ライフサイエンスコーパス: Wilms' tumor

1 ome) and is described in some cancers (e.g., Wilms' tumor).

2 All six developed Wilms tumor.

3 is lost or mutated in up to 30% of cases of Wilms tumor.

4 he WTX gene is frequently lost or mutated in Wilms tumor.

5 ted evidence of DIS3L2 mutations in sporadic Wilms tumor.

6 should be considered in all individuals with Wilms tumor.

7 ered growth, some of which include a risk of Wilms tumor.

8 enotypes from those of children with BWS and Wilms tumor.

9 reases risk for embryonal cancers, including Wilms tumor.

10 tion gene accounting for approximately 2% of Wilms tumor.

11 paralog in a significant percentage of human Wilms tumor.

12 sulting in a pathology highly reminiscent of Wilms tumor.

13 IGF1R to be associated with poor outcome in Wilms tumors.

14 embled malignant rhabdoid tumors rather than Wilms tumors.

15 mors, followed by targeted sequencing of 651 Wilms tumors.

16 of 4,900 cancer-related genes in 26 primary Wilms tumors.

17 histone methylation state that characterizes Wilms tumors.

18 pathogenesis of a significant percentage of Wilms tumors.

19 ic malignancies such as rhabdomyosarcoma and Wilms' tumor.

20 l trials for the management of children with Wilms' tumor.

21 ecognized as important prognostic factors in Wilms' tumor.

22 s now the most common known gene mutation in Wilms' tumor.

23 potecan in pediatric patients with recurrent Wilms' tumor.

24 urvivors of acute lymphoblastic leukemia and Wilms' tumor.

25 chanism for chemotherapeutic intervention in Wilms' tumor.

26 36 in an orthotopic xenograft model of human Wilms' tumor.

27 cators for patients with favorable-histology Wilms' tumor.

28 lassification schema for favorable-histology Wilms' tumor.

29 pression data separated these two classes of Wilms' tumor.

30 clear region of the blastemal cells in 6% of Wilms' tumors.

31 ion and proliferation program of a subset of Wilms' tumors.

32 nal development, is mutated in 10% to 15% of Wilms' tumors.

33 profiles in WT1-mutant versus WT1 wild-type Wilms' tumors.

34 entiviral transfer of a TCR specific for the Wilms tumor 1 (WT1) antigen, these TCR-edited cells expr

35 entified a role for the transcription factor Wilms tumor 1 (WT1) as a critical regulator of senescenc

36 icent et al. report on the identification of Wilms tumor 1 (Wt1) as a Kras synthetic-lethal gene in a

37 ter analysis identified transcription factor Wilms tumor 1 (WT1) binding sites, and WT1 knockdown res

38 Furthermore, microarray analyses showed that Wilms tumor 1 (WT1) gene was overexpressed by trisomy 8

39 The aberrant overexpression of Wilms tumor 1 (WT1) in myeloid leukemia plays an importa

40 LCs electroporated with Wilms tumor 1 (WT1) mRNA achieve sufficiently sustained

41 n with leukemia-associated antigens, such as Wilms Tumor 1 (WT1) peptides, induces a T-cell populatio

42 In this study, we assessed the expression of Wilms tumor 1 (WT1), a known marker of mesothelial cells

43 Conditional linage tracing with Wilms tumor 1 (Wt1)-CreERT2 and Rosa26 reporter mice fou

44 ochemical labeling with the podocyte markers Wilms tumor 1 and p57 identified parietal epithelial cel

45 ion of the villous protrusions of the PE and Wilms tumor 1 and transcription factor 21 expression.

46 t side induced ectopic expression domains of Wilms tumor 1 and transcription factor 21.

47 The Wilms tumor 1 gene (WT1) can either repress or induce th

48 ly reported the adverse prognostic impact of Wilms tumor 1 gene (WT1) mutations in younger adult cyto

49 nalysis has demonstrated that MCs expressing Wilms tumor 1 give rise to HSCs and myofibroblasts durin

50 NA directed against the transcription factor Wilms tumor 1 in transgenic mice reduces that protein sp

51 ly striking with regard to the appearance of Wilms tumor 1 protein-specific CD8 T-cell responses in l

52 nt and is associated with the suppression of Wilms' tumor 1 (WT-1) transcription factor expression.

