ライフサイエンスコーパス: metastatic cancer

1 tructive uropathy, urothelial carcinoma, and metastatic cancer.

2 cancer, lymphoma, leukemia, and unspecified metastatic cancer.

3 nging from neurodegeneration to diabetes and metastatic cancer.

4 reach of TCR gene therapy for patients with metastatic cancer.

5 onale for targeting ICMT in the treatment of metastatic cancer.

6 eir significance in prognosis and therapy of metastatic cancer.

7 estrates the progression from a primary to a metastatic cancer.

8 tional deregulation is a defining feature of metastatic cancer.

9 zation is needed to better prevent and treat metastatic cancer.

10 n attractive and novel immunotherapy against metastatic cancer.

11 both in cell culture and in animal models of metastatic cancer.

12 re among the most common oncogenic events in metastatic cancer.

13 ptor and is involved in immune responses and metastatic cancer.

14 the efficacy of cell-based immunotherapy for metastatic cancer.

15 therapeutic opportunity in the management of metastatic cancer.

16 actively cycling cells may be needed to halt metastatic cancer.

17 dermining the success of therapies targeting metastatic cancer.

18 ratory burst, sperm motility, apoptosis, and metastatic cancer.

19 nically relevant therapeutic target to treat metastatic cancer.

20 lt in abscopal responses among patients with metastatic cancer.

21 ed TLR7/8 agonist and checkpoint blockade in metastatic cancer.

22 al interactions between the brain milieu and metastatic cancer.

23 opportunity to analyze disease evolution in metastatic cancer.

24 pies have led to patients living longer with metastatic cancer.

25 ated with MEK inhibitor use for treatment of metastatic cancer.

26 ogen-activated protein kinase enzyme MEK for metastatic cancer.

27 ectly act on multiple cell types to suppress metastatic cancer.

28 improving the efficacy of immunotherapy for metastatic cancer.

29 nfection, to study other pathologies such as metastatic cancer.

30 ches are needed for utility in patients with metastatic cancer.

31 sufficient in the majority of patients with metastatic cancer.

32 e for the detection of CTCs in patients with metastatic cancer.

33 f anti-PD-1/PD-L1 inhibitors in advanced and metastatic cancer.

34 arring, tissue fibrosis, celiac disease, and metastatic cancer.

35 expression of RhoGDI2 in xenograft models of metastatic cancer.

36 have shown efficacy in preclinical models of metastatic cancer.

37 ent to trigger regressions of an established metastatic cancer.

38 ment and cell migration are altered, such as metastatic cancer.

39 ional therapies for treatment of advanced or metastatic cancer.

40 ndscape of studies exploring the genomics of metastatic cancer.

41 munotherapies for treatment of patients with metastatic cancer.

42 favorable prognostic factor in patients with metastatic cancer.

43 ndications ranging from vascular diseases to metastatic cancer.

44 improved clinical outcomes in patients with metastatic cancer.

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

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

47 stromal tissue is a hallmark of high grade, metastatic cancers.

48 is used clinically to treat certain types of metastatic cancers.

49 molecular landscape and microenvironment of metastatic cancers.

50 therapeutically viable approach for treating metastatic cancers.

51 on gene signature, a feature of invasive and metastatic cancers.

52 nt of ovarian cancer and other transcoelomic metastatic cancers.

53 ormation and the development of invasive and metastatic cancers.

54 wn to be down-regulated in some aggressively metastatic cancers.

55 DD9 is an established marker of invasive and metastatic cancers.

56 magic bullet is not enough for treatment of metastatic cancers.

57 particular as new targets for the therapy of metastatic cancers.

58 aling and also have a prominent role in some metastatic cancers.

59 n, is enriched in the serum of patients with metastatic cancers.

60 a rational strategy to treat Twist1-positive metastatic cancers.

61 onse in preclinical models of orthotopic and metastatic cancers.

62 aggressive chemoradiotherapy for eradicating metastatic cancers.

63 ental contributions to ischemic diseases and metastatic cancers.

