Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Genetic and epigenetic alterations on the short arm of chromosome 11 are involved in a majority of sporadic Wilms' tumours.

British journal of cancer - 21 Aug 2006

Satoh Y, Nakadate H, Nakagawachi T, Higashimoto K, Joh K, Masaki Z, Uozumi J, Kaneko Y, Mukai T, Soejima H

Abstract excerpt

Wilms' tumour is one of the most common solid tumours of childhood. 11p13 (WT1 locus) and 11p15.5 (WT2 locus) are known to have genetic or epigenetic aberrations in these tumours. In Wilms' tumours, mutation of the Wilms tumour 1 (WT1) gene at the WT1 locus has been reported, and the WT2 locus, comprising the two independent imprinted domains IGF2/H19 and KIP2/LIT1, can undergo maternal deletion or alterations...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to beta Catenin
Share to Chromosomes, Human, Pair 11

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Cyclin-Dependent Kinase Inhibitor p57

Share to Genes, Wilms Tumor

Share to Insulin-Like Growth Factor II

Share to Kidney Neoplasms

Share to Loss of Heterozygosity

Share to Wilms Tumor

Source

Open in PubMed Open full text

Identifiers

PMID: 16909133
DOI: 10.1038/sj.bjc.6603302
PMCID: PMC2360663

Genes

IGF2
CTNNB1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Genetic and epigenetic alterations on the short arm of chromosome 11 are involved in a majority of sporadic Wilms' tumours.PMID 16909133Read ↗

Duplication of paternal IGF2 or loss of maternal IGF2 imprinting occurs in half of Wilms tumors with various structural WT1 abnormalities.Semantic proximity Read ↗

Genomic profiling maps loss of heterozygosity and defines the timing and stage dependence of epigenetic and genetic events in Wilms' tumors.Semantic proximity Read ↗

Genomic imbalances pinpoint potential oncogenes and tumor suppressors in Wilms tumorsSemantic proximity Read ↗

Allelotyping in Wilms tumors identifies a putative third tumor suppressor gene on chromosome 11.Semantic proximity Read ↗

Loss of heterozygosity at 11p13 in Wilms' tumours does not necessarily involve mutations in the WT1 gene.Semantic proximity Read ↗

The Genetic and Epigenetic Features of Bilateral Wilms Tumor Predisposition: A Report from the Children's Oncology Group AREN18B5-Q StudySemantic proximity Read ↗

The molecular biology of Wilms' tumourSemantic proximity Read ↗

Multiple genetic abnormalities of 11p15 in Wilms' tumor.Semantic proximity Read ↗

Stratification of Wilms tumor by genetic and epigenetic analysis.Semantic proximity Read ↗

Tumor development in the Beckwith-Wiedemann syndrome is associated with a variety of constitutional molecular 11p15 alterations including imprinting defects of KCNQ1OT1.Semantic proximity Read ↗

Recent advances in Wilms' tumor predisposition.Semantic proximity Read ↗

Wilms tumor genetics: mutations in WT1, WTX, and CTNNB1 account for only about one-third of tumors.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.