ライフサイエンスコーパス: renal cancer

1 he CDCP1 gene through the HIF-1/2 pathway in renal cancer.

2 e as novel therapeutics for the treatment of renal cancer.

3 lms' tumor (WT) is the most common childhood renal cancer.

4 tility in promoting MDA-7/IL-24 lethality in renal cancer.

5 ntagonist sFRP3 has not been investigated in renal cancer.

6 on of POX in human cancer tissues, including renal cancer.

7 RP3 may play an important role in metastatic renal cancer.

8 rapeutic value for the clinical treatment of renal cancer.

9 GF) and promote a rapid progression of human renal cancer.

10 many human malignancies including clear cell renal cancer.

11 a critical role in the rapid progression of renal cancer.

12 ntreated patients with metastatic clear cell renal cancer.

13 is an antiangiogenic agent with activity in renal cancer.

14 arding the robotic approach to management of renal cancer.

15 laparoscopic approach for the management of renal cancer.

16 f sorafenib and its role in the treatment of renal cancer.

17 atic breast, colorectal, prostate, lung, and renal cancer.

18 was recently approved for use in metastatic renal cancer.

19 ease and facilitate translational studies in renal cancer.

20 alling has recently been implicated in human renal cancer.

21 manifestations of Birt-Hogg-Dube syndrome or renal cancer.

22 s in immune intact patients with melanoma or renal cancer.

23 e in the early detection and surveillance of renal cancer.

24 n renal proximal tubules, precursor cells of renal cancer.

25 croarrays, has advanced our understanding of renal cancer.

26 y trigger a host immune response against the renal cancer.

27 -muscle tumors of the skin and uterus and/or renal cancer.

28 hysiology of the diverse types of epithelial renal cancer.

29 osis in survival of patients with metastatic renal cancer.

30 creases survival in patients with metastatic renal cancer.

31 with intermediate-risk metastatic clear cell renal cancer.

32 tic, have been identified in human papillary renal cancer.

33 in this trial, is ineffective in metastatic renal cancer.

34 Wilms tumor is the most common childhood renal cancer.

35 e associated with a highly malignant form of renal cancer.

36 nephroblastoma, is the most common pediatric renal cancer.

37 us, we sought to determine a role for DDT in renal cancer.

38 form of collecting duct and type 2 papillary renal cancer.

39 ons in patients with metastatic melanoma and renal cancer.

40 cell lines and in a mouse xenograft model of renal cancer.

41 and sufficient follow-up, 50 (11%) developed renal cancer.

42 cells in syngeneic models of colorectal and renal cancer.

43 bition of Src-mediated oncogenic pathways in renal cancer.

44 tic potential of miR-205 in the treatment of renal cancer.

45 interest for the treatment of prostatic and renal cancers.

46 ly in the setting of breast, thyroid, and/or renal cancers.

47 implications for the choice of treatment for renal cancers.

48 opsy can help subtype and grade many primary renal cancers.

49 occur at a younger age than do nonhereditary renal cancers.

50 /1A2 induction, such as breast, ovarian, and renal cancers.

51 e (VHL) is the causative gene for most adult renal cancers.

52 dings in breast, ovarian, head and neck, and renal cancers.

53 breast and lung cancers and lowest levels in renal cancers.

54 e needs to be bypassed for the initiation of renal cancers.

55 ed risk of breast, thyroid, endometrial, and renal cancers.

56 (thyroid cancer) and 22 (uveal melanoma plus renal cancer) 28-day cycles.

57 8%), breast cancer (16%), sarcoma (13%), and renal cancer (7%).

58 In renal cancer, a radiolabeled antibody, iodine-124 cG250,

59 2)) was associated with an increased risk of renal cancer (adjusted hazard ratio [HR], 1.39; 95% conf

60 ollow-up, six (0.52%) subsequently developed renal cancers, all of which were separate from the simpl

61 bearing murine colon adenocarcinoma or human renal cancer and drugs with anticachexia properties rest

62 undergoing investigation in locally advanced renal cancer and in other tumor types.

