𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Chromosome arm 16q in Wilms tumors: Unbalanced chromosomal translocations, loss of heterozygosity, and assessment of the CTCF gene

✍ Scribed by Albert Yeh; Michelle Wei; Samuel B. Golub; Darrell J. Yamashiro; Vundavali V. Murty; Benjamin Tycko

Book ID
102844877
Publisher
John Wiley and Sons
Year
2002
Tongue
English
Weight
666 KB
Volume
35
Category
Article
ISSN
1045-2257

No coin nor oath required. For personal study only.

✦ Synopsis

Abstract

Chromosome arm 16q is a common site of loss of heterozygosity (LOH) in Wilms tumors (WTs). The mechanism and consequences of 16q LOH are not known, but the CTCF gene, in band 16q22, is a candidate target gene. CTCF protein binds to DNA upstream of the H19 gene on chromosome band 11p15, and maintains normal imprinting of H19 and IGF2. Thus, its loss might predispose to de novo methylation of the maternal allele of H19 and loss of imprinting (LOI) of IGF2 in WTs. We mapped Chr16 LOH in WTs and correlated this with unbalanced chromosomal translocations and histopathology. We also analyzed the CTCF gene for its mRNA and protein expression and DNA sequence, and we investigated correlations with methylation of H19^mat^. In our series, unbalanced t(1;16) chromosomal translocations were a major pathway for Chr16 loss of heterozygosity, and this LOH was correlated significantly with tumor anaplasia. CTCF mapped in the minimal region of Chr16 LOH. However, we found no correlation between Chr16 LOH, or loss of CTCF mRNA or protein, and methylation of H19^mat^. Some WTs contained reduced amounts of CTCF protein, but among these were cases with and without H19^mat^ methylation. Rare WTs with simultaneous 16q LOH and H19^mat^ methylation lacked CTCF mutations. These data argue against the CTCF gene as a target of Chr16 LOH in WTs, but leave open the possibility that post‐transcriptional loss of CTCF protein may account for some instances of LOI. Β© 2002 Wiley‐Liss, Inc.

πŸ“œ SIMILAR VOLUMES

Allele loss in Wilms tumors of chromosom
Allele loss in Wilms tumors of chromosome arms 11q, 16q, and 22q correlates with clinicopathological parameters
✍ Barbara Klamt; Michael Schulze; Claudia ThΓ€te; Jaroslav Mares; Peter Goetz; Roma πŸ“‚ Article πŸ“… 1998 πŸ› John Wiley and Sons 🌐 English βš– 101 KB πŸ‘ 1 views

An extended analysis for loss of heterozygosity (LOH) on eight chromosomes was conducted in a series of 82 Wilms tumors. Observed rates of allele loss were: 9.5% (1p), 5% (4q), 6% (6p), 3% (7p), 9.8% (11q), 28% (11p15), 13.4% (16q), 8.8% (18p), and 13.8% (22q). Known regions of frequent allele loss

Mutations/deletions of the WT1 gene, los
Mutations/deletions of the WT1 gene, loss of heterozygosity on chromosome arms 11p and 11q, chromosome ploidy and histology in Wilms' tumors in Japan
✍ Hisaya Nakadate; Kinji Yokomori; Naoki Watanabe; Takashi Tsuchiya; Takeshi Namik πŸ“‚ Article πŸ“… 2001 πŸ› John Wiley and Sons 🌐 French βš– 110 KB πŸ‘ 2 views

## Incidence rates of Wilms' tumor (WT) markedly differ in East Asian and Caucasian children. In the present study, we examined WT1 deletions/mutations and loss of heterozygosity (LOH) on 11p and 11q in a large number of WTs and compared our findings with those from 4 series of Caucasian WTs. Inci

Association of chromosome arm 16q loss w
Association of chromosome arm 16q loss with loss of imprinting of insulin-like growth factor–II in Wilms tumor
✍ Stephanie K. Mummert; Victor A. Lobanenkov; Andrew P. Feinberg πŸ“‚ Article πŸ“… 2005 πŸ› John Wiley and Sons 🌐 English βš– 128 KB πŸ‘ 2 views

## Abstract The most common known molecular defect in Wilms tumor (WT) of the kidney, the most frequent solid tumor of childhood, is loss of imprinting (LOI) of the insulin‐like growth factor–II gene (__IGF2__), which involves activation of the normally silent maternal allele of the gene and hyperm

Germline mutations of the POU6F2 gene in
Germline mutations of the POU6F2 gene in Wilms tumors with loss of heterozygosity on chromosome 7p14
✍ Daniela Perotti; Giovanna De Vecchi; Maria A. Testi; Elena Lualdi; Piergiorgio M πŸ“‚ Article πŸ“… 2004 πŸ› John Wiley and Sons 🌐 English βš– 201 KB πŸ‘ 2 views

Wilms tumor (WT) is a kidney malignancy of childhood characterized by highly heterogeneous genetic alterations. We previously reported the molecular and cytogenetic characterization of a WT (Case 30) carrying an interstitial deletion in chromosome 7p14 between markers D7S555 and D7S668. Loss of hete