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 paralog in a significant percentage of human Wilms tumor.

3 sulting in a pathology highly reminiscent of Wilms tumor.

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

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

6 ted evidence of DIS3L2 mutations in sporadic Wilms tumor.

7 utcomes in patients with favorable histology Wilms tumor.

8 should be considered in all individuals with Wilms tumor.

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

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

11 reases risk for embryonal cancers, including Wilms tumor.

12 All six developed Wilms tumor.

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

14 nomas, papillary thyroid cancers (PTCs), and Wilms tumors.

15 pathogenesis of a significant percentage of Wilms tumors.

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

17 embled malignant rhabdoid tumors rather than Wilms tumors.

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

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

20 histone methylation state that characterizes Wilms tumors.

21 ic malignancies such as rhabdomyosarcoma and Wilms' tumor.

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

23 ecognized as important prognostic factors in Wilms' tumor.

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

25 potecan in pediatric patients with recurrent Wilms' tumor.

26 chanism for chemotherapeutic intervention in Wilms' tumor.

27 36 in an orthotopic xenograft model of human Wilms' tumor.

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

29 lassification schema for favorable-histology Wilms' tumor.

30 urvivors of acute lymphoblastic leukemia and Wilms' tumor.

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

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

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

34 Wilms tumor 1 (WT1) and beta-catenin are two master regu

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

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

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

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

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

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

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

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

43 model of atrial cardiomyopathy in rat and in Wilms tumor 1 (WT1)(CreERT2/+);ROSA-tdT(+/-) mice.

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

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

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

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

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

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

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

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

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

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

54 e-like 3-methyltransferase-like 14 (METTL14)-Wilms tumor 1-associated protein complex dynamically reg

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

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

57 ts affecting the fourth zinc finger (ZF4) of Wilms' tumor 1 (WT1) (p.Ser478Thrfs*17, p.Pro481Leufs*15

58 y the expression of the transcription factor Wilms' Tumor 1 (WT1) and colony stimulating factor 1 (CS

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

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

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

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

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

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

65 cells that express the transcription factor Wilms' Tumor 1 (WT1), which drives the expression of two

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

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

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

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

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

71 fferential expression of three marker genes: Wilms' tumor 1, transgelin, and myxovirus 1.

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

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

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

75 have proposed WBP5, and its association with Wilms Tumor-1 (WT1) expression, as part of a gene expres

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

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

78 diated cross-regulating feedback mechanisms: Wilms Tumor-1-YAP-mediated downregulation of E-cadherin,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 ed EFS for patients with favorable histology Wilms tumor and LOH1p/16q compared with the historical N

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

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

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

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

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

107 e variant identified is a somatic hotspot in Wilms tumors and has been identified in 2 PTCs.

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

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

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

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

112 dence of such childhood cancers as lymphoma, Wilms tumor, and neuroblastoma.

113 mary tumors, including 24 neuroblastomas, 24 Wilms tumors, and 8 rhabdomyosarcomas.

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

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

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

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

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

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

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

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

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

123 We therefore isolated a high-affinity Wilms' Tumor Antigen 1-specific TCR (TCR(C4)) from HLA-A

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

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

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

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

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

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

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

131 (WTX) is a putative tumor suppressor gene in Wilms tumor, but its expression and functions in other t

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

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

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

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

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

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

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

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

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

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

142 By contrast, Wilms tumor cells established orthotopically within the

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

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

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

146 2 study enrolled patients with very low-risk Wilms tumor confirmed by central review of pathology, di

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

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

149 ents with newly diagnosed diffuse anaplastic Wilms tumor (DAWT) and whether a regimen containing carb

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

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

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

153 hylation of the H19 locus, a known driver of Wilms tumor development, in 58% of the expansions.

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

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

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

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

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

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

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

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

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

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

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

165 e safety of administering TAA-Ts that target Wilms tumor gene 1, preferentially expressed antigen of

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

167 Wilms tumor gene on the X chromosome (WTX) is a putative

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

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

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

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

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

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

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

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

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

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

178 Wilms tumor is a pediatric kidney cancer associated with

179 Wilms tumor is the most common childhood renal cancer.

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

181 Wilms tumor is the most common renal malignancy of child

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

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

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

185 To investigate whether Wilms tumor (nephroblastoma; a childhood kidney cancer)

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

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

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

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

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

191 Wilms' tumor or nephroblastoma is believed to arise from

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

214 RNA profiling of PTCs, MNG, schwannomas, and Wilms tumors revealed a common profile among E518K hemiz

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

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

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

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

219 sensitivity in the detection of preoperative Wilms tumor rupture.

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

221 Wilms' tumor shares similarities with neuro- and gliobla

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

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

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

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

226 In National Wilms Tumor Study 5 (NWTS-5), tumor-specific combined lo

227 ion to regimen I agents used in the National Wilms Tumor Study 5 (NWTS-5; vincristine, doxorubicin, c

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

229 2, 6,185 patients enrolled onto the National Wilms Tumor Study between 1969 and 1995 were actively ob

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 uroblastoma and rhabdomyosarcoma, whereas in Wilms tumor, they are late events.

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

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

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

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

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

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

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

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

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

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

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

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

278 These included the KT-10 Wilms' tumor with a PALB2 mutation, the BRCA1-deficient

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

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

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

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

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

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

285 Wilms tumor (WT) is a genetically heterogeneous childhoo

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

287 nical discovery and testing of therapies for Wilms tumor (WT) patients who have poor outcomes.

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

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

290 that capture the biological heterogeneity of Wilms tumor (WT).

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

292 Wilms' tumor (WT) morphologically resembles the embryoni

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

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

295 Wilms' tumor (WT), the most common childhood kidney canc

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