ライフサイエンスコーパス: Wilms' tumour

1 nal development result in the development of Wilms tumour.

2 these defects define a distinct subclass of Wilms tumours.

3 te abnormally, possibly mimicking aspects of Wilms' tumour.

4 of blastemal cells in human fetal kidney and Wilms' tumours.

5 of childhood renal malignancies known as non-Wilms' tumours.

6 A hypermethylation in 21 of 39 (54%) primary Wilms' tumours.

7 3 (methyltransferase-like 3), METTL14, WTAP (Wilms tumour 1-associated protein) and KIAA1429.

8 Here, we show that Wilms' tumour 1 (WT1), a developmental master regulator

9 lling complex, is required for expression of Wilms' tumour 1 (Wt1), fetal EPDC activation and subsequ

10 One such gene is Wilms' tumour 1 (WT1), which plays multiple roles in dev

11 Mutations of the Wilms' tumour-1 (WT1) gene in humans can lead to childho

12 process of PGP midline convergence, we used Wilms' tumour 1a (wt1a) as a marker to label kidney prim

13 ressor gene, mutation of which is a cause of Wilms' tumour, a childhood renal nephroblastoma.

14 mary tumours) at CASP8, SLIT2 and RASSF1A in Wilms' tumour and at RASSF1A, TIMP3, DAPK, SLIT2, MT1G a

15 ma, brain tumours, adrenocortical carcinoma, Wilms' tumour and phyllodes tumour.

16 de novo promoter methylation is frequent in Wilms' tumour and RCC, and these data enable methylation

17 enetic gene silencing in the pathogenesis of Wilms' tumour and renal cell carcinoma (RCC), we determi

18 K, MGMT, NORE1A, p14ARF and RARB2 in primary Wilms' tumours and CASP8, CDH1, CDH13, CRBP1, DAPK, MGMT

19 uppressor gene, WT1, is mutated in 10-15% of Wilms' tumours and encodes zinc-finger proteins with div

20 des a zinc-finger protein that is mutated in Wilms' tumours and highly expressed in a wide variety of

21 presentation, imaging, and pathology of non-Wilms' tumours and this second part provides an updated

22 Thus, 40 Wilms' tumours and up to 49 adult RCC were analysed by m

23 involved in the management of patients with Wilms' tumour are increasingly focusing their efforts on

24 Children with stage II-III intermediate-risk Wilms' tumours assessed after delayed nephrectomy were r

25 ecessary for the initiation of some familial Wilms' tumours but subsequently the maintenance of the n

26 s for Wilms tumour development by regulating Wilms tumour cell proliferation.

27 xperiments showed that they are required for Wilms tumour cell proliferation.

28 -interfering RNAs leads to reduced DNMT3A in Wilms' tumour cells and human embryonal kidney-derived c

29 Finally, we show that depletion of WT1 in Wilms' tumour cells can lead to reactivation of gene exp

30 lso demonstrated at hypermethylated genes in Wilms' tumour cells, including a region of long-range ep

31 Wilms' tumours demonstrated a high incidence of methylat

32 trast to RASSF1A, only a minority (10.3%) of Wilms' tumours demonstrated p16 promoter methylation.

33 WT1 is a suppressor for Wilms tumour development and an oncogene for diverse mal

34 a gain-of-function and act as oncogenes for Wilms tumour development by regulating Wilms tumour cell

35 al overgrowth and causes a predisposition to Wilms' tumour development.

36 Wilms' tumours display biallelic AWT1 expression, indica

37 kitt's lymphoma, CNS tumours, neuroblastoma, Wilms' tumour, Ewing's sarcoma, osteosarcoma, and rhabdo

38 ntify inactivating CTR9 mutations in 3 of 35 Wilms tumour families, through exome and Sanger sequenci

39 le loss was not detected in nine informative Wilms' tumours (five with RASSF1A methylation).