63 e assessed the expression of DLL4 in primary renal cancer and investigated the biological function of

64 pression of miR-200 and the EMT signature in renal cancer and is associated with poor clinical outcom

65 t-line treatment of patients with metastatic renal cancer and is currently being trialled in other ca

66 approximately 8% of patients with metastatic renal cancer and melanoma.

67 One partial response in a patient with renal cancer and minor responses (n=3) in patients with

68 d may play a key role in the pathogenesis of renal cancer and von Hippel-Lindau disease.

69 gnificant fraction of patients with sporadic renal cancers and idiopathic cystic lung disease, and li

70 es, including the resistant cell lines TK10 (renal cancer) and SKMEL28 (melanoma).

71 tabolic signature of metastatic melanoma and renal cancer, and metastatic cell lines.

72 of incident cancer; the primary outcome was renal cancer, and secondary outcomes were any cancer and

73 neate clinically distinct forms of inherited renal cancer, and to identify and characterize the genes

74 biomarkers to screen, diagnose, and monitor renal cancers are clearly needed.

75 Renal cancers are highly aggressive and clinically chall

76 Fumarate hydratase-deficient renal cancers are highly aggressive and metastasize even

77 Renal cancers are increasingly being diagnosed incidenta

78 Renal cancers are likely to be particularly sensitive to

79 tream signaling consequences contributing to renal cancer as a result of loss of the tumor suppressor

80 dy, we identified the upregulated miR-23b in renal cancer as an important regulator of POX.

81 d clinical specimens of breast, ovarian, and renal cancer as well as glioblastomas.

82 itinib, an anti-angiogenic drug approved for renal cancer, as an inhibitor for ABL1 gatekeeper mutant

83 However, while the diagnosis of renal cancer at a curable stage remains the first priori

84 ncreased frequencies of breast, thyroid, and renal cancers beyond those conferred by germline PTEN mu

85 ly significant new roles for coregulators in renal cancer biology.

86 es: tuberous sclerosis, hereditary papillary renal cancer, Birt-Hogg-Dube syndrome, hereditary leiomy

87 e future, with responses already reported in renal cancer, bladder cancer, and Hodgkin's lymphoma amo

88 result in fibrofolliculomas, lung cysts and renal cancers, but the precise mechanisms of tumour supp

89 hat CNI may mediate the progression of human renal cancer by downregulating CXCR3-B and by promoting

90 pidermoid carcinoma of the nasopharynx (KB), renal cancer (CAKI-1), and melanoma cancer (SKMEL-2).

91 gh-risk (pT3, pT4, node-positive) clear cell renal cancer (ccRCC) in the ASSURE trial (adjuvant sunit

92 necessary for the pathogenesis of clear cell renal cancer (ccRCC); however, the molecular mechanisms

93 Therefore, Jade-1 may suppress renal cancer cell growth in part by increasing apoptosis

94 Jade-1 inhibited renal cancer cell growth, colony formation, and tumor fo

95 e we report that prostaglandin E(2) promotes renal cancer cell invasion through a signal transduction

96 croRNA hsa-miR-29b in the VHL-overexpressing renal cancer cell line 786-O.

97 of apoptotic cells in the sFRP3-transfected renal cancer cell line A498.

98 We isolated a clone (R331) of the murine renal cancer cell line Renca that was strikingly more se

99 ine NCI/ADR-RES (GI(5)(0) = 0.0169 muM), and renal cancer cell line RXF 393 (GI(5)(0) = 0.0197 muM).

100 pproach for treatment follow-up, utilizing a renal cancer cell line with rapamycin as a tool compound

101 n of miR-205 was significantly suppressed in renal cancer cell lines and tumors when compared with no

102 helial cells, human renal cancer tissues and renal cancer cell lines demonstrated higher expression o

103 Knockdown of galectin-1 gene expression in renal cancer cell lines reduced cell invasion, clonogeni

104 pression was barely detectable in all tested renal cancer cell lines, regardless of VHL status.

105 or activity against human breast, colon, and renal cancer cell lines, undergoes hydrolysis in aqueous

106 lation was confirmed in three additional VHL-renal cancer cell lines, was insensitive to the prolyl h

107 lective inhibitor of the growth of six human renal cancer cell lines.

108 d aid investigators in analysing appropriate renal cancer cell lines.