64 facilitating tumor growth and progression in metastatic cancers.

65 omarker and potential therapeutic target for metastatic cancers.

66 for consideration in studies in advanced or metastatic cancers.

67 e a new avenue for therapeutic inhibition of metastatic cancers.

68 omising results for the treatment of certain metastatic cancers.

69 ies for targeting cachexia in the context of metastatic cancers.

70 growing evidence of embryonic signatures in metastatic cancers.

71 limiting the risk of premature death due to metastatic cancers.

72 strategies for the treatment of advanced and metastatic cancers.

73 ak recommendation against its routine use in metastatic cancers.

74 alysis is available from clinically acquired metastatic cancers.

75 5, 2010, and July 30, 2012, 52 patients with metastatic cancer (18 tumour types) received anti-interl

76 erly patients within three broad stages: (1) metastatic cancer, (2) early-stage cancer after surgery,

77 as liver failure (9.9% vs 4.2%; p < 0.001), metastatic cancer (5.9% vs 3.2%; p < 0.001), and diabete

78 We identified 10 patients with metastatic cancer (7 pathologically proven) who develope

79 The majority of hospitalized patients had metastatic cancer (81%).

80 e CXCR4 is highly expressed in a majority of metastatic cancers, a CXCR4-auristatin ADC may be useful

81 ratio, 1.54; 95% CI, 1.51-1.58), and having metastatic cancer (adjusted hazard ratio, 1.46; 95% CI,

82 pect of NIS-mediated radionuclide therapy of metastatic cancer after MSC-mediated gene delivery.

83 properties correlate with the progression of metastatic cancer along the epithelial-to-mesenchymal tr

84 Cell lines are widely-used models to study metastatic cancer although the extent to which they reca

85 nt cancer stages, including precancerous and metastatic cancers, although not in normal tissues.

86 as follows: septic shock, 7.27 (7.19-7.35); metastatic cancer and acute leukemia (Hierarchical Condi

87 LS3BP and galectin-3 as new targets to treat metastatic cancer and fibrosing diseases.

88 ree HIV(+) cART(+) individuals who died with metastatic cancer and had no detectable plasma viral loa

89 85 years who did not have newly diagnosed or metastatic cancer and lived within a study site catchmen

90 inin (HPA) has been shown to bind aggressive metastatic cancer and was produced in recombinant form (

91 n the course of illness for any patient with metastatic cancer and/or high symptom burden.

92 essel growth contributes to the pathology of metastatic cancers and age-related retinopathies.

93 enocarcinoma is one of the most invasive and metastatic cancers and has a dismal 5-year survival rate

94 abuse, heart failure, nonmetastatic cancer, metastatic cancer, and chronic kidney disease; 24.2% of

95 s highly expressed in steroidogenic tissues, metastatic cancer, and inflammatory and neurological dis

96 commendation for administration in other non-metastatic cancers, and a weak recommendation against it

97 ctivation, rapid regression of localized and metastatic cancers, and long-term disease control.

98 ing tumor cells (CTCs) shed from primary and metastatic cancers are admixed with blood components and

99 further reveals the disruptive reality that metastatic cancers are tremendously complex and individu

100 l find a prominent place in the treatment of metastatic cancer as a consolidative partner with system

101 therapy is associated with the regression of metastatic cancer at a distance from the irradiated site

102 individuals with undetectable viral load and metastatic cancer at death and performed time-scaled Bay

103 n, and phase 1 study of MABp1 in adults with metastatic cancer at the MD Anderson Clinical Center for

104 the role of fluidic forces as modulators of metastatic cancer biology in a customizable microfluidic

105 unotherapy can be an effective treatment for metastatic cancer, but a significant subpopulation will

106 as PD-1) elicits durable tumor regression in metastatic cancer, but these dramatic responses are conf

107 bitors produce durable responses in numerous metastatic cancers, but immune-related adverse events (i

108 (ICI) treatments benefit some patients with metastatic cancers, but predictive biomarkers are needed

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

110 generative medicine may be expanded to treat metastatic cancer by revitalizing an exhausted and senes

111 w as established in control tests with a non-metastatic cancer cell line (HeLa).

