Allelic loss on chromosome 11p is a less frequent event in bilateral than in unilateral Wilms' tumours

Little, Melissa H.; Clarke, Jo; Byrne, Jennifer A.; Dunn, Roseanne S.; Smith, Peter J.

doi:10.1016/0959-8049(92)90027-y

Cited by 16 publications

(4 citation statements)

References 18 publications

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“…In sporadic WT, at least 5% carry intragenic WT1 mutations with a further 10% demonstrating gross WT1 rearrangements. 11p LOH is lower in bilateral Wilms' tumour (Little et al, 1992a), whereas bilateral tumours appear to show intragenic WT1 mutations more often. As earlier discussed, familial WT represents only 1% of all WT, is rarely associated with other anomalies and has never been linked to 11p13 (Huff et al, 1988), suggesting that WT1 screening is not useful here.…”

Section: A Clinical Perspectivementioning

confidence: 90%

A clinical overview of WT1 gene mutations

1997

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Section: A Clinical Perspectivementioning

confidence: 90%

A clinical overview of WT1 gene mutations

1997

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“… 25 ) and LOI by LOH was shown to occur infrequently in bilateral tumours compared with unilateral (Ref. 38 ). Therefore, despite a relatively low penetrance level, LOI by gain of methylation at 11p15 is clearly associated with both unilateral and bilateral WTs, indicating a disruption in normal epigenetic control.…”

Section: Wt Predisposition Syndromesmentioning

confidence: 99%

Bilateral Wilms tumour: a review of clinical and molecular features

Charlton

Irtan

Bergeron

et al. 2017

Expert Rev. Mol. Med.

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Wilms tumour (WT) is the most common paediatric kidney cancer and affects approximately one in 10 000 children. The tumour is associated with undifferentiated embryonic lesions called nephrogenic rests (NRs) or, when diffuse, nephroblastomatosis. WT or NRs can occur in both kidneys, termed bilateral disease, found in only 5–8% of cases. Management of bilateral WT presents a major clinical challenge in terms of maximising survival, preserving renal function and understanding underlying genetic risk. In this review, we compile clinical data from 545 published cases of bilateral WT and discuss recent progress in understanding the molecular basis of bilateral WT and its associated precursor NRs in the context of the latest radiological, surgical and epidemiological features.

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“…T h e majority of imprinted genes identified to date, including ZGFZ and H19, are expressed from the same parental allele in both species. Loss of the presumed maternally expressed ~57~"' allele in Wilms' tumor with LOH of llp15.5 would result in functional Five patient samples were chosen in which RFLP analysis by Southern blotting had identified complete loss of heterozygosity (LOH) of the llp15.5 region in primary Wilms' tumor using methods previously described (data not shown) (Little et al, 1992). RNA prepared from Wilms' tumor and normal kidney tissue were reverse transcribed using AMV reverse transcriptase (Promega) and resulting cDNA was amplified by PCR.…”

Section: ~5 7~' "mentioning

confidence: 99%