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1 tructures resembling those observed in human Wilms tumour.
2 e cancers at higher rates than patients with Wilms tumour.
3 was to identify new predisposition genes for Wilms tumour.
4 nal development result in the development of Wilms tumour.
5  these defects define a distinct subclass of Wilms tumours.
6 te abnormally, possibly mimicking aspects of Wilms' tumour.
7 of blastemal cells in human fetal kidney and Wilms' tumours.
8 of childhood renal malignancies known as non-Wilms' tumours.
9 A hypermethylation in 21 of 39 (54%) primary Wilms' tumours.
10 3 (methyltransferase-like 3), METTL14, WTAP (Wilms tumour 1-associated protein) and KIAA1429.
11                           Here, we show that Wilms' tumour 1 (WT1), a developmental master regulator
12 lling complex, is required for expression of Wilms' tumour 1 (Wt1), fetal EPDC activation and subsequ
13                             One such gene is Wilms' tumour 1 (WT1), which plays multiple roles in dev
14 xpression of the epicardial master regulator Wilms' tumour 1 (WT1).
15                             Mutations of the Wilms' tumour-1 (WT1) gene in humans can lead to childho
16  process of PGP midline convergence, we used Wilms' tumour 1a (wt1a) as a marker to label kidney prim
17 s have been found in the ENL YEATS domain in Wilms tumour(2,3), the most common type of paediatric ki
18 ts with renal tumours are diagnosed with non-Wilms tumour, a broad heterogeneous group of tumours tha
19 ressor gene, mutation of which is a cause of Wilms' tumour, a childhood renal nephroblastoma.
20 ing FBXW7 mutations in four individuals with Wilms tumour and a de-novo non-synonymous FBXW7 mutation
21 mary tumours) at CASP8, SLIT2 and RASSF1A in Wilms' tumour and at RASSF1A, TIMP3, DAPK, SLIT2, MT1G a
22 ma, brain tumours, adrenocortical carcinoma, Wilms' tumour and phyllodes tumour.
23  de novo promoter methylation is frequent in Wilms' tumour and RCC, and these data enable methylation
24 enetic gene silencing in the pathogenesis of Wilms' tumour and renal cell carcinoma (RCC), we determi
25 K, MGMT, NORE1A, p14ARF and RARB2 in primary Wilms' tumours and CASP8, CDH1, CDH13, CRBP1, DAPK, MGMT
26 uppressor gene, WT1, is mutated in 10-15% of Wilms' tumours and encodes zinc-finger proteins with div
27 des a zinc-finger protein that is mutated in Wilms' tumours and highly expressed in a wide variety of
28  presentation, imaging, and pathology of non-Wilms' tumours and this second part provides an updated
29                                     Thus, 40 Wilms' tumours and up to 49 adult RCC were analysed by m
30 phoma, malignant CNS tumours, neuroblastoma, Wilms' tumours, and bone and soft tissue sarcomas.
31  involved in the management of patients with Wilms' tumour are increasingly focusing their efforts on
32 Children with stage II-III intermediate-risk Wilms' tumours assessed after delayed nephrectomy were r
33 ecessary for the initiation of some familial Wilms' tumours but subsequently the maintenance of the n
34 arrant further exploration include targeting Wilms tumour cancer genes with a non-redundant role in n
35 edisposition genes, account for about 10% of Wilms tumour cases.
36 s for Wilms tumour development by regulating Wilms tumour cell proliferation.
37 xperiments showed that they are required for Wilms tumour cell proliferation.
38 -interfering RNAs leads to reduced DNMT3A in Wilms' tumour cells and human embryonal kidney-derived c
39    Finally, we show that depletion of WT1 in Wilms' tumour cells can lead to reactivation of gene exp
40 lso demonstrated at hypermethylated genes in Wilms' tumour cells, including a region of long-range ep
41                 Only a third of the familial Wilms tumour clusters we analysed were attributable to k
42 onstrate that organoid cultures derived from Wilms tumours consist of multiple different cell types,
43 of entities with outcomes that diverged from Wilms tumour, corroborated with immunohistochemistry and
44                                              Wilms' tumours demonstrated a high incidence of methylat
45 trast to RASSF1A, only a minority (10.3%) of Wilms' tumours demonstrated p16 promoter methylation.
46                      WT1 is a suppressor for Wilms tumour development and an oncogene for diverse mal
47  a gain-of-function and act as oncogenes for Wilms tumour development by regulating Wilms tumour cell
48 al overgrowth and causes a predisposition to Wilms' tumour development.
49                                              Wilms' tumours display biallelic AWT1 expression, indica
50 kitt's lymphoma, CNS tumours, neuroblastoma, Wilms' tumour, Ewing's sarcoma, osteosarcoma, and rhabdo
51 ntify inactivating CTR9 mutations in 3 of 35 Wilms tumour families, through exome and Sanger sequenci
52 sis of the upcoming COG favourable-histology Wilms tumour (FHWT) study.
53 le loss was not detected in nine informative Wilms' tumours (five with RASSF1A methylation).
54                                          Non-Wilms' tumours form a small heterogeneous group of clini
55                                         Four Wilms' tumours from a family showing strong evidence of
56 and suggests that hnRNP-U may be a candidate Wilms' tumour gene at 1q44.
