to identify genes that promote distant metastasis in mice.

197 cated as critical drivers of cell growth and metastasis in numerous Ras-driven cancers.

198 ty for both early detection and the study of metastasis in preclinical models.

199 l, thereby influencing the global pattern of metastasis in that animal.

200 primary tumour growth and experimental lung metastasis in the HT1080 xenograft model and highlight t

201 effectively inhibit tumor growth as well as metastasis in the tumor-bearing mouse models.

202 l cells markedly enhances tumor invasion and metastasis in Trp53DeltaIEC mice (Trp53DeltaIECAktE17K)

203 tance, mesothelial clearance, and peritoneal metastasis in vitro and in vivo.

204 data demonstrate that IQGAP1 is crucial for metastasis in vivo through regulation of extravasation a

205 s pathway prevents breast tumor invasion and metastasis in vivo.

206 d by active proliferation, and propensity to metastasis in vivo.

207 AK signaling in CAF to promote breast cancer metastasis in vivo.

208 n and invasion in vitro and tumor growth and metastasis in vivo.

209 mation in vitro, as well as tumor growth and metastasis in vivo.

210 cells reduced the ability of CAV1 to induce metastasis in vivo.

211 Bone metastasis incidence was not significantly associated wi

212 ition and is therefore an ideal target for a metastasis inhibitor.

213 in in blood vessel remodeling, tumor growth, metastasis, integrin binding, and proteolytic regulation

214 Our findings illustrate that metastasis is a selective process favoring motile and so

215 Brain metastasis is an important cause of mortality in patient

216 Metastasis is generally considered a characteristic of m

217 The reduced risk of metastasis is mainly due to distant metastasis but not r

218 e incidence, risk factors, and timing of CNS metastasis is needed to inform surveillance strategies f

219 standing of the molecular mechanisms driving metastasis is rudimentary.

220 hese data suggest that the natural course of metastasis is selectively relaxed relative to early tumo

221 Metastasis is the cause for 90% of cancer-related mortal

222 sites of distant metastases, and spinal bone metastasis is the most common source of neurological mor

223 Metastasis is the primary cause of cancer mortality.

224 Metastasis is the primary cause of death of cancer patie

225 Metastasis is the ultimate "survival of the fittest" tes

226 ve been linked to increased tumor growth and metastasis, largely on the basis of overexpression studi

227 s one of lethal cancers among women with its metastasis leading to cancer-related morbidity and morta

228 Although MCC has a high propensity for metastasis, little is known about the underlying mechani

229 dominant effect on MDSC programming in liver metastasis (LM).

230 fies stem cell populations that mediate lung metastasis, mechanisms underlying the role of this cell

231 In a spontaneous breast-to-lung metastasis model, we found that primary tumor cells acti

232 Because of this difference, inhibitors of metastasis must account for each migration mode.

233 suboptimal, suggesting that AKT-driven tumor metastasis needs to be further understood.

234 Breast cancer metastasis occurs via blood and lymphatic vessels.

235 with lipid utilization to fuel invasion and metastasis occurs.

236 cific Akt1 deletion is sufficient to inhibit metastasis of Akt-proficient tumors.

237 idea that periodontal inflammation promotes metastasis of breast cancer by recruiting MDSC in part b

238 drug delivery systems against malignant lung metastasis of breast cancer have been extensively studie

239 asingly recognized for its role in promoting metastasis of breast cancer, prostate cancer, and melano

240 lonal interactions are sufficient to promote metastasis of CL31.

241 new mechanism by which platelets promote the metastasis of colon and breast cancer cells and suggests

242 ude mouse model of a highly aggressive liver metastasis of colon cancer.

243 provide novel therapeutic strategies for the metastasis of GC.

244 or players that can suppress progression and metastasis of mouse and human cutaneous squamous cell ca

245 arget cells, inhibits growth and spontaneous metastasis of triple-negative breast cancer.

246 These sEVs promote metastasis of xenograft and pancreatic tumors to lung in

247 no surgical resection due to intraoperative metastasis or locally irresectable tumor, 2) macroscopic

248 , nondiagnostic biopsy, and extensive spinal metastasis or prior kyphoplasty.