112 Results with metastatic cancer cell lines show that some of the effec

113 on of lasp-2 in either SW620 or PC-3B1 cells-metastatic cancer cell lines-increases cell migration bu

114 CBFbeta can determine the plasticity of the metastatic cancer cell phenotype, suggesting that its re

115 Equol also increased metastatic cancer cell viability.

116 demonstrate that systemic injection of brain metastatic cancer cell-derived EVs promoted brain metast

117 Trp consumption and Kyn production by highly metastatic cancer cells (HT29) were significantly higher

118 Yet, it is largely unknown how metastatic cancer cells acquire an ability to cope with

119 the genes that control the transmigration of metastatic cancer cells across the BBB, offering new tar

120 opy to analyze the complex interplay between metastatic cancer cells and a functional artificial micr

121 Not much is known about metastatic cancer cells and endothelial cross-talk, whic

122 vels of p-hnRNP E1 are highly upregulated in metastatic cancer cells and low in normal epithelial tis

123 g as a synthetic premetastatic niche recruit metastatic cancer cells and provide a survival advantage

124 ractility is responsive to interactions with metastatic cancer cells and that reducing endothelial ce

125 molecular interactions between platelets and metastatic cancer cells are not well understood.

126 assess ATP, ADP, and pH levels in MDA-MB-231 metastatic cancer cells as a function of the local colla

127 S100A4 regulates the motility of metastatic cancer cells by binding to non-muscle (NM) my

128 Once transformed, metastatic cancer cells can migrate persistently by adap

129 asion and that MTA1 overexpression in highly metastatic cancer cells drives cell migration and invasi

130 dynamics have not been used to differentiate metastatic cancer cells from less invasive ones.

131 emonstrate a strategy capable of eliminating metastatic cancer cells in a selective manner.

132 hat can facilitate the seeding and growth of metastatic cancer cells in distant organs, but the effec

133 bition of the channel abrogated migration of metastatic cancer cells in vitro Silencing or pharmacolo

134 The invasive phenotype of metastatic cancer cells is accompanied by the formation

135 der to establish themselves in distal sites, metastatic cancer cells need to acquire organ-specific t

136 Metastatic cancer cells often reside in distal tissues a

137 d antihepsin treatment, we demonstrated that metastatic cancer cells preferentially colonized the hep

138 ATM depletion in metastatic cancer cells reduced cell migration and invas

139 Here we present a system in which metastatic cancer cells release a cell-penetrating fluor

140 impact tissues that are rarely inhabited by metastatic cancer cells such as skeletal muscle and adip

141 loss of AP-1B expression in highly migratory metastatic cancer cells suggesting that AP-1B's novel ro

142 Compared with other metastatic cancer cells tested, RCC and STS cells exhibi

143 We propose that Arg acts as a switch in metastatic cancer cells that governs the decision to 'gr

144 -016 inhibits Rac activity in the MDA-MB-435 metastatic cancer cells that overexpress Rac and exhibit

145 Implanted scaffolds recruited metastatic cancer cells that were inoculated into the ma

146 parts metastatic competence on otherwise non-metastatic cancer cells through decreased inter-cellular

147 flammatory circuitry that can be co-opted by metastatic cancer cells to facilitate lung colonization,

148 promote the invasion of cells, ranging from metastatic cancer cells to immune cells, into tissue.

149 o enhance the metastasis of otherwise weakly metastatic cancer cells to the lungs and bones.