57                                          The Wilms' Tumour gene WT1 has important functions during de
58            The genetic changes that underpin Wilms tumour have been defined by studies of familial ca
59                                Patients with Wilms tumour have benefited from the results of decades
60                            Childhood ALL and Wilms' tumour have long-term effects on interpersonal fu
61 e we report the whole-exome sequencing of 44 Wilms tumours, identifying missense mutations in the mic
62                Each mutation segregates with Wilms tumour in the family and a second mutational event
63 evelopmental disorders and susceptibility to Wilms' tumour in children.
64                           Most patients with Wilms' tumour in Europe and North America can be cured w
65 sed lymphocyte DNA from 890 individuals with Wilms tumour, including 91 affected individuals from 49
66                                              Wilms tumour is a childhood kidney cancer.
67                                              Wilms tumour is an embryonal tumour of childhood that cl
68 on genes and 20 genes somatically mutated in Wilms tumour is limited, consisting of only four genes.
69                                              Wilms tumour is the most common childhood kidney cancer.
70                                              Wilms tumour is the most common childhood renal cancer a
71                                              Wilms tumour is the most common renal malignancy of chil
72                                              Wilms' tumour is the most common childhood kidney tumour
73 fferent subtypes of kidney cancer, including Wilms tumours, malignant rhabdoid tumours, renal cell ca
74 dscape of cancer genes that are operative in Wilms tumour, many of which are intricately linked to th
75 ne and somatic genetic changes that underlie Wilms tumour may translate into better patient outcomes.
76 mportant regulators of MYCN, LIN28 and other Wilms tumour oncogenes.
77 ing 91 affected individuals from 49 familial Wilms tumour pedigrees.
78 our tissues, including the first analysis of Wilms' tumour precursor lesions, nephrogenic rests.
79 able to known genes, indicating that further Wilms tumour predisposition factors await discovery.
80               These data establish CTR9 as a Wilms tumour predisposition gene and suggest it acts as
81                                While several Wilms tumour predisposition genes have been identified,
82                                 The four new Wilms tumour predisposition genes identified-TRIM28, FBX
83 cesses and, together with the other 17 known Wilms tumour predisposition genes, account for about 10%
84 rative chemotherapy regimen for stage II-III Wilms' tumour pretreated with chemotherapy was to includ
85 sible for the development of the majority of Wilms tumours remain largely unknown.
86 hylation results were also available for the Wilms' tumour samples.
87       We recommend that all individuals with Wilms tumour should be offered genetic testing and parti
88 ting and particularly, those with epithelial Wilms tumour should be offered TRIM28 genetic testing.
89 aemia, lymphoma, CNS tumours, neuroblastoma, Wilms tumour, soft-tissue sarcomas, and bone cancer) by
90                                          The Wilms' tumour suppressor gene WT1 is essential for the n
91 (DDS) is caused by dominant mutations of the Wilms' tumour suppressor gene, WT1, and characterized by
92                                          The Wilms' tumour suppressor gene, WT1, encodes a zinc-finge
93                                          The Wilms' tumour suppressor gene, WT1, is mutated in 10-15%
94          One highly conserved feature of the Wilms' tumour suppressor gene, WT1, is the potential, fo
95 erozygosity (LOH) indicate the presence of a Wilms' tumour suppressor gene.
96 ggests that PTH-B1 is a candidate for the 7p Wilms' tumour suppressor gene.
97                                          The Wilms' tumour suppressor protein WT1 contains a transcri
98                                          The Wilms' tumour suppressor protein WT1 plays a central rol
99  all these cell types frequently express the Wilms' tumour suppressor Wt1, which transcriptionally co
100                                          The Wilms' tumour suppressor, WT1, is a zinc finger protein
101 vivors odds ratio 10.83 [95% CI 3.87-30.82], Wilms' tumour survivors 4.85 [1.43-16.47]), which was as
102                                   A familial Wilms' tumour susceptibility gene, known as FWT1, has re
103  Here we identify recurrent mutations within Wilms tumours that involve the highly conserved YEATS do
104 nd, if mutated, can lead to the formation of Wilms' tumour, the most common paediatric kidney cancer.
105 at LOH on chromosome 17q is rare in sporadic Wilms' tumour, the results suggest that FWT1 is not a tu
106 hood acute lymphoblastic leukaemia (ALL) and Wilms' tumour to address previous methods limitations.
107  tumorigenesis, we have analysed 40 sporadic Wilms tumours using a panel of 10 microsatellite polymor
108            However, the alleles lost in this Wilms' tumour were those segregating with the disease in
109 stage II-III, histological intermediate-risk Wilms' tumour when a newly defined high-risk blastemal s
110  treatment of stage II-III intermediate risk Wilms' tumour when the histological response to preopera
111 IN were identified in three individuals with Wilms tumour, which is highly unlikely to have occurred
112  assessed 102 survivors of childhood ALL and Wilms' tumour, who had been free from relapse for 5 year
113            However, one in ten children with Wilms tumour will die of their disease despite modern tr
114 recently established cell lines from primary Wilms tumours with different WT1 mutations.
115                       We studied 18 cases of Wilms' tumour with favourable histological findings.
116 ociation with the rare epithelial subtype of Wilms tumour, with 14 of 16 tumours being epithelial or
117                                              Wilms tumour (WT) is a childhood embryonal tumour that i
118                      Cytogenetic analysis of Wilms tumours (WT) have shown that abnormalities involvi
119                                              Wilms' tumour (WT) has a diverse and complex molecular a
120                                              Wilms' tumour (WT) is one of the most common solid tumou

 
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