40 Non-Wilms' tumours form a small heterogeneous group of clini

41 Four Wilms' tumours from a family showing strong evidence of

42 and suggests that hnRNP-U may be a candidate Wilms' tumour gene at 1q44.

43 The Wilms' Tumour gene WT1 has important functions during de

44 Childhood ALL and Wilms' tumour have long-term effects on interpersonal fu

45 e we report the whole-exome sequencing of 44 Wilms tumours, identifying missense mutations in the mic

46 Each mutation segregates with Wilms tumour in the family and a second mutational event

47 evelopmental disorders and susceptibility to Wilms' tumour in children.

48 Most patients with Wilms' tumour in Europe and North America can be cured w

49 Wilms tumour is a childhood kidney cancer.

50 Wilms tumour is an embryonal tumour of childhood that cl

51 Wilms tumour is the most common childhood kidney cancer.

52 Wilms' tumour is the most common childhood kidney tumour

53 mportant regulators of MYCN, LIN28 and other Wilms tumour oncogenes.

54 our tissues, including the first analysis of Wilms' tumour precursor lesions, nephrogenic rests.

55 These data establish CTR9 as a Wilms tumour predisposition gene and suggest it acts as

56 rative chemotherapy regimen for stage II-III Wilms' tumour pretreated with chemotherapy was to includ

57 sible for the development of the majority of Wilms tumours remain largely unknown.

58 hylation results were also available for the Wilms' tumour samples.

59 The Wilms' tumour suppressor gene WT1 is essential for the n

60 (DDS) is caused by dominant mutations of the Wilms' tumour suppressor gene, WT1, and characterized by

61 The Wilms' tumour suppressor gene, WT1, encodes a zinc-finge

62 The Wilms' tumour suppressor gene, WT1, is mutated in 10-15%

63 One highly conserved feature of the Wilms' tumour suppressor gene, WT1, is the potential, fo

64 erozygosity (LOH) indicate the presence of a Wilms' tumour suppressor gene.

65 ggests that PTH-B1 is a candidate for the 7p Wilms' tumour suppressor gene.

66 The Wilms' tumour suppressor protein WT1 contains a transcri

67 The Wilms' tumour suppressor protein WT1 plays a central rol

68 all these cell types frequently express the Wilms' tumour suppressor Wt1, which transcriptionally co

69 The Wilms' tumour suppressor, WT1, is a zinc finger protein

70 vivors odds ratio 10.83 [95% CI 3.87-30.82], Wilms' tumour survivors 4.85 [1.43-16.47]), which was as

71 A familial Wilms' tumour susceptibility gene, known as FWT1, has re

72 Here we identify recurrent mutations within Wilms tumours that involve the highly conserved YEATS do

73 nd, if mutated, can lead to the formation of Wilms' tumour, the most common paediatric kidney cancer.

74 at LOH on chromosome 17q is rare in sporadic Wilms' tumour, the results suggest that FWT1 is not a tu

75 hood acute lymphoblastic leukaemia (ALL) and Wilms' tumour to address previous methods limitations.

76 tumorigenesis, we have analysed 40 sporadic Wilms tumours using a panel of 10 microsatellite polymor

77 However, the alleles lost in this Wilms' tumour were those segregating with the disease in

78 stage II-III, histological intermediate-risk Wilms' tumour when a newly defined high-risk blastemal s

79 treatment of stage II-III intermediate risk Wilms' tumour when the histological response to preopera

80 assessed 102 survivors of childhood ALL and Wilms' tumour, who had been free from relapse for 5 year

81 recently established cell lines from primary Wilms tumours with different WT1 mutations.

82 We studied 18 cases of Wilms' tumour with favourable histological findings.

83 Cytogenetic analysis of Wilms tumours (WT) have shown that abnormalities involvi

84 Wilms' tumour (WT) has a diverse and complex molecular a

85 Wilms' tumour (WT) is one of the most common solid tumou