53 t stem cells expressing stem cell antigen-1, Wilms' tumor 1 (WT-1), and CD34, suggesting active, heal

54 se mutation of the transcriptional regulator Wilms' Tumor 1 (WT1) as the cause of nonsyndromic, autos

55 ific and faithfully recapitulated endogenous Wilms' tumor 1 (Wt1) gene expression.

56 The Wilms' tumor 1 (WT1) gene plays an important role in mam

57 Wilms' tumor 1 (WT1) is essential for the development an

58 Here, we found that the transcription factor Wilms' Tumor 1 (WT1) modulates VEGFA and FGF2 signaling

59 High levels of the Wilms' Tumor 1 (WT1) protein and mRNA had been associate

60 As (miRNA) are made, we demonstrate that the Wilms' tumor 1 (WT1) transcription factor has an essenti

61 fibrosis (IPF); however, the contribution of Wilms' tumor 1 (Wt1)-positive PMCs to the generation of

62 A significant loss of podocytes, assessed by Wilms' tumor 1 and nephrin staining and urinary nephrin

63 te differentiation through downregulation of Wilms' tumor 1 in mice.

64 Here, we identify a crucial role for the Wilms' tumor 1 protein (WT1) in circumvallate (CV) papil

65 ecessary for normal podocyte function (e.g., Wilms' tumor 1 protein [WT1], transcription factor pod1,

66 Wilms' tumor 1-associating protein (WTAP) is a putative

67 on of the podocyte proteins synaptopodin and Wilms' tumor 1.

68 reen fluorescent protein (GFP) driven by the Wilms tumor-1 (WT-1) promoter, we demonstrate PMC traffi

69 se was monitored by quantitative analysis of Wilms tumor-1 (WT1), a leukemia-associated gene.

70 Wilms tumor-1 (Wt1)-positive epicardial cells were highe

71 rdial-specific knockout of the gene encoding Wilms' tumor-1 (Wt1) leads to a reduction in mesenchymal

72 fluorescence detection of antibodies against Wilms' tumor-1 or transducin-like enhancer of split 4.

73 The Wilms' tumor-1 protein (WT1) is a transcriptional regula

74 cut from paraffin-embedded tissue to measure Wilms' tumor-1 protein-positive podocyte nuclear number

75 d TFEB expression also induced expression of Wilms' tumor-1, another E-cadherin activator.

76 Similar genetic mapping of Wilms' tumor-1-positive mesothelial cells indicated that

77 fl(2)d, the Drosophila homolog of Wilms'-tumor-1-associated protein (WTAP), regulates the

78 Wilms' tumors (13%) exhibited a low-level gain correspon

79 is inactivated in approximately one-third of Wilms tumors (15 of 51 tumors).

80 ermethylation of H19 in children with IH and Wilms tumor, 20% (3/15), was significantly lower than th

81 in the 1990s), of abdominal radiotherapy for Wilms' tumor (78%, 53%, and 43%, respectively), of chest

82 than the frequency in children with BWS and Wilms tumor, 79% (11/14; P = .0028).

83 In a large family affected with Wilms tumor, 84% of variants uniquely identified by FamS

84 ginally identified as an inactivated gene in Wilms tumor, a childhood kidney cancer.

85 idney share a number of characteristics with Wilms tumor, a common pediatric kidney cancer.

86 suppressor targeted by somatic mutations in Wilms tumor, a pediatric kidney cancer, and by germline

87 Mutation of WT1 in humans leads to Wilms' tumor, a pediatric kidney tumor, or other kidney

88 Wilms' tumor accounts for nearly 6% of all pediatric can

89 treatment regimens for anaplastic histology Wilms' tumor (AH).

90 therapy regimen or with anaplastic histology Wilms' tumor (AHWT) in first or subsequent recurrence we

91 d missense mutations have been identified in Wilms tumor and acute myeloid leukemia.

