Association of 11q loss, trisomy 12, and possible 16q loss with loss of imprinting of insulin-like growth factor-II in Wilms tumor

Naoki Watanabe, Hisaya Nakadate, Masayuki Haruta, Waka Sugawara, Fumiaki Sasaki, Yukiko Tsunematsu, Atsushi Kikuta, Masahiro Fukuzawa, Hajime Okita, Jun Ichi Hata, Hidenobu Soejima, Yasuhiko Kaneko

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

We evaluated the WT1 and IGF2 status and performed chromosome and/or comparative genomic hybridization analysis in 43 tumor samples from patients with Wilms tumor. On this basis, we classified them into 4 groups: WT1 abnormality, loss of heterozygosity (LOH) of IGF2, loss of imprinting (LOI) of IGF2, and retention of imprinting (ROI) of IGF2, which were seen in 12%, 30%, 16%, and 42% of the tumors, respectively. Patients in the LOI group were older than those in other groups (P < 0.01), and tumors in the WT1 group had fewer cytogenetic changes than did those in the other groups (P < 0.01). It was found that 11q- and +12 were more frequent in the LOI group than in the WT1+LOH+ROI group (P < 0.01 and P < 0.01). There was no difference in the incidence of 16q- between the LOI group and the other groups; however, when we excluded 16 tumors with LOH on 11p15, 16q- tended to be more frequent in the LOI group than in the WT1/+ROI group (P = 0.06). The association of 11q- or +12 with LOI of IGF2 found in the present study suggests that many tumors with no WT1 abnormalities need overexpression of IGF2 together with biallelic inactivation of the tumor-suppressor gene on 11q and/or overexpression of growth-promoting genes on chromosome 12. The 11q gene may code for one of the proteins that constitute a CTCF insulator complex, and its mutation, deletion, or haploinsufficiency may cause insulator abnormalities that might lead to LOI of IGF2.

Original languageEnglish
Pages (from-to)592-601
Number of pages10
JournalGenes Chromosomes and Cancer
Volume45
Issue number6
DOIs
Publication statusPublished - 2006 Jun
Externally publishedYes

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Insulin-Like Growth Factor II
Wilms Tumor
Loss of Heterozygosity
Neoplasms
Haploinsufficiency
Chromosomes, Human, Pair 12
Comparative Genomic Hybridization
Sequence Deletion
Tumor Suppressor Genes
Cytogenetics
Genes
Chromosomes
Chromosome 11q trisomy
Incidence
Growth
Proteins

ASJC Scopus subject areas

  • Cancer Research
  • Genetics

Cite this

Association of 11q loss, trisomy 12, and possible 16q loss with loss of imprinting of insulin-like growth factor-II in Wilms tumor. / Watanabe, Naoki; Nakadate, Hisaya; Haruta, Masayuki; Sugawara, Waka; Sasaki, Fumiaki; Tsunematsu, Yukiko; Kikuta, Atsushi; Fukuzawa, Masahiro; Okita, Hajime; Hata, Jun Ichi; Soejima, Hidenobu; Kaneko, Yasuhiko.

In: Genes Chromosomes and Cancer, Vol. 45, No. 6, 06.2006, p. 592-601.

Research output: Contribution to journalArticle

Watanabe, N, Nakadate, H, Haruta, M, Sugawara, W, Sasaki, F, Tsunematsu, Y, Kikuta, A, Fukuzawa, M, Okita, H, Hata, JI, Soejima, H & Kaneko, Y 2006, 'Association of 11q loss, trisomy 12, and possible 16q loss with loss of imprinting of insulin-like growth factor-II in Wilms tumor', Genes Chromosomes and Cancer, vol. 45, no. 6, pp. 592-601. https://doi.org/10.1002/gcc.20321
Watanabe, Naoki ; Nakadate, Hisaya ; Haruta, Masayuki ; Sugawara, Waka ; Sasaki, Fumiaki ; Tsunematsu, Yukiko ; Kikuta, Atsushi ; Fukuzawa, Masahiro ; Okita, Hajime ; Hata, Jun Ichi ; Soejima, Hidenobu ; Kaneko, Yasuhiko. / Association of 11q loss, trisomy 12, and possible 16q loss with loss of imprinting of insulin-like growth factor-II in Wilms tumor. In: Genes Chromosomes and Cancer. 2006 ; Vol. 45, No. 6. pp. 592-601.
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abstract = "We evaluated the WT1 and IGF2 status and performed chromosome and/or comparative genomic hybridization analysis in 43 tumor samples from patients with Wilms tumor. On this basis, we classified them into 4 groups: WT1 abnormality, loss of heterozygosity (LOH) of IGF2, loss of imprinting (LOI) of IGF2, and retention of imprinting (ROI) of IGF2, which were seen in 12{\%}, 30{\%}, 16{\%}, and 42{\%} of the tumors, respectively. Patients in the LOI group were older than those in other groups (P < 0.01), and tumors in the WT1 group had fewer cytogenetic changes than did those in the other groups (P < 0.01). It was found that 11q- and +12 were more frequent in the LOI group than in the WT1+LOH+ROI group (P < 0.01 and P < 0.01). There was no difference in the incidence of 16q- between the LOI group and the other groups; however, when we excluded 16 tumors with LOH on 11p15, 16q- tended to be more frequent in the LOI group than in the WT1/+ROI group (P = 0.06). The association of 11q- or +12 with LOI of IGF2 found in the present study suggests that many tumors with no WT1 abnormalities need overexpression of IGF2 together with biallelic inactivation of the tumor-suppressor gene on 11q and/or overexpression of growth-promoting genes on chromosome 12. The 11q gene may code for one of the proteins that constitute a CTCF insulator complex, and its mutation, deletion, or haploinsufficiency may cause insulator abnormalities that might lead to LOI of IGF2.",
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AU - Watanabe, Naoki

AU - Nakadate, Hisaya

AU - Haruta, Masayuki

AU - Sugawara, Waka

AU - Sasaki, Fumiaki

AU - Tsunematsu, Yukiko

AU - Kikuta, Atsushi

AU - Fukuzawa, Masahiro

AU - Okita, Hajime

AU - Hata, Jun Ichi

AU - Soejima, Hidenobu

AU - Kaneko, Yasuhiko

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N2 - We evaluated the WT1 and IGF2 status and performed chromosome and/or comparative genomic hybridization analysis in 43 tumor samples from patients with Wilms tumor. On this basis, we classified them into 4 groups: WT1 abnormality, loss of heterozygosity (LOH) of IGF2, loss of imprinting (LOI) of IGF2, and retention of imprinting (ROI) of IGF2, which were seen in 12%, 30%, 16%, and 42% of the tumors, respectively. Patients in the LOI group were older than those in other groups (P < 0.01), and tumors in the WT1 group had fewer cytogenetic changes than did those in the other groups (P < 0.01). It was found that 11q- and +12 were more frequent in the LOI group than in the WT1+LOH+ROI group (P < 0.01 and P < 0.01). There was no difference in the incidence of 16q- between the LOI group and the other groups; however, when we excluded 16 tumors with LOH on 11p15, 16q- tended to be more frequent in the LOI group than in the WT1/+ROI group (P = 0.06). The association of 11q- or +12 with LOI of IGF2 found in the present study suggests that many tumors with no WT1 abnormalities need overexpression of IGF2 together with biallelic inactivation of the tumor-suppressor gene on 11q and/or overexpression of growth-promoting genes on chromosome 12. The 11q gene may code for one of the proteins that constitute a CTCF insulator complex, and its mutation, deletion, or haploinsufficiency may cause insulator abnormalities that might lead to LOI of IGF2.

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