ライフサイエンスコーパス: metastatic cancer

1 tructive uropathy, urothelial carcinoma, and metastatic cancer.

2 lt in abscopal responses among patients with metastatic cancer.

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

4 al interactions between the brain milieu and metastatic cancer.

5 opportunity to analyze disease evolution in metastatic cancer.

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

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

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

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

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

11 improving the efficacy of immunotherapy for metastatic cancer.

12 nging from neurodegeneration to diabetes and metastatic cancer.

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

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

15 sufficient in the majority of patients with metastatic cancer.

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

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

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

19 expression of RhoGDI2 in xenograft models of metastatic cancer.

20 have shown efficacy in preclinical models of metastatic cancer.

21 ent to trigger regressions of an established metastatic cancer.

22 pression is suppressed in cancer, especially metastatic cancer.

23 ediated objective responses in patients with metastatic cancer.

24 nregulated or lost in the advanced stages of metastatic cancer.

25 ent, may be developed as a means of treating metastatic cancer.

26 central feature of embryonic development and metastatic cancer.

27 ts undergoing hepatic resection for 1(o) and metastatic cancer.

28 eir significance in prognosis and therapy of metastatic cancer.

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

30 tional deregulation is a defining feature of metastatic cancer.

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

32 n attractive and novel immunotherapy against metastatic cancer.

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

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

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

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

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

38 therapeutic opportunity in the management of metastatic cancer.

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

40 dermining the success of therapies targeting metastatic cancer.

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

42 nically relevant therapeutic target to treat metastatic cancer.

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

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

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

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

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

48 onse in preclinical models of orthotopic and metastatic cancers.

49 aggressive chemoradiotherapy for eradicating metastatic cancers.

50 ental contributions to ischemic diseases and metastatic cancers.

51 omarker and potential therapeutic target for metastatic cancers.

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

53 for consideration in studies in advanced or metastatic cancers.

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

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

56 r cellular function, which is linked to many metastatic cancers.

57 e the clonal relationships among primary and metastatic cancers.

58 often indicative of recurrent, advanced, or metastatic cancers.

59 ies for diagnosis, prognosis, and therapy of metastatic cancers.

60 ents for the treatment of murine primary and metastatic cancers.

61 s to differentiate among the three different metastatic cancers.

62 molecular landscape and microenvironment of metastatic cancers.

63 therapeutically viable approach for treating metastatic cancers.

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

65 alysis is available from clinically acquired metastatic cancers.

66 nt of ovarian cancer and other transcoelomic metastatic cancers.

67 ormation and the development of invasive and metastatic cancers.

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

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

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

71 5, 2010, and July 30, 2012, 52 patients with metastatic cancer (18 tumour types) received anti-interl

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

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

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

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

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

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

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

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

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

81 low-dose IL-2 treatment in 12 patients with metastatic cancer and 9 patients with chronic myelogenou

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

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

84 85 years who did not have newly diagnosed or metastatic cancer and lived within a study site catchmen

85 Comparison of metastatic cancer and localized disease in multiple expr

86 hich we believe to be novel, is operative in metastatic cancer and should be considered in tumor immu

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

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

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

90 at caveolin-1 is up-regulated in a number of metastatic cancers and can influence various aspects of

91 l kinase activity is elevated in a number of metastatic cancers and these kinases are activated downs

92 preference-sensitive (palliative therapy for metastatic cancer), and treatment modality, influenced p

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

94 dex), recently approved for the treatment of metastatic cancer, and GW5638/DPC974, a SERD that is cur

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

96 evels of fascin expression are found in many metastatic cancers, and inhibition of fascin function by

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

100 embrane molecule highly expressed in several metastatic cancers as well as on CD34(+)CD133(+) myeloid

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 e most effective in primary tumors and early metastatic cancers, before selection for TRAIL resistanc

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

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

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

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

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

110 promising target for manipulation to inhibit metastatic cancer cell adhesion.

111 those organs as fertile soil for subsequent metastatic cancer cell colonization.

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

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

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

115 g are effective tools to interrogate diverse metastatic cancer cell phenotypes as well as the metasta

116 Equol also increased metastatic cancer cell viability.

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

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

119 Metastatic cancer cells (seeds) preferentially grow in t

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

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

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

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

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 one mechanism by which the organotropism of metastatic cancer cells can arise.

128 upregulated and seven were downregulated in metastatic cancer cells compared with TMD-231 cells.

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

130 Successful removal of metastatic cancer cells from the abdominal cavity and ci

131 ased convection of drugs, growth factors, or metastatic cancer cells from the tumor margin into the p

132 Metastatic cancer cells have the ability to both degrade

133 Early and specific detection of metastatic cancer cells in the lung (the most common org

134 n early growth advantage to the accompanying metastatic cancer cells in the lungs.

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

136 Metastatic cancer cells increase glucose consumption and

137 These results suggest that metastatic cancer cells increase specific oncogenic sign

138 t time that increased expression of CD147 in metastatic cancer cells is coupled to the up-regulation

139 mors, we found that viability of circulating metastatic cancer cells is higher if they are incorporat

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

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

142 Bone metastatic cancer cells produce factors such as parathyr

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

144 Furthermore, the metastatic cancer cells tested exhibited higher ROS gene

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

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

147 -016 inhibits Rac activity in the MDA-MB-435 metastatic cancer cells that overexpress Rac and exhibit

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

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

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

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

152 g vasculature mediates the initial homing of metastatic cancer cells to specific foci in the lungs.

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

154 -selectin, leading to preferential homing of metastatic cancer cells to these foci.

