PMID- 10598141 OWN - NLM STAT- MEDLINE DCOM- 20000105 LR - 20190816 IS - 0165-4608 (Print) IS - 0165-4608 (Linking) VI - 115 IP - 2 DP - 1999 Dec TI - Hemizygous deletions of chromosome band 16q24 in Wilms tumor: detection by fluorescence in situ hybridization. PG - 100-5 AB - Loss of heterozygosity (LOH) for markers on chromosome arm 16q in Wilms tumor has been linked to an increased risk of treatment failure. We