Loss of heterozygosity at 7p in Wilms’ tumour development

Powlesland, Rachel M.; Charles, Adrian; Malik, Karim; Reynolds, Paul A.; Pires, Sara Xavier; Boavida, Maria Guida; Brown, Keith

doi:10.1054/bjoc.1999.0922

Cited by 35 publications

(40 citation statements)

References 39 publications

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“…To investigate the relationship between LOI at 11p13 and LOI at 11p15 in WT, we initially characterized a cohort of 51 WTs for LOH status using RFLP and/or microsatellite polymorphisms on 11p (23,24). We found 28 WTs that retained heterozygosity at 11p13 and 11p15 (and one that was heterozygous at 11p13 but had LOH at 11p15) and were therefore suitable for LOI analysis.…”

Section: Resultsmentioning

confidence: 99%

“…We therefore examined 11p13 and 11p15 imprinting in two examples of hyperplastic perilobar NRs dissected from adjacent to tumors WT62 and WT65 to determine the timing of LOI at 11p13 and 11p15 and their relationship to LOH at 16q and 7p, two loci associated with WT progression (24,29). These two patients had multiple perilobar NRs that were macroscopically visible and well separated from tumor tissue (see Supplementary Fig.…”

Section: Imprinting Changes During Wt Progressionmentioning

confidence: 99%

“…Previously, we have used this approach to show that 11p LOH and WT1 mutation are relatively early events in WT development, being found in NRs, whereas 16q and 7p LOH appear as later events, being confined to tumor tissue (24,29).…”

Section: Loi In Wt Progressionmentioning

confidence: 99%

“…LOH was assessed using RFLP and/or microsatellite polymorphisms on 7p, 11p, and 16q as previously described (23,24).…”

Section: Loh Analysismentioning

confidence: 99%

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Frequency and Timing of Loss of Imprinting at 11p13 and 11p15 in Wilms' Tumor Development

Brown

Power

Moore

et al. 2008

Molecular Cancer Research

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Epigenetic changes occur frequently in Wilms' tumor (WT), especially loss of imprinting (LOI) of IGF2/H19 at 11p15. Our previous results have identified imprinted transcripts (WT1-AS and AWT1) from the WT1 locus at 11p13 and showed LOI of these in some WTs. In this article, we set out to test the relationship between LOI at 11p13 and 11p15 and their timing in WT progression relative to other genetic changes. We found a higher level (83%) of 11p13 LOI in WT than of 11p15 LOI (71%). There was no correlation between methylation levels at the 11p13 and 11p15 differentially methylated regions or between allelic expression of WT1-AS/AWT1 and IGF2. Interestingly, retention of normal imprinting at 11p13 was associated with a small group of relatively late-onset, high-stage WTs. An examination of genetic and epigenetic alterations in nephrogenic rests, which are premalignant WT precursors, showed that LOI at both 11p13 and 11p15 occurred before either 16q loss of heterozygosity (LOH) or 7p LOH. This suggests that these LOH events are very unlikely to be a cause of LOI but that LOH may act by potentiating the effects of overexpression of IGF2 and/or WT1-AS/AWT1 that

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Section: Resultsmentioning

confidence: 99%

Section: Imprinting Changes During Wt Progressionmentioning

confidence: 99%

Section: Loi In Wt Progressionmentioning

confidence: 99%

“…LOH was assessed using RFLP and/or microsatellite polymorphisms on 7p, 11p, and 16q as previously described (23,24).…”

Section: Loh Analysismentioning

confidence: 99%

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Frequency and Timing of Loss of Imprinting at 11p13 and 11p15 in Wilms' Tumor Development

Brown

Power

Moore

et al. 2008

Molecular Cancer Research

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“…The resulting 16q hemizygosity correlates positively with tumor anaplasia (14,15). Other chromosomes previously implicated by cytogenetics and/or LOH include losses and gains of portions of chromosome 1 (16), abnormalities of chromosome 7, notably i(7p) in which the p-arm is lost and q-arm is reduplicated (17)(18)(19)(20)(21), and loss of chromosome 14q (22). To examine LOH at higher resolution and with complete genomic coverage and to gain insights into the relationship between genetic and epigenetic events in Wilms' tumors, we have carried out a genome-wide scan at high resolution in syndromic (WAGR or Denys-Drash) and sporadic Wilms' tumors using Affymetrix 10K single nucleotide polymorphism (SNP) chips.…”

Section: Introductionmentioning

confidence: 99%

Genomic Profiling Maps Loss of Heterozygosity and Defines the Timing and Stage Dependence of Epigenetic and Genetic Events in Wilms' Tumors

Yuan

Yamashiro³

et al. 2005

Molecular Cancer Research

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To understand genetic and epigenetic pathways in Wilms' tumors, we carried out a genome scan for loss of heterozygosity (LOH) using Affymetrix 10K single nucleotide polymorphism (SNP) chips and supplemented the data with karyotype information. To score loss of imprinting (LOI) of the IGF2 gene, we assessed DNA methylation of the H19 5V differentially methylated region (DMR). Few chromosomal regions other than band 11p13 (WT1) were lost in Wilms' tumors from Denys-Drash and Wilms' tumor-aniridia syndromes, whereas sporadic Wilms' tumors showed LOH of several regions, most frequently 11p15 but also 1p, 4q, 7p, 11q, 14q, 16q, and 17p. LOI was common in the sporadic Wilms' tumors but absent in the syndromic cases. The SNP chips identified novel centers of LOH in the sporadic tumors, including a 2.4-Mb minimal region on chromosome 4q24-q25. Losses of chromosomes 1p, 14q, 16q, and 17p were more common in tumors presenting at an advanced stage; 11p15 LOH was seen at all stages, whereas LOI was associated with early-stage presentation. Wilms' tumors with LOI often completely lacked LOH in the genome-wide analysis, and in some tumors with concomitant 16q LOH and LOI, the loss of chromosome 16q was mosaic, whereas the H19 DMR methylation was complete. These findings confirm molecular differences between sporadic and syndromic Wilms' tumors, define regions of recurrent LOH, and indicate that gain of methylation at the H19 DMR is an early event in Wilms' tumorigenesis that is independent of chromosomal losses. The data further suggest a biological difference between sporadic Wilms' tumors with and without LOI. (Mol Cancer Res 2005;3(9):493 -502)

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Characterization of a Wilms tumor in a 9‐year‐old girl with trisomy 18

Anderson

Punnett

Huff

et al. 2003

American J of Med Genetics Pt A

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This is a report of a trisomy 18 patient who developed Wilms tumor in conjunction with perilobar nephroblastomatosis (NB) at 9 years and 5 months of age. Review of the literature revealed that most patients with trisomy 18 who develop Wilms tumor, do so at a later than expected age for a tumor related to NB, and are females. In this case, no chromosome 11 WT1 mutation was detected by PCR/SSCP analysis, but the tumor had in addition to the trisomy, an isochromosome 7q and loss of heterozygosity at 16q, two mutations that have been linked independently to Wilms tumorigenesis.

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Loss of heterozygosity at 7p in Wilms’ tumour development

Cited by 35 publications

References 39 publications

Frequency and Timing of Loss of Imprinting at 11p13 and 11p15 in Wilms' Tumor Development

Frequency and Timing of Loss of Imprinting at 11p13 and 11p15 in Wilms' Tumor Development

Genomic Profiling Maps Loss of Heterozygosity and Defines the Timing and Stage Dependence of Epigenetic and Genetic Events in Wilms' Tumors

Characterization of a Wilms tumor in a 9‐year‐old girl with trisomy 18

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