title: Mutations/deletions of the WT1 gene, loss of heterozygosity on chromosome arms 11p and 11q, chromosome ploidy and histology in Wilms' tumors in Japan.
abstract: Incidence rates of Wilms' tumor (WT) markedly differ in East Asian and Caucasian children. In the present study, we examined WT1 deletions/mutations and loss of heterozygosity (LOH) on 11p and 11q in a large number of WTs and compared our findings with those from 4 series of Caucasian WTs. Incidence rates of the subtle WT1 mutation in 3 of the 5 series of sporadic and unilateral WTs including ours were 4.3-6.2% and similar. However, gross homozygous WT1 deletion was more frequent in our series than in some others. In addition, our series tended to show a higher incidence of LOH limited to 11p13 and a lower incidence of LOH including 11p15 than the Caucasian one. These findings indicate some genetic differences in WT between the 2 regions. One of the 4 Caucasian series reported a correlation of germinal WT1 mutation with the predominantly stromal histology. The present study not only confirms the correlation of germinal WT1 deletion/mutation with predominant stromal histology but also establishes a correlation with somatic WT1 deletion/mutations with predominant stromal histology. While WTs with WT1 abnormalities usually showed pseudodiploidy and predominant stromal histology, those without WT1 abnormalities showed various chromosome numbers and histologic subtypes.
authors.affiliation: Saitama Cancer Center Hospital, Saitama, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Nakadate
authors.forename: K
authors.initials: K
authors.lastname: Yokomori
authors.forename: N
authors.initials: N
authors.lastname: Watanabe
authors.forename: T
authors.initials: T
authors.lastname: Tsuchiya
authors.forename: T
authors.initials: T
authors.lastname: Namiki
authors.forename: H
authors.initials: H
authors.lastname: Kobayshi
authors.forename: S
authors.initials: S
authors.lastname: Suita
authors.forename: Y
authors.initials: Y
authors.lastname: Tsunematsu
authors.forename: Y
authors.initials: Y
authors.lastname: Horikoshi
authors.forename: Y
authors.initials: Y
authors.lastname: Hatae
authors.forename: M
authors.initials: M
authors.lastname: Endo
authors.forename: Y
authors.initials: Y
authors.lastname: Komada
authors.forename: H
authors.initials: H
authors.lastname: Eguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Toyoda
authors.forename: A
authors.initials: A
authors.lastname: Kikuta
authors.forename: R
authors.initials: R
authors.lastname: Kobayashi
authors.forename: Y
authors.initials: Y
authors.lastname: Kaneko
mesh_terms: D000483:Alleles; D044466:Asian People; D002648:Child; D002675:Child, Preschool; D002869:Chromosome Aberrations; D002880:Chromosomes, Human, Pair 11; D005260:Female; D017353:Gene Deletion; D006720:Homozygote; D006801:Humans; D007223:Infant; D007564:Japan; D019656:Loss of Heterozygosity; D008297:Male; D009154:Mutation; D011003:Ploidies; D025721:WT1 Proteins / Q000235:genetics*; D044465:White People; D009396:Wilms Tumor / Q000208:ethnology / Q000235:genetics*
chemical_list: D025721:WT1 Proteins