92 their possible contribution to nonsyndromic Wilms tumor and identified constitutional 11p15 abnormal

93 or implicated in the pediatric kidney cancer Wilms tumor and in mesenchymal differentiation with pote

94 p-ERK 1/2 (Thr202/Tyr204) expression in the Wilms tumor and metastatic Ewing's sarcoma, but not in t

95 and protein expression was down-regulated in Wilms tumor and RCC.

96 codes a tumor suppressor gene inactivated in Wilms tumor and recently implicated in WNT signaling thr

97 c stem cell rescue in patients with relapsed Wilms tumor and rhabdomyosarcoma suggests that some pati

98 c stem cell rescue in patients with relapsed Wilms tumor and rhabdomyosarcoma suggests that some pati

99 is pilot study assessed patients with DSRCT, Wilms' tumor and Ewing's sarcoma.

100 or 8 to > or = 60 weeks in two patients with Wilms' tumor and two with brainstem glioma (one exophyti

101 mors, and 25 informative, well-characterized Wilms' tumors and determined the relationship between IG

102 ression in the blastemal compartment of some Wilms' tumors and is associated with an adverse outcome

103 aturing the triad of congenital nephropathy, Wilms tumor, and intersex disorders (XY under-virilizati

104 TX gene is the most commonly mutated gene in Wilms tumor, and its product enhances Wilms tumor gene 1

105 hese data highlight two molecular classes of Wilms' tumor, and indicate strong selection for stabiliz

106 rse prognostic factor in favorable histology Wilms' tumor, and the utilization of molecular markers t

107 Unlike WAGR (Wilms tumor, aniridia, genitourinary anomalies, and ment

108 S), Frasier syndrome (FS) and WAGR syndrome (Wilms tumor, aniridia, genitourinary malformations, and

109 centromeric to BDNF (11p14.1), result in the Wilms' tumor, aniridia, genitourinary anomalies, and men

110 Patients with Wilms' tumor, aniridia, major genitourinary malformation

111 To determine whether the leukemia-associated Wilms tumor antigen (WT1) contributes to a graft-versus-

112 Recent studies have detected Wilms tumor antigen (WT1)-specific cytotoxic T lymphocyt

113 Recently, vaccines against the Wilms Tumor antigen 1 (WT1) have been tested in cancer p

114 ming of naive T cells from healthy donors to Wilms tumor antigen 1 (WT1), a protein overexpressed in

115 of cytotoxic T lymphocytes specific for the Wilms tumor antigen 1, resulting in more than an 80% dec

116 ic syndrome and laparoscopic nephrectomy for Wilms tumor are presented.

117 Wilms tumors are a heterogeneous class of tumors in whic

118 ressive means of diagnosis and treatment for Wilms' tumor are continuing to achieve very good cure ra

119 Most Wilms' tumors are of low stage, favorable histology, and

120 These data support the hypothesis that Wilms' tumors arise, in part, because WT1 mutant protein

121 The WTX, Wilms tumor-associated tumor-suppressor gene, is present

122 syndrome/idiopathic hemihypertrophy and the Wilms' tumor-associated syndromes.

123 Furthermore, cell lines derived from Wilms' tumors but not those from renal cell carcinomas w

124 ectomy is successful for low risk unilateral Wilms tumor, but its indications remain controversial.

125 ith therapy resistance and poor prognosis of Wilms tumor, but the molecular basis for this phenotype

126 (NSS) in patients with synchronous bilateral Wilms tumor (BWT) operated on between 2001 and 2014.

127 tic clinic trials in children with bilateral Wilms tumors (BWT) exist.

128 this subgroup, we analyzed 58 blastemal type Wilms tumors by exome and transcriptome sequencing and v

129 er a plausible explanation for the fact that Wilms tumors can arise either from loss of WT1 or loss o

130 The recent identification of Wilms' tumor cancer stem cells could provide a framework

131 Seventy Wilms tumor cases with rupture were matched to 70 Wilms

132 de association study in 757 individuals with Wilms tumor (cases) and 1,879 controls.