150 Metastatic cancer cells undergo an epithelial-mesenchyma

151 A variety of metastatic cancer cells use actin-rich membrane protrusi

152 Recently extravasated metastatic cancer cells use the Rif/mDia2 actin-nucleati

153 the astrocyte gap-junctional network, brain metastatic cancer cells use these channels to transfer t

154 cancer, beta3 was strongly expressed on bone metastatic cancer cells, but not primary mammary tumors

155 Compared with poorly metastatic cancer cells, highly metastatic cells express

156 For highly metastatic cancer cells, the pH measured at the surface

157 rs, and anoikis resistance is a hallmark for metastatic cancer cells, this study suggests a pro-metas

158 irpin RNA to knock down CD29 and/or CD49f in metastatic cancer cells, we demonstrated that while acut

159 nd carcinoma cells- but not in normal or non-metastatic cancer cells-, and likely involves the downst

160 o explain the unleashed TGFbeta responses in metastatic cancer cells.

161 a marked upregulation of EREG in primary and metastatic cancer cells.

162 ting two mutually exclusive pathways for the metastatic cancer cells.

163 such as imparting therapeutic resistance to metastatic cancer cells.

164 and), contributing to bone marrow tropism of metastatic cancer cells.

165 ify the SLN, which is most likely to contain metastatic cancer cells.

166 nel LN biopsy--is generally used to identify metastatic cancer cells.

167 tumor growth and a frequent destination for metastatic cancer cells.

168 ly reduced the invasive capacity of proximal metastatic cancer cells.

169 Myc controls the generation of self-renewing metastatic cancer cells.

170 dhesion molecule (sICAM1) secreted from bone-metastatic cancer cells.

171 atrix remodeling and tumor cell migration in metastatic cancer cells.

172 adherens junctions and in the diapedesis of metastatic cancer cells.

173 kinase 1) activity and directed migration of metastatic cancer cells.

174 2 with an antagonist blocks proliferation of metastatic cancer cells.

175 immune system to eliminate the residual and metastatic cancer cells.

176 ortunities to effectively target SPP1-driven metastatic cancers characterized by FSTL1 downregulation

177 In fact, the majority of patients with metastatic cancer develop a debilitating muscle-wasting

178 An increasing fraction of patients with metastatic cancer develop leptomeningeal dissemination o

179 ing target for biomarkers or drug target for metastatic cancer diagnosis and therapy, perhaps mediate

180 m)Tc-PAMA-cobalamin imaging in patients with metastatic cancer disease and show that tumor targeting

181 Care concepts for patients with metastatic cancer emphasized the potential of interdisci

182 The clinical records of all patients with metastatic cancer enrolled in clinical trials requiring

183 f vulnerabilities between primary tumors and metastatic cancer, even in the same patient or experimen

184 mors to kinase inhibitors, but patients with metastatic cancer eventually develop disease progression

185 We identified 40 genes overexpressed in metastatic cancers from patients reporting high pain (n

186 hat pain mediators would be overexpressed in metastatic cancers from patients reporting high pain.

187 e pre-metastatic niche formation and promote metastatic cancer growth by secreting pro-inflammatory c

188 ways synergistically may inhibit primary and metastatic cancer growth.

189 els of pro-inflammatory cytokines to promote metastatic cancer growth.

190 , the comprehensive methylation landscape of metastatic cancer has never been defined.

191 effective therapeutic targets, treatment of metastatic cancer has progressed minimally.

192 l transition (EMT), considered essential for metastatic cancer, has been a focus of much research, bu

193 re becoming more pertinent, as patients with metastatic cancer have extended overall survival because

194 he mutational landscape of a heavily treated metastatic cancer, identify novel mechanisms of AR signa

195 s a potentially useful framework for viewing metastatic cancer in terms of predictability, complexity

196 uantify, with single cell sensitivity, human metastatic cancer in the mouse skeleton, concurrently wi

197 plasma samples to track genomic evolution of metastatic cancers in response to therapy.

198 tinctions suggest a strategy for eradicating metastatic cancers in which initial therapy, by reducing

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

200 ily pretreated patients with HER2-expressing metastatic cancer, including HER2-positive trastuzumab e

201 alignancies encompass a range of primary and metastatic cancers, including low-grade and high-grade g

202 Metastatic cancer involving spread to the peritoneal cav

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

204 Metastatic cancer is a major cause of death and remains

205 afety of sodium thiosulfate in patients with metastatic cancer is encouraged.

