Results of the United Kingdom Children's Cancer Study Group first Wilms' Tumor Study.

Pritchard, Jon; Imeson, John; Barnes, Janet M.; Cotterill, SJ; Gough, D. C. S.; Marsden, H. B.; Morris‐Jones, P. H.; Pearson, D

doi:10.1200/jco.1995.13.1.124

Cited by 121 publications

(70 citation statements)

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“…With this approach, SIOP reported a 4-year EFS rate of 83% [53]. In contrast, the first Wilms' tumor study by the United Kingdom Children's Cancer Study Group reported a survival rate of only 65% when radiation therapy was not given to patients with lung metastases [54]. This finding raises the question about the role of lung irradiation.…”

Section: Pros and Cons Of The Nwtsg And Siop Approachescontrasting

confidence: 46%

Current Therapy for Wilms’ Tumor

2005

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Section: Pros and Cons Of The Nwtsg And Siop Approachescontrasting

confidence: 46%

Current Therapy for Wilms’ Tumor

2005

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“…The average age at onset of Wilms tumour in this group is 34 months, considerably younger than expected for unilateral cases, raising the possibility of a Wilms tumour predisposition gene in this locus (Breslow et al, 1993). The distribution of stage-ofdisease at presentation is also skewed towards presentation with higher stage disease, 36% of patients having stage 4 disease compared to around 14% in the National Wilms tumour studies and the United Kingdom trials (Pritchard et al, 1995;D'Angio et al, 1989). Although the numbers in this review are very small, the possibility of an association between LOH for markers on 7p with earlier onset and more advanced disease is worth further investigation in a larger number of patients.…”

Section: Discussionmentioning

confidence: 92%

Loss of heterozygosity for the short arm of chromosome 7 in sporadic Wilms tumour

et al. 1998

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“…All patients referred to the Hospital for Sick Children, Great Ormond Street. with a histopathological diagnosis of Wilms' tumour were treated on sequential United Kingdom Children's Cancer Study Group protocols UKWI and UKW2 (Pritchard et al, 1995;CD Mitchell, personnal communication). All children received uniform treatment as per the protocol and have been followed up for at least 7 years.…”

Section: Methodsmentioning

confidence: 99%

“…a consequence of consistent improvement in treatment strategies (D'Ancio et al 1989: Pritchard et al 1995 (D'Angio et al 1981). The addition of doxorubicin to vincristine and actinomycin D in the National Wilms' Tumour Study (NWTS-3) improxed the relapse-free sun-ival bv 10%c and the overall survival by 5% in patients with favourable histology' stage 3 disease (D'Angio et al 1989).…”

mentioning

confidence: 99%

Loss of heterozygosity on chromosome 16 in sporadic Wilms' tumour

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Pritchard²,

Scambler³

et al. 1998

Br J Cancer

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Summary To establish whether loss of heterozygosity (LOH) for chromosome 16q in Wilms' tumours confers an adverse prognosis, DNA from 40 Wilms' tumour/normal pairs were analysed using highly polymorphic microsatellite markers along the length of 1 6q. Fifteen per cent of tumours showed LOH for 16q. Although the common region of allele loss spanned the 16q24-qter region, a second distinct region of LOH was identified in 16q21. (Coppes et al. 1992: Maw et al. 1992: Grundy et al. 1994: Austruy et al. 1995: Redeker et al 1996. Using a panel of informative markers for the region 16ql2.2-qter. Maw et al (1992) were the first to demonstrate LOH for 16q in 9 (20%c) of 45 informatiVe patients by Southem blot analysis. A larger follow--on study. as part of NWTS4. involving 232 patients. found a similar frequency of LOH at 17%7. but used only polymorphic markers that mapped to the distal 16q22-qter region (Grundv et al. 1994). In the study by Coppes et al (1992). using only two polymorphic markers mapping to 16q22.2 and 16q24.3. LOH was identified in 20% of tumours. The most recent studv. albeit in a relatively small group of patients (Austruy et al. 1995). found the highest level of LOH (25%7c) using a large panel of restriction length polymorphisms and microsatellite probes. Furthermore. LOH for 16q has been associated with a worse outcome because these patients have a relapse rate 3.3 times higher than those with tumours retaining heterozygosity for 16q (Grundy et al 1994).Because cytogenetic and molecular studies of Wilms' tumours clearly suggest a role for grenes on 16q in the molecular pathology of this tumour. we have undertaken LOH analysis for 16q markers using a large. well-characterized series of sporadic Wilms' tumours. Our results clearly show that LOH is relatively frequent in Wilms' tumours. especially in patients with an adverse outcome. MATERIALS AND METHODSDNA was prepared from tumour tissue and lymphocNies using standard phenol-chloroform extraction procedures described by Wadey et al (1990). The optimal polymerase chain reaction (PCR) conditions

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Results of the United Kingdom Children's Cancer Study Group first Wilms' Tumor Study.

Cited by 121 publications

References 14 publications

Current Therapy for Wilms’ Tumor

Current Therapy for Wilms’ Tumor

Loss of heterozygosity for the short arm of chromosome 7 in sporadic Wilms tumour

Loss of heterozygosity on chromosome 16 in sporadic Wilms' tumour

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