109 e role of sFRP3 using primary and metastatic renal cancer cell lines.

110 The effect of rapamycin on renal cancer cell phenotype, molecules (E-cadherin, p27

111 ence for a novel mechanism for IGF-1R-driven renal cancer cell proliferation involving miR-214 and mT

112 miR-214 significantly blocked IGF-1R-forced renal cancer cell proliferation, which was reversed by e

113 olimus, and the effect of treatment on mouse renal cancer cell pulmonary metastasis was investigated.

114 In human renal cancer cells (786-0 and Caki-1) and renal epitheli

115 uld induce HO-1, and promote the survival of renal cancer cells (786-0 and Caki-1).

116 uman normal renal epithelial cells (REC) and renal cancer cells (786-0 and Caki-1).

117 that the overexpression of CXCR3-B in human renal cancer cells (Caki-1) promoted cellular apoptosis

118 e phenotypes of isogenic pairs of clear cell renal cancer cells (ccRCC), with or without VHL, upon th

119 (expressing PD-L1 receptor PD-1) and murine renal cancer cells (RENCA, expressing high PD-L1).

120 FILNC1 deficiency in renal cancer cells alleviates energy stress-induced apop

121 or tyrosine kinase c-Met is overexpressed in renal cancer cells and can play major role in the growth

122 -A*0201-restricted antigen expressed by both renal cancer cells and normal kidney cells.

123 ur data signify that HO-1 is up-regulated in renal cancer cells as a survival strategy against chemot

124 overexpressed HO-1 promotes the survival of renal cancer cells by inhibiting cellular apoptosis; we

125 apoptosis and immune escape mechanism(s) of renal cancer cells by the regulations of novel molecules

126 ent, were found to induce HO-1 expression in renal cancer cells Caki-1 and 786-O; and the apoptotic e

127 issues; and the overexpression of CXCR3-B in renal cancer cells can significantly inhibit cell prolif

128 Increased expression of IGF-1R in renal cancer cells correlates with their potency of tumo

129 uced and HO-1-mediated pathway could protect renal cancer cells from apoptosis.

130 reduced cyclinD1, and arrested the growth of renal cancer cells in G1/S phase.

131 inhibits the growth of FLCN-deficient human renal cancer cells in mouse xenografts.

132 to block proliferation and invasion of 786-O renal cancer cells in vitro.

133 VHL reintroduction into renal cancer cells increases endogenous Jade-1 protein a

134 n of IGF-1R levels and miR-214 expression in renal cancer cells independent of VHL status.

135 uced AKT Ser473 phosphorylation and rendered renal cancer cells more susceptible to NVP-BEZ235-mediat

136 olonged the survival of mice inoculated with renal cancer cells or T24 human bladder cancer cells.

137 e report that VHL-deficient and VHL-positive renal cancer cells possess significantly decreased level

138 HIF2alpha expression is dependent on PLD in renal cancer cells suggests that targeting PLD signals m

139 he translocation behaviors of the metastatic renal cancer cells through plain and nanotextured PDMS m

140 n, migration, EMT and stem-like phenotype in renal cancer cells through the AKT/GSK3beta/CTNNB1 pathw

141 hich c-Met can promote increased survival of renal cancer cells through the regulation of HO-1 and PD

142 Here, we used 786-0 human renal cancer cells to investigate the effect of cyclospo

143 Rapamycin conditioning of renal cancer cells upregulated E-cadherin expression and

144 Proliferation of renal cancer cells was suppressed by miR-205, mediated b

145 In a xenograft model wherein, live renal cancer cells were implanted under the kidney capsu

146 etic conditions was also dependent on PLD in renal cancer cells with restored pVHL expression.

147 Interestingly, like renal cancer cells, in AsPC-1 cells PKC-zeta leads to di

148 In renal cancer cells, the inactivation of the tumor suppre

149 Using renal cancer cells, we confirmed that stauprimide inhibi

150 expression of any apoptosis-related genes in renal cancer cells, we performed a protein array.

151 colony formation, migration, and invasion in renal cancer cells.

152 in vivo in human prostate, breast, lung, and renal cancer cells.