206 Metastatic cancer is extremely difficult to treat, and t

207 deaths, and one poorly understood aspect of metastatic cancer is the adaptability of cells from a pr

208 (CTCs) from the blood of patients at risk of metastatic cancers is a promising approach to improving

209 Curative therapy for metastatic cancers is equivalent to causing extinction o

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

211 therapy, traditionally limited to refractory metastatic cancer, is being increasingly used at earlier

212 l canal compression, a major complication of metastatic cancer, is managed with radiotherapy to maint

213 ted protein (GIV), a protein up-regulated in metastatic cancers, is also required for outside-in inte

214 -binding protein upregulated in a variety of metastatic cancers, is essential for efficient plasma me

215 y from early-stage cancers to late-stage and metastatic cancers, microRNAs that promote relapse and m

216 In both metazoan development and metastatic cancer, migrating cells must carry out a deta

217 s a single agent in murine colon and mammary metastatic cancer models, entolimod rapidly induces CXCL

218 igh-grade glioblastoma and melanoma, even in metastatic cancer models.

219 before death) and patients with progressive metastatic cancer (N = 312) following at least 1 chemoth

220 t from the point of diagnosis onward for all metastatic cancer, new and ambitious research is require

221 their reproduction without triggering fatal metastatic cancers, nor even maintain a normal reproduct

222 present, there are no "cures" for secondary metastatic cancer of any form and there is an urgent unm

223 (aged >=18 years) had relapsed, advanced, or metastatic cancer of the ovary, cervix, endometrium, bla

224 duce long lasting responses in patients with metastatic cancers of a wide range of histologies.

225 ectly act on multiple cell types to suppress metastatic cancer.Oncogene advance online publication, 1

226 18), older age (OR 1.02, 95% CI 1.0071.03-), metastatic cancer (OR 2.89, 95% CI 1.46-5.73) and CaUTI

227 , lymphoma, fluid and electrolyte disorders, metastatic cancer, other neurological disorders, periphe

228 of care, and even survival in patients with metastatic cancer, palliative care has increasing releva

229 The liver is host to many metastatic cancers, particularly colorectal cancer, for

230 However, metastatic cancer patients treated with immunotherapy sh

231 Using EpCAM targeted MBs CTCs from metastatic cancer patients were isolated, suggesting tha

232 preferable treatment option for advanced or metastatic cancer patients who are male, aged < 65 years

233 chment of peripheral memory T cells from six metastatic cancer patients, we identified and isolated C

234 and is associated with a shorter survival in metastatic cancer patients.

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

236 3 years per 1000 men screened and 3 cases of metastatic cancer per 1000 men screened, with no reducti

237 Metastatic cancers produce exosomes that condition pre-m

238 sitively correlated with RSK2 expression and metastatic cancer progression in primary patient tumor s

239 The classic view of metastatic cancer progression is that it is a unidirecti

240 ffectiveness through analysis of data on (i) metastatic cancer progression, (ii) drug treatment in hu

241 itiating various signaling events leading to metastatic cancer progression.

242 a potential drug target in the prevention of metastatic cancer progression.

243 ecular link between SMYD3 overexpression and metastatic cancer progression.

244 Patients with metastatic cancer receiving first course palliative radi

245 ession in different cancers and what renders metastatic cancer refractory to available therapies.

246 that promote metabolic adaptations to drive metastatic cancer remain unclear.

247 Secondary metastatic cancer remains the single biggest cause of mo

248 However, its potential for treating metastatic cancer remains unknown.

249 oradiotherapy during treatment of late-stage metastatic cancers remains a key clinical challenge.

250 Developing selective strategies to treat metastatic cancers remains a significant challenge.

251 tory failure, heart failure, cardiac arrest, metastatic cancer (requiring ICU), end-stage dementia (r

252 ortunity to evaluate the utility of them for metastatic cancer research.