133 ful therapeutic strategy by using a panel of Wilms tumor cell lines.

134 hat C/EBPB is a critical survival factor for Wilms tumor cells and that its expression contributes to

135 By contrast, Wilms tumor cells established orthotopically within the

136 this concern, we obtained and tested primary Wilms tumor cells, finding no detectable SOCE in this ce

137 Because Wilms' tumor cells may similarly depend on CXCR2 signali

138 In hereditary Wilms tumors, clonal loss of WT1 precludes the beta-cate

139 2 study enrolled patients with very low-risk Wilms tumor confirmed by central review of pathology, di

140 The management of Wilms' tumor continues to evolve with two different appr

141 tumor cases with rupture were matched to 70 Wilms tumor controls without rupture according to age an

142 ion alone after nephrectomy in very low-risk Wilms tumor (defined as stage I favorable histology Wilm

143 are associated with WT1 mutations, including Wilms tumors, Denys-Drash syndrome (DDS), Frasier syndro

144 tend our insights in the genetics underlying Wilms tumor development and emphasize the importance of

145 ch to treating stage III favorable-histology Wilms tumor (FHWT) is Regimen DD4A (vincristine, dactino

146 Patients with favorable histology Wilms' tumor (FHWT) and recurrence after at least one sa

147 on/deletion mutations in favorable histology Wilms tumors (FHWTs) to occur within SIX1/2 (7% of 534 t

148 opy number gain of 1q in favorable-histology Wilms tumors (FHWTs) with event-free survival (EFS) and

149 ent to examine the expression profiles of 54 Wilms tumors, five normal kidneys and fetal kidney.

150 DNA copy number, and DNA methylation in 117 Wilms tumors, followed by targeted sequencing of 651 Wil

151 dysplasia but do not appear to predispose to Wilms tumor formation.

152 WTX, a protein encoded by a gene mutated in Wilms tumors, forms a complex with beta-catenin, AXIN1,

153 variants of the WT1 gene are susceptible to Wilms' tumors (Frasier and Denys-Drash syndromes).

154 stered ESTs that clearly separate anaplastic Wilms tumors from tumors with favorable histology.

155 the prostate cancer epithelial cells was the Wilms tumor gene (WT1).

156 activity, and immunogenicity of a polyvalent Wilms tumor gene 1 (WT1) peptide vaccine in patients wit

157 lls, demonstrate increased expression of the Wilms tumor gene 1 product (WT1), making WT1 an attracti

158 ene in Wilms tumor, and its product enhances Wilms tumor gene 1-mediated transcription.

159 ey development requires the functions of the Wilms tumor gene WT1 and the WNT/beta-catenin signaling

160 , we review recent findings showing that the Wilms' tumor gene (Wt1) is a key regulator of mesenchyme

161 ins known to be overexpressed in AML such as Wilms' tumor gene, and multiparameter flow cytometry to

162 ntified constitutional epigenetic defects in Wilms tumor genes extend the understanding of Wilms tumo

163 e results indicate that children with IH and Wilms tumor have different constitutional epigenotypes f

164 otential mutation sites in the p53 gene from Wilms' tumor, head and neck tumor, and colorectal tumor.

165 oblastoma (HR, 0.47; 95% CI, 0.40-0.54), and Wilms tumor (HR, 0.70; 95% CI, 0.59-0.82).

166 A microRNA (miRNA) screen of primary Wilms' tumors identified specific overexpression of miR-

167 e discuss genetic and epigenetic findings in Wilms' tumor in the context of renal development.

