PMID- 17639583
OWN - NLM
STAT- MEDLINE
DCOM- 20071025
LR  - 20070807
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 46
IP  - 10
DP  - 2007 Oct
TI  - Duplication of the paternal IGF2 allele in trisomy 11 and elevated expression 
      levels of IGF2 mRNA in congenital mesoblastic nephroma of the cellular or mixed 
      type.
PG  - 929-35
AB  - In a metaphase comparative genomic hybridization and fluorescence in situ 
      hybridization study of 13 congenital mesoblastic nephroma (CMN) tumors, trisomy 
      11 was found in seven cellular or mixed type tumors, disomy 11 with other 
      chromosome changes in two cellular type tumors, and no chromosome changes in four 
      classical type tumors. Reverse-transcription (RT)-PCR analysis detected the 
      ETV6-NTRK3 fusion transcript in all eight cellular or mixed type tumors examined, 
      but not in four classical type tumors. All seven tumors with trisomy 11 showed 
      duplication of the paternal IGF2 allele, and six cellular or classical type 
      tumors with disomy 11 showed one paternal and one maternal allele of IGF2, 
      analyzing the methylation status of the sixth CTCF site of the H19-differentially 
      methylated region. Allelic expression study using the ApaI/AvaII polymorphism 
      site at exon 9 of IGF2 showed retention of imprinting in all seven tumors 
      examined. Quantitative real-time RT-PCR analysis showed higher expression levels 
      of IGF2 mRNA in three of three cellular type tumors with trisomy 11, in one 
      cellular type tumor with disomy 11, and in three of four classical tumors than in 
      fetal kidneys or normal kidney tissues. Thus, duplicated paternal IGF2 resulted 
      in elevated IGF2 mRNA levels, and may provide CMN or its precursor cells with a 
      proliferative advantage. The mechanism explaining that some cellular or classical 
      type tumors with disomy 11 also showed elevated IGF2 mRNA levels remains 
      unresolved. IGF2 clearly plays an important role in the tumorigenic process of 
      CMN, although it is difficult to assess its exact role.
CI  - Copyright (c) 2007 Wiley-Liss, Inc.
FAU - Watanabe, Naoki
AU  - Watanabe N
AD  - Department of Cancer Diagnosis, Research Institute for Clinical Oncology, Saitama 
      Cancer Center, Ina, Saitama, and Department of Pediatrics, Juntendo University, 
      Nerima Hospital, Tokyo, Japan.
FAU - Haruta, Masayuki
AU  - Haruta M
FAU - Soejima, Hidenobu
AU  - Soejima H
FAU - Fukushi, Daisuke
AU  - Fukushi D
FAU - Yokomori, Kinji
AU  - Yokomori K
FAU - Nakadate, Hisaya
AU  - Nakadate H
FAU - Okita, Hajime
AU  - Okita H
FAU - Hata, Jun-ich
AU  - Hata JI
FAU - Fukuzawa, Masahiro
AU  - Fukuzawa M
FAU - Kaneko, Yasuhiko
AU  - Kaneko Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
RN  - 0 (ETV6-NTRK3 fusion protein, human)
RN  - 0 (Oncogene Proteins, Fusion)
RN  - 0 (RNA, Messenger)
RN  - 67763-97-7 (Insulin-Like Growth Factor II)
SB  - IM
MH  - Alleles
MH  - Chromosomes, Human, Pair 11/*genetics
MH  - Female
MH  - *Gene Duplication
MH  - Genomic Imprinting
MH  - Humans
MH  - Infant
MH  - Infant, Newborn
MH  - Insulin-Like Growth Factor II/*genetics
MH  - Kidney Neoplasms/congenital/genetics/metabolism
MH  - Male
MH  - Nephroma, Mesoblastic/congenital/*genetics/metabolism
MH  - Oncogene Proteins, Fusion/genetics/metabolism
MH  - RNA, Messenger/*genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Translocation, Genetic
MH  - *Trisomy
EDAT- 2007/07/20 09:00
MHDA- 2007/10/27 09:00
CRDT- 2007/07/20 09:00
PHST- 2007/07/20 09:00 [pubmed]
PHST- 2007/10/27 09:00 [medline]
PHST- 2007/07/20 09:00 [entrez]
AID - 10.1002/gcc.20481 [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2007 Oct;46(10):929-35. doi: 10.1002/gcc.20481.