253 30 are also frequently present in lymph node metastatic cancer samples from the breast, colon and ova

254 Many clinical trials in the early and metastatic cancer setting now include CTCs as a monitori

255 daptation of the multi-cellular ecosystem of metastatic cancer shapes clinical outcomes.

256 Metastatic cancer spread is responsible for most cancer-

257 wn comparably inhibited RENCA cell pulmonary metastatic cancer spread.

258 tissue, both impeding diagnosis of early and metastatic cancer stages and leading to costly and invas

259 erating the transformation of normal LSCs to metastatic cancer stem cells (mCSCs).

260 cer subtypes and activity in patient-derived metastatic cancer stem-like cells indicating a potential

261 ecently been implicated in accelerating bone metastatic cancers, such as acute myelogenous leukemia a

262 lder with ALK-rearranged locally advanced or metastatic cancer that had progressed despite standard t

263 Nasopharyngeal carcinoma (NPC) is a highly metastatic cancer that is consistently associated with E

264 vation in that it unveils a heterogeneity to metastatic cancer that may be ill-suited to canonical cl

265 hylome and whole-transcriptome sequencing in metastatic cancer that provides a comprehensive overview

266 Uveal melanoma (UM) is a highly metastatic cancer that, in contrast to cutaneous melanom

267 Six kidney transplant recipients with metastatic cancers that were not responding to first-lin

268 In metastatic cancer, the degree of heterogeneity of the tu

269 e populations such as the cells that compose metastatic cancers, the emergence of cells that are resi

270 Despite the high mortality from metastatic cancer, therapeutic targets to prevent metast

271 Besides applications to wound healing and metastatic cancer, these studies are relevant for tissue

272 he contrary, the prognosis for children with metastatic cancer, though significantly improved from a

273 lasma-derived cell-free DNA and eight frozen metastatic cancer tissues collected during rapid autopsy

274 samples to 19.3% and 21.8% in localized and metastatic cancer tissues, respectively (P-value < 2 x 1

275 trospective study examined all patients with metastatic cancer treated between February 2010 and Octo

276 1), or its ligand PD-L1, are the mainstay of metastatic cancer treatment.

277 er (SCLC) is one of the most lethal and most metastatic cancer types.

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

279 ion of therapeutic response in patients with metastatic cancer undergoing systemic cytotoxic and/or t

280 sensory retinal detachments in patients with metastatic cancer undergoing systemic therapy with MEK i

281 Conclusion In patients with metastatic cancer undergoing systemic treatment, differe

282 ta from 51 patients with locally advanced or metastatic cancer undergoing treatment with the MEK inhi

283 gnificantly higher risk of presentation with metastatic cancer, undertreatment, and death resulting f

284 undred sixteen consecutive participants with metastatic cancer underwent 932 CT examinations to monit

285 mic therapy may be used to treat advanced or metastatic cancer using the same indications and combina

286 7, 2003, to April 3, 2012, 41 patients with metastatic cancer were enrolled.

287 Ten patients with biopsy-proven metastatic cancer were included.

288 ormal pairs from 97 patients with a range of metastatic cancers were sequenced, with a mean coverage

289 f the lung, head and neck, esophagus, or any metastatic cancer) were excluded.

290 benefits of palliative care in patients with metastatic cancer who are also receiving standard oncolo

291 review of kidney transplant recipients with metastatic cancer who received checkpoint inhibitors at

292 Patients with metastatic cancer who were hospitalized between January

293 One hundred twenty patients with metastatic cancer who were no longer being treated with

294 ients with progressive, treatment-refractory metastatic cancer who were treated with a single dose ea

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

296 as the first broadly successful strategy for metastatic cancer will require clinicians to integrate t

297 R5 as an exciting new therapeutic target for metastatic cancer with clinical trials now targeting bre

298 Eligible patients (n = 686) had metastatic cancer with spinal cord or cauda equina compr

299 geted therapeutic agent for the treatment of metastatic cancers with high Rac activity.

300 in a prospective study of 124 patients with metastatic cancer, with contemporaneous matched tumor ti