168 to the epithelial cells of fetal kidney and Wilms' tumors in most cases, 12% of tumors were also fou

169 f an observation alone strategy for low-risk Wilms tumor incorporating both clinical features and bio

170 Wilms tumor is a pediatric kidney cancer associated with

171 Wilms tumor is the most common childhood renal cancer.

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

173 Wilms tumor is the most common renal malignancy of child

174 Fortunately, survival for patients with Wilms' tumor is generally excellent.

175 Despite the high cure rate of Wilms tumor, long-term survivors remain at risk of death

176 ons of WT1; recently, it has been found that Wilms tumors may also be associated with biallelic mutat

177 histology in chemotherapy-treated pediatric Wilms tumors (nephroblastoma) is associated with adverse

178 We further validated MSNP in a Wilms' tumor/normal kidney comparison, comparing the res

179 mprinting patterns than has been reported in Wilms tumors of all ages.

180 ty to the RMF peptide from the intracellular Wilms tumor oncoprotein WT1 in complex with HLA-A*02:01.

181 et Lin28 to specific cell types, we observed Wilms tumor only when Lin28 is aberrantly expressed in m

182 Wilms' tumor or nephroblastoma is believed to arise from

183 Wilms' tumor, or nephroblastoma, is the most common pedi

184 t REST may act as a tumor-suppressor gene in Wilms tumor pathogenesis.

185 Objective responses were noted in three Wilms tumor patients and one each of medulloblastoma and

186 s expression contributes to the prognosis of Wilms tumor patients.

187 d with higher relapse and mortality rates in Wilms tumor patients.

188 ateral cases (P = 0.001) and in one familial Wilms tumor pedigree.

189 ncing transcription factor) in four familial Wilms tumor pedigrees and nine non-familial cases.

190 These data establish REST as a Wilms tumor predisposition gene accounting for approxima

191 Approximately 5% of children with Wilms tumor present with disease in both kidneys.

192 The Wilms tumor protein (WT-1) is widely recognized as a tum

193 lls recognizing tumor-associated Ags such as Wilms tumor protein (WT1) are thought to exert potent an

194 Wilms tumor protein 1 (WT1) has been implicated in the c

195 s early growth response protein 1 (Egr1) and Wilms tumor protein 1 (WT1) to different forms of modifi

196 omerular tuft expressed the podocyte markers Wilms tumor protein 1, nephrin, podocin, and synaptopodi

197 nistically, this function of Pk3 may involve Wilms tumor protein 1-interacting protein (Wtip), which

198 podocytes (coexpression of synaptopodin and Wilms tumor protein), parietal epithelial cells (PAX 8),

199 The Wilms tumor protein, WT-1, is a widely recognized tumor

200 hat murine Adamts16 is co-expressed with the Wilms tumor protein, Wt1, in the developing glomeruli of

201 We report here that the Wilms tumor protein, WT1, which is necessary for normal

202 ts as one of the most common known causes of Wilms tumor, provide mechanistic insights into imprintin

203 ction in very young children with stage I FH Wilms' tumor, regardless of tumor size, and we suggest t

204 atment of anaplastic histology and bilateral Wilms' tumor remains a challenge.

205 WiT49, a cell line derived from a metastatic Wilms tumor, resulted in spontaneous apoptosis.

206 me that is associated with susceptibility to Wilms' tumor, rhabdomyosarcoma and hepatoblastoma.

207 ilms tumor genes extend the understanding of Wilms tumor risk in children lacking syndromic features,

208 The diagnosis of Wilms tumor rupture was established by central review of

209 he sensitivity and specificity for detecting Wilms tumor rupture were 54% (36 of 67 cases) and 88% (6

210 sensitivity in the detection of preoperative Wilms tumor rupture.

211 tive genomic hybridization (aCGH) data on 68 Wilms' tumor samples, we identified a significant correl

212 clinical trials for patients with recurrent Wilms' tumor should be considered.

213 no longer be recommended in future National Wilms Tumor Studies.

214 A total of 142 patients studied on National Wilms' Tumor Studies 1, 2, 3, 4, and 5 were analyzed.

215 mic Medical Center (n = 1,349), the National Wilms Tumor Study (n = 364), the St Jude Lifetime Cohort

216 Background The National Wilms Tumor Study (NWTS) approach to treating stage III

217 A primary objective of the fifth National Wilms Tumor Study (NWTS-5) was to identify prognostic in

218 cation rate was similar between the National Wilms Tumor Study and the International Society of Pedia

219 2, 6,185 patients enrolled onto the National Wilms Tumor Study between 1969 and 1995 were actively ob

220 abdomyosarcoma Study Group, and the National Wilms Tumor Study Group in 2000 offered the newly formed

221 rolled between 1969 and 2002 by the National Wilms Tumor Study Group.

