Epigenetic differences between Wilms' tumours in white and east-Asian children. (Q51037846)

27 March 2018

title

Epigenetic differences between Wilms' tumours in white and east-Asian children. (English)

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27 March 2018

author

Ian Morison

3

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27 March 2018

Tony Reeve

10

object named as

Anthony E Reeve

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27 March 2018

author name string

Ryuji Fukuzawa

1

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27 March 2018

Norman E Breslow

2

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27 March 2018

Patrick Dwyer

4

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27 March 2018

Takeshi Kusafuka

5

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27 March 2018

Yasutsugu Kobayashi

6

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27 March 2018

David M Becroft

7

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27 March 2018

J Bruce Beckwith

8

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27 March 2018

Elizabeth J Perlman

9

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27 March 2018

language of work or name

English

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publication date

1 February 2004

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27 March 2018

published in

The Lancet

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27 March 2018

volume

363

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27 March 2018

issue

9407

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27 March 2018

page(s)

446-451

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27 March 2018

Epidemiology of Wilms tumor

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Epigenetic lesions at the H19 locus in Wilms' tumour patients

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Epigenetic changes encompassing the IGF2/H19 locus associated with relaxation of IGF2 imprinting and silencing of H19 in Wilms tumor

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Increased expression of the insulin-like growth factor-II gene in Wilms' tumor is not dependent on loss of genomic imprinting or loss of heterozygosity

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Epigenetic changes at the insulin-like growth factor II/H19 locus in developing kidney is an early event in Wilms tumorigenesis.

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Nephrogenic rests and the pathogenesis of Wilms tumor: developmental and clinical considerations

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Loss of Imprinting of Insulin-Like Growth Factor-II (IGF2) Gene in Distinguishing Specific Biologic Subtypes of Wilms Tumor

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Loss of allelic heterozygosity at a second locus on chromosome 11 in sporadic Wilms' tumor cells

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Methylation sequencing analysis refines the region of H19 epimutation in Wilms tumor

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Loss of imprinting of a paternally expressed transcript, with antisense orientation to KVLQT1, occurs frequently in Beckwith-Wiedemann syndrome and is independent of insulin-like growth factor II imprinting

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Loss of methylation at chromosome 11p15.5 is common in human adult tumors

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The treatment of Wilms' Tumor: Results of the second national Wilms' Tumor study

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

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Mutations/deletions of the WT1 gene, loss of heterozygosity on chromosome arms 11p and 11q, chromosome ploidy and histology in Wilms' tumors in Japan

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Loss of IGF2 imprinting: a potential marker of colorectal cancer risk

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Disruption of imprinting caused by deletion of the H19 gene region in mice

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7 January 2021

Disruption of insulin-like growth factor 2 imprinting in Beckwith-Wiedemann syndrome

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7 January 2021

10.1016/S0140-6736(04)15491-3

Identifiers

DOI

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27 March 2018

1 reference

27 March 2018