155 Metastatic cancer cells undergo an epithelial-mesenchyma

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

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

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

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

160 Metastatic cancer cells, in contrast, show sufficient FA

161 uced the IL-6/IL-8-dependent invasiveness of metastatic cancer cells, indicating that IL-1alpha regul

162 neously spread to the lung tissue along with metastatic cancer cells, significantly decreases the num

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

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

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

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

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

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

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

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

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

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

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

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

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

176 and miR-22 was consistently downregulated in metastatic cancer cells.

177 ades the other tissue, in the same manner as metastatic cancer cells.

178 of ROS-inducing agents such as 4HPR against metastatic cancer cells.

179 racellular matrix, is often dysfunctional in metastatic cancer cells.

180 einase (MMP) inducer, is highly expressed in metastatic cancer cells.

181 r selective delivery to alphavbeta3 positive metastatic cancer cells.

182 and independent of the physical presence of metastatic cancer cells.

183 egrin receptors that are highly expressed in metastatic cancer cells.

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

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

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

187 such as imparting therapeutic resistance to metastatic cancer cells.

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

189 Patients with metastatic cancer commonly have increased serum galectin

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

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

192 In particular, metastatic cancers, drug-resistant cancers, and cancer s

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

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

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

196 cy for p53 and Rb tumor suppressors leads to metastatic cancer, exhibiting features of both luminal a

197 be repeatedly administered to patients with metastatic cancer expressing the tumor antigen carcinoem

198 te during normal embryonic development or in metastatic cancer first detach from an epithelium.

199 Metastatic cancer foci as small as a few hundred cells w

200 ways synergistically may inhibit primary and metastatic cancer growth.

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

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

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

204 to poor visibility in 246 patients (14.6%), metastatic cancer in 69 patients (4.1%), bleeding in 49

205 ression was also seen in 7/7 (100%) cases of metastatic cancer in bone.

206 Intraoperative analysis for the presence of metastatic cancer in SLNs from breast cancer patients la

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

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

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

210 tic efficacy against established primary and metastatic cancers in syngeneic mice and activate tumor-

211 2) is overexpressed in 40%-80% of late-stage metastatic cancers in the absence of gene amplification.

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

213 to those found in the sera of patients with metastatic cancer increased adhesion of MUC1-expressing

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

215 al event in the pathogenesis of invasive and metastatic cancer is E-cadherin loss of function.

216 Metastatic cancer is extremely difficult to treat, and t

217 lopment of effective, systemic therapies for metastatic cancer is highly desired.

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

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

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

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

222 Patients with preburn HIV/AIDS, metastatic cancer, liver disease, and renal disease have

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

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

225 ould home to and kill cancer cells in a lung metastatic cancer model.

226 Our metastatic cancer models, combined with noninvasive imag

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

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

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

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

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

232 antly prolongs the survival of patients with metastatic cancers of the colorectum, breast and lung.

233 curative outcome in a variety of primary and metastatic cancers of the liver.

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

235 isease (OR = 5.1), liver disease (OR = 4.8), metastatic cancer (OR = 4.6), pulmonary circulation diso

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

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

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

239 immunomagnetically enriched for CTCs from 74 metastatic cancer patients and 50 normal donors were use

240 me quantitative PCR in blood samples from 81 metastatic cancer patients and 55 healthy donors that we

241 ial cells (CEpCs) in the peripheral blood of metastatic cancer patients has shown promise for improve

242 However, metastatic cancer patients treated with immunotherapy sh

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

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

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

246 s study was to compare in an animal model of metastatic cancer PDT alone and PDT combined with low-do

247 ehavior (SPP1, CHI3L1, MUM1), and aggressive metastatic cancer phenotype (SPP1, CHI3L1).

248 Metastatic cancers produce exosomes that condition pre-m

249 umor B7-H1 was significantly associated with metastatic cancer progression (RR, 3.46; P < 0.001) and

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

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

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

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

254 ecular link between SMYD3 overexpression and metastatic cancer progression.

255 dysregulation of these same processes during metastatic cancer progression.

256 itiating various signaling events leading to metastatic cancer progression.

257 Forty-nine patients with metastatic cancer received intravenous imexon over 30 to

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

259 Secondary metastatic cancer remains the single biggest cause of mo

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

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

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

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

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

265 in the tumor stroma of human pancreatic and metastatic cancer specimens was confirmed by quantitativ

266 wn comparably inhibited RENCA cell pulmonary metastatic cancer spread.

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

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

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

270 Decisions about treatments for metastatic cancers tended to be more physician controlle

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

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

273 ty has gone awry in what diseases, including metastatic cancers that are of special interest to our l

274 In a syngeneic model of metastatic cancer, the down-regulation of Crry on i.v.-i

275 de a molecular link between two hallmarks of metastatic cancer: the glycolytic switch and increased e

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

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

278 The small GTPase RalA is activated in metastatic cancers through multiple mechanisms and speci

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

280 inase (MMP) is strongly associated with many metastatic cancer types.

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

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

283 In a small cohort of patients with metastatic cancer undergoing systemic treatment, tempora

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

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

286 A model of hepatic metastatic cancer was developed with portal vein infusio

287 Because aerobic glycolysis is a hallmark of metastatic cancer, we examined whether increases in CD14

288 7, 2003, to April 3, 2012, 41 patients with metastatic cancer were enrolled.

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

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

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

292 elop tumor specific thermal therapy (Rx) for metastatic cancer when inductively heated by an external

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

294 Patients with metastatic cancer who were hospitalized between January

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

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

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

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

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

300 sease; no prior chemotherapy for advanced or metastatic cancer; Zubrod performance status (PS) of 0 t