222 erent approaches being taken by the National Wilms Tumor Study in North America and the International

223 l (Amsterdam, the Netherlands), the National Wilms Tumor Study, and the St Jude Lifetime Cohort Study

224 simulations based on data from the National Wilms Tumor Study, the authors demonstrate that such adj

225 WTs from 1,114 patients enrolled in National Wilms Tumor Study-5 that were informative for 1p and 16q

226 Stage III designation in NWTS-5 (National Wilms Tumor Study-5) was determined by four pathologic c

227 An objective of the fifth National Wilms' Tumor Study (NWTS-5) was to evaluate the efficacy

228 Mutations in the Wilms tumor suppressor 1 (WT1) gene are as frequent in a

229 se elements to the zinc-finger proteins WT1 (Wilms tumor suppressor 1) and EGR1 (early growth respons

230 Notably, WTX binds WT1, another Wilms tumor suppressor and stem cell marker that encodes

231 ociated with constitutional mutations in the Wilms tumor suppressor gene WT1.

232 bryogenesis, progenitor cells expressing the Wilms tumor suppressor gene, WT1, are induced to differe

233 The zinc finger domain of the Wilms tumor suppressor protein (WT1) contains four canon

234 are a heterogeneous class of tumors in which Wilms tumor suppressor-1 (WT1) and the p53 tumor suppres

235 The Wilms' tumor suppressor 1 (WT1) gene encodes a DNA- and

236 The transcription factor Wilms' tumor suppressor 1 (WT1) is key to podocyte devel

237 (FGF) signaling and the transcription factor Wilms' tumor suppressor 1 (WT1).

238 The Wilms' tumor suppressor gene (WT1) encodes a zinc finger

239 ional deletion of the ST/PE lineage-specific Wilms' tumor suppressor gene (Wt1) in the ST/PE of G2-Ga

240 knock-out mouse embryos have shown that the Wilms' tumor suppressor gene (Wt1) is indispensable for

241 The Wilms' tumor suppressor gene 1 (WT1) encodes a zinc fing

242 The Wilms' tumor suppressor gene, Wt1, encodes a transcripti

243 The Wilms' tumor suppressor protein WT1 functions as a trans

244 The Wilms' tumor suppressor protein WT1 is a transcriptional

245 pronephric podocyte progenitors express the Wilms' tumor suppressor wt1a but do not undergo glomerul

246 podocytes (colocalized with synaptopodin and Wilms' tumor suppressor) and present in lower abundance

247 The Wilms' tumor suppressor-1 (Wt1) and the FoxC1/2 transcri

248 f podocytes required wt1a, which encodes the Wilms' tumor suppressor-1 transcription factor, and rbpj

249 mal recessive manner that is associated with Wilms tumor susceptibility.

250 ute myeloid leukemia with t(9;11), bilateral Wilms' tumor, systemic lupus erythematosus, and conditio

251 versely, genes expressed at a lower level in Wilms tumors tend to be expressed less in uninduced meta

252 nd that genes expressed at a higher level in Wilms tumors tend to be expressed more in uninduced meta

253 49 cell line is characteristic of anaplastic Wilms tumors that are refractory to treatment and expres

254 In Wilms' tumors that demonstrate maintenance of imprinting

255 3 of beta-catenin (CTNNB1) are specific for Wilms' tumors that have lost WT1, but 50% of WT1-mutant

256 Wilms Tumor, the most common pediatric kidney cancer, ev

257 iously recognized as recurrently involved in Wilms tumors, the most frequent being BCOR, BCORL1, NONO

258 crine effects of enhanced IGF2 expression in Wilms tumor, this disease may be acutely dependent on si

259 rentially expressed between fetal kidney and Wilms tumors to kidney morphogenesis, we found that gene

260 currently being used to assign patients with Wilms' tumor to specific protocol-based therapies.

