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 1
Externally publishedYes

ASJC Scopus subject areas

  • Genetics
  • Cancer Research

Fingerprint Dive into the research topics of 'Association of 11q loss, trisomy 12, and possible 16q loss with loss of imprinting of insulin-like growth factor-II in Wilms tumor'. Together they form a unique fingerprint.

  • Cite this

    Watanabe, N., Nakadate, H., Haruta, M., Sugawara, W., Sasaki, F., Tsunematsu, Y., Kikuta, A., Fukuzawa, M., Okita, H., Hata, J. I., 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, 45(6), 592-601. https://doi.org/10.1002/gcc.20321