153 e mRNA stability of VEGF in 786-0 and Caki-1 renal cancer cells.

154 iR-23b was knocked down by its antagomirs in renal cancer cells.

155 th, invasion, and inhibition of apoptosis in renal cancer cells.

156 expression using siRNA promoted apoptosis of renal cancer cells.

157 rough modulation of TIS11B protein levels in renal cancer cells.

158 ited CNI-mediated augmented proliferation of renal cancer cells.

159 oth HIF1alpha and HIF2alpha in VHL-deficient renal cancer cells.

160 has been shown to reverse tumorigenesis with renal cancer cells.

161 gulatory component of HIFalpha expression in renal cancer cells.

162 poptosis induced by serum deprivation in the renal cancer cells.

163 c-Met phosphorylation and Ras activation in renal cancer cells.

164 ary and sufficient to suppress E-cadherin in renal cancer cells.

165 tion of Akt kinase activity in both types of renal cancer cells.

166 tly inhibited IGF-1R-driven proliferation of renal cancer cells.

167 er473 in response to NVP-BEZ235 treatment in renal cancer cells.

168 pathway induces HO-1 to promote survival of renal cancer cells.

169 in increased proliferation and migration of renal cancer cells; CNI-mediated cell proliferation invo

170 rcinomas were shown to be different types of renal cancer characterized by specific genetic alteratio

171 D1 (encoding cyclin D1) that is specific for renal cancers characterized by inactivation of the von H

172 , making the relationship between Jade-1 and renal cancer compelling.

173 laparoscopic renal nephrectomy for localized renal cancer confers equivalent long-term oncologic resu

174 ations, which are severe and associated with renal cancer development, prevented Jade-1 stabilization

175 Medical records were reviewed for subsequent renal cancer diagnoses.

176 ectively evaluate the prevalence of ACKD and renal cancer during renal transplant evaluation.

177 ated in the treatment of advanced clear cell renal cancer, either as first-line treatment or after tr

178 As the array of biologic therapies for renal cancer expands with the approval of tyrosine kinas

179 he von Hippel-Lindau (VHL) gene is the major renal cancer gene in adults.

180 ally distinct, inherited forms of epithelial renal cancer; genes responsible for five inherited predi

181 The presentation of renal cancer has evolved.

182 Treatment of advanced renal cancer has made little progress in the past 30 yr.

183 The approach to treatment of renal cancer has shifted dramatically from radical surge

184 rtial nephrectomy for the treatment of small renal cancers has led to the development of energy ablat

185 Most renal cancers have defects in the von Hippel-Lindau tumo

186 ) tumor suppressor gene predispose people to renal cancer, hemangioblastomas, and pheochromocytomas i

187 of the variant hereditary leiomyomatosis and renal cancer (HLRCC) syndrome, and have shown that these

188 have achieved durable responses in melanoma, renal cancer, Hodgkin's diseases and lung cancer.

189 In the RENCA model of mouse renal cancer, however, combining CVX-060 with sunitinib

190 rome, which allows for early surveillance of renal cancer in affected patients as well as disease scr

191 Wilms tumor is the most common renal cancer in children.

192 y may prevent the development/progression of renal cancer in CNI-treated patients.

193 tive nephrectomy in patients with metastatic renal cancer in the era of targeted therapy is uncertain

194 Whereas previously, the list of hereditary renal cancers in adults included von Hippel-Lindau disea

195 hazards regression model was used to compare renal cancer incidence for patients who had simple cyst-

196 Renal cancer incidence has increased progressively in th

197 There was no difference in renal cancer incidence in patients with simple cyst-appe

198 Minimally invasive treatments of renal cancer (including percutaneous ablation) show prom

199 us disease that consists of various types of renal cancer, including tumors with indolent, multifocal

200 Traditionally, curative therapy for most renal cancers involved open radical nephrectomy.

201 The genetics of renal cancer is dominated by inactivation of the VHL tum

202 e of immunotherapy for metastatic clear-cell renal cancer is its curative potential, as demonstrated

203 The primary therapy of renal cancer is the surgical removal.

204 e in a better understanding of the causes of renal cancer, its prevention, and, ultimately, its cure.