249 ilure, local or regional recurrence, distant metastasis, or death from any cause, or was censored at

250 f the prognostic factors of PCa and the bone metastasis pattern of patients would be helpful for pati

251 Cancer metastasis poses a challenging problem both clinically a

252 evious diagnosis of breast cancer with liver metastasis presented with a complaint of increasing pain

253 xed relative to early tumorigenesis and that metastasis-private mutations are not drivers of cancer s

254 ar how this would contribute to blocking the metastasis promoting function of CAV1.

255 entified ~30 genes with a functional role in metastasis promotion and characterized detailed mechanis

256 In contrast, KDELR1 deficiency enhances metastasis, providing the first example of different dis

257 Metastasis reduces survival in oral cancer patients and

258 cancer have been extensively studied, while metastasis remains a challenging issue.

259 Although metastasis remains the cause of most cancer-related mort

260 AS-ERK signaling regulates colorectal cancer metastasis remains unknown.

261 chemia reperfusion injury (IRI) during liver-metastasis resection for treatment of colon cancer may i

262 7.0]) of 37 patients in cohort 1 had a brain metastasis response.

263 increases chemotherapy efficacy and reduces metastasis risk in patients with TNBC.

264 ctions in both animal models and human brain metastasis samples.

265 e- and post-EMT tumor cells in breast cancer metastasis.See related commentary by Bunz, p.

266 and TRAF3IP2 each inhibited tumor growth and metastasis, silencing TRAF3IP2 is more effective; target

267 identified as top gene sets associated with metastasis-specific lethality.

268 th different socioeconomic statuses and bone metastasis statuses was compared by Kaplan-Meier analysi

269 NME1 is a metastasis suppressor, a class of proteins which inhibit

270 ional staging of HNSCC using the tumour-node-metastasis system has been supplemented by the 2017 AJCC

271 ation of survival without relapse or distant metastasis than placebo with no apparent long-term toxic

272 one group was closer to primary tumors with metastasis than the other group.

273 7/MMP9 signalling hub in primary bone cancer metastasis that is clinically actionable.

274 umor growth, microenvironmental changes, and metastasis, the epigenetic regulation of NF-kappaB in tu

275 in clinical oncology trials, its effects on metastasis, the principal cause of cancer mortality, rem

276 ant roles in tumour development, relapse and metastasis; the intrinsic self-renewal characteristics a

277 nant cells including motility, invasion, and metastasis, thereby affecting tumor progression.

278 ests that chemotherapeutic drugs can promote metastasis through poorly defined mechanisms.

279 g of genes that suppress tumor formation and metastasis through trimethylation of histone H3 at lysin

280 ed with cancer development, progression, and metastasis, thus they hold promise as next generation bi

281 ional Cancer Control (AJCC/UICC) tumour-node-metastasis (TNM) staging system provides the current gui

282 the role of patrolling monocytes in melanoma metastasis to lungs, we generated C57BL/6J mice in which

283 For metastasis to occur, cancer cells must exocytose proteas

284 umors in omega3-fed mice and inhibited their metastasis to the liver and/or lung, but had the opposit

285 ating tumor cells, and increased spontaneous metastasis to the liver or lungs in two mouse models.

286 longer survival in synchronous single-organ metastasis to the lung compared to no resection (14.0 +/

287 st cancer patients, as well as breast cancer metastasis to the lung.

288 , leading to extensive bone destruction, and metastasis to the lungs.

289 learn risk factors for 5 year breast cancer metastasis using a clinical dataset we curated.

290 gated the role of circular RNAs (circRNA) in metastasis, using melanoma as a model aggressive tumor.

291 ntly, inhibition of neutrophil-mediated lung metastasis via the sustained release of Zileuton.

292 nction of IL-33 and ILC2s in promoting tumor metastasis via their capacity to suppress innate type 1

293 The effect of pioglitazone on liver metastasis was assessed.

294 Metastasis was the commonest lesion, followed by spondyl

295 ole of plectin in prostate cancer growth and metastasis, we performed proteomic analysis of prostate

296 e emerges that initiates and drives systemic metastasis, where polyclonal seeding between sites is co

297 ible to lung inflammation, tumorigenesis and metastasis, which resembles the pathological features in

298 expression of Trop2 induces tumor growth and metastasis while loss of Trop2 suppresses these abilitie

299 k of pain identifies patients at low risk of metastasis with sensitivity = 0.94 and negative predicti

300 We evaluated total LNY and LN metastasis with/without NAT and clinical and pathologica