261 een associated with relapse in very low-risk Wilms tumors treated with surgery alone and may help red

262 een associated with relapse in very low-risk Wilms tumors treated with surgery alone and may help red

263 ldren's Oncology Group defines very low-risk Wilms tumors (VLRWT) as stage I favorable histology Wilm

264 To identify mutations that predispose to Wilms tumor, we are conducting exome sequencing studies.

265 ommon variants that confer susceptibility to Wilms tumor, we conducted a genome-wide association stud

266 on screen for DNA copy-number alterations in Wilms tumor, we identified somatic deletions targeting a

267 role of mutations of WT1 in the etiology of Wilms' tumor, we used an inducible cellular system for e

268 the role of WT1 as a transcription factor in Wilms' tumors, we used cDNA microarrays to compare the e

269 umors (VLRWT) as stage I favorable histology Wilms tumors weighing less than 550 g in children younge

270 h small (<550 g) Stage I favorable histology Wilms tumors were treated with surgery only.

271 A total of 2,596 patients with Wilms' tumor were enrolled onto NWTS-5, of whom 281 (10.

272 1986 to 2001), 242 children with stage I FH Wilms' tumor were treated with immediate nephrectomy fol

273 Thirteen children with relapsed Wilms' tumor were treated with one or two cycles of high

274 ry tumor samples were analyzed, and 15 of 16 Wilms' tumors were found to be CXCR2 positive, whereas g

275 Survival for patients with Wilms' tumor when considered as a whole, once less than

276 uring development leads to the initiation of Wilms tumor, whereas EMT contributes to the development

277 lent survival for children being treated for Wilms' tumor, while minimizing therapy-related toxicity.

278 is an effective treatment for patients with Wilms' tumor who experience relapse.

279 and alterations in LIN28-LET7 expression in Wilms tumor will be explored.

280 our genes predicts future relapse of primary Wilms tumors with high accuracy, independent of anaplasi

281 umor (defined as stage I favorable histology Wilms tumors with nephrectomy weight <550g and age at di

282 tumor suppressor, frequently inactivated in Wilms tumor, with both plasma membrane and nuclear local

283 tissue, in colon, lung, breast, thyroid and Wilms' tumors, with intermediate variation in adenomas.

284 rom 13 of 437 individuals (3%) with sporadic Wilms tumor without features of growth disorders, includ

285 Survivors of Wilms tumor (WT) are at risk for adverse health and soci

286 ation therapy or chemotherapy for unilateral Wilms tumor (WT) diagnosed during childhood on pregnancy

287 Clinical trials in Wilms tumor (WT) have resulted in overall survival rates

288 Wilms tumor (WT) is a genetically heterogeneous childhoo

289 Wilms tumor (WT) is the most common pediatric renal tumo

290 Children with stage III Wilms tumor (WT) treated in NWTS-5 were assessed for eve

291 an chromosome 11p15 that is commonly lost in Wilms tumor (WT), encodes an imprinted untranslated RNA.

292 Children with the rare Wilms tumor (WT)-aniridia (WAGR) syndrome have not had s

293 Wilms' tumor (WT) is the most common childhood renal can

294 ression profiling of both mRNA and miRNAs in Wilms' tumor (WT) samples to provide the first evidence

295 Wilms' tumor (WT), one of the most common pediatric soli

296 odal evaluation performance in children with Wilms' Tumors (WT), to determined factors associated wit

297 n addition to genes previously implicated in Wilms tumors (WT1, CTNNB1, AMER1, DROSHA, DGCR8, XPO5, D

298 n of the Ewing's sarcoma (EWS) gene with the Wilms' tumor (WT1) gene.

299 CT (EWS-WT1), Ewing's sarcoma (EWS-FLI1) and Wilms' tumor (WT1) to better understand the signaling pa

300 athway mediated cytoplasmic retention of the Wilms tumor (WTI) protein, which strongly suppressed the