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

研究成果: Article査読

21 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)592-601
ページ数10
ジャーナルGenes Chromosomes and Cancer
45
6
DOI
出版ステータスPublished - 2006 6月
外部発表はい

ASJC Scopus subject areas

  • 遺伝学
  • 癌研究

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