205 data suggest that inactivation of JARID1C in renal cancer leads to heterochromatin disruption, genomi

206 Endogenous Jade-1 in stable renal cancer lines also exhibited VHL mutation-dependent

207 Interestingly, a number of human renal cancer lines were also susceptible to FasL-mediate

208 This practice is based on reliable data that renal cancers <3 cm in diameter behave with minimal mali

209 cal studies in patients with ovarian cancer, renal cancer, lymphoma, and neuroblastoma, where they ha

210 results are used to confirm the diagnosis of renal cancers, metastases, and infections, and there is

211 in combination were investigated in a murine renal cancer model (Renca).

212 , the only modality that can cure widespread renal cancer, must not be overlooked.

213 ents with non-Hodgkin's lymphoma, colon, and renal cancer occurred.

214 urine DNA from patients with organ-confined renal cancers of all histological types.

215 es characteristic of benign renal tumors and renal cancers of different grades.

216 spontaneously arising renal adenocarcinoma (renal cancer) of BALB/c origin was used as the model tum

217 ith neural-network analysis to either detect renal cancer or to identify proteins of potential use as

218 ssociated with increased risks of breast and renal cancer over PTEN mutation-positive individuals.

219 herefore contribute to VHL renal disease and renal cancer pathogenesis.

220 This new landscape of renal cancer patients can be offered an expanded list of

221 ned from end-stage chronic kidney disease or renal cancer patients contain round, multilamellar miner

222 may prove more efficacious than sunitinib in renal cancer patients whose tumours express FGF2.

223 By combination of urine or serum analysis of renal cancer patients, hypermethylation was detected in

224 alterations remained as high as 92% in 7/10 renal cancer patients.

225 or serum can be detected in the majority of renal cancer patients.

226 ethylation in the urine and serum samples of renal cancer patients.

227 rum sample (total, 18) also were tested from renal cancer patients.

228 potentially therapeutic T-cell responses in renal cancer patients.

229 P3 correlates with poor clinical outcomes in renal cancer patients.

230 iferation that must be overcome generally in renal cancer, perhaps initially by pVHL inactivation and

231 proximal tubule cells, which are clear-cell renal cancer precursors, and expression increases with d

232 We review the changes in renal cancer presentation and our understanding of its c

233 Renal cancer presents a unique opportunity to explore th

234 ycosphingolipid synthesis with tumor growth, renal cancer progression and regression can be evaluated

235 t MCPIP1 protein levels are decreased during renal cancer progression.

236 strategy for the prevention of CNI-mediated renal cancer progression.

237 r (253J-BV), pancreatic cancer (L3.6pl), and renal cancer (RBM1-IT) but not in the EGF/TGF-alpha-nega

238 it the growth of a small percentage of human renal cancers (RCs), although the majority of RCs both i

239 eled monoclonal antibodies (11 patients with renal cancer receiving (124)I-cG250 and 5 patients with

240 ntreated patients with metastatic clear cell renal cancer recruited between June 2008 and October 201

241 nephrectomy in the management of metastatic renal cancer remains controversial.

242 Therapy for metastatic renal cancer remains inadequate, but recent developments

243 It is clear that renal cancer remains one of the most immunoresponsive of

244 Mice bearing the experimental murine renal cancer Renca can be successfully treated with some

245 The murine renal cancer Renca has been used as a model for developi

246 Using a mouse renal cancer (Renca), we show that NKG2D recognition by

247 murine myeloid leukemia, C1498, and a murine renal cancer, Renca.

248 .3% of patients with metastatic melanoma and renal cancer, respectively.

249 Jade-1 stabilization by pVHL correlates with renal cancer risk, making the relationship between Jade-

250 at TCE exposure is associated with increased renal cancer risk, particularly among individuals carryi

251 teraction of Jade-1 and pVHL correlates with renal cancer risk.

252 loss of Jade-1 stability may correlate with renal cancer risk.

253 Finally, analysis of clinical renal-cancer samples demonstrates that a large proportio

254 IR, 18.81; 95% CI, 3.88 to 54.95; P < .001), renal cancer (SIR, 11.22; 95% CI, 2.31 to 32.79; P < .00

255 reast cancer (SIR, 5.5; 95% CI, 4.5 to 6.7), renal cancer (SIR, 3.9; 95% CI, 2.0 to 7.5), soft tissue

256 Renal cancer size at presentation has decreased.

257 M1-IT) but not in the EGF/TGF-alpha-negative renal cancer SN12-PM6, tumor-associated endothelial cell

258 Medical therapies are lacking for advanced renal cancer, so there is a great need to understand its

259 ples demonstrates that a large proportion of renal cancers strongly express FGF2.

260 a and the COSMIC Cell Lines Project to three renal cancer subtypes from The Cancer Genome Atlas: clea

261 missense mutations commonly associated with renal cancer, such as Leu118Pro or Arg167Trp, did not st

262 nse mutations that cause VHL disease without renal cancer, such as Tyr98His and Tyr112His, stabilized

263 A recent genome-wide association study on renal cancer susceptibility identified single-nucleotide

264 Hereditary renal cancer syndromes can lead to multiple bilateral ki

265 Genetic and phenotypic characterization of renal cancer syndromes includes von Hippel-Lindau diseas

266 ying genetic mutations that cause hereditary renal cancer syndromes will have profound implications f

267 iple renal cell carcinomas, and/or heritable renal cancer syndromes.

268 genic mouse model of von Hippel-Lindau (VHL) renal cancer termed the TRACK model (transgenic model of

269 olves a transcription factor translocated in renal cancer, TFEB.

270 underlying vulnerability of all VHL mutated renal cancers that could be therapeutically exploited.

271 y established in culture from a patient with renal cancer, the patient's tumor cells were efficiently

272 for improving management of small clear-cell renal cancers through noninvasive immunologic identifica

273 that DCs transfected with RNA isolated from renal cancer tissue are remarkably effective in stimulat

274 tomatically classify sample regions in human renal cancer tissue ex-vivo into tumor or benign tissue

275 al tissues and renal epithelial cells, human renal cancer tissues and renal cancer cell lines demonst

276 Finally, we observed that human renal cancer tissues expressing low amounts of CXCR3-B s

277 in was high in normal kidney, low in primary renal cancer tissues, and high in metastatic renal cance

278 renal cancer tissues, and high in metastatic renal cancer tissues.

279 antly up-regulated and co-localized in human renal cancer tissues.

280 CXCR3-B is markedly down-regulated in human renal cancer tissues; and the overexpression of CXCR3-B

281 families with multiple members affected with renal cancer to delineate clinically distinct forms of i

282 imaging biomarker of response of metastatic renal cancer to targeted therapy.

283 somal fragile site at 3p14.2, the hereditary renal cancer translocation breakpoint, and cancer cell h

284 ) and sorafenib, two commonly used drugs for renal cancer treatment, were found to induce HO-1 expres

285 -specific PCR may enhance early detection of renal cancer using a noninvasive urine test.

286 Aldosterone mediates metastatic spread of renal cancer via the G protein-coupled estrogen receptor

287 The incidence of renal cancer was significantly lower in patients with si

288 view of the involvement of RASSF1A in adult renal cancers we investigated RASSF1A as a candidate Wil

289 protein partners with potential relevance to renal cancer, we screened a human kidney library against

290 Patients without renal cancer were evaluated for a minimum of 5 years (me

291 Fifteen patients with measurable metastatic renal cancer were studied.

292 ed and for breast, thyroid, endometrial, and renal cancers were calculated.

293 n have an increased prevalence of breast and renal cancers when compared with PTEN mutation carriers.

294 rapeutic strategy for targeting HIF2alpha in renal cancers where HIF2alpha is critical for tumorigene

295 routinely used circulating tumor markers for renal cancer, which is often detected incidentally and i

296 t tumors such as prostate, breast, lung, and renal cancers, which can lead to various complications,

297 ost frequent TIMP-3 methylation was found in renal cancers, which originate in the tissue that normal

298 patients with either metastatic melanoma or renal cancer who were treated with high-dose bolus IL-2

299 identifies FILNC1 as a negative regulator of renal cancer with potential clinical value, but also rev

300 hanges in tumor pO2 in highly vascular 786-0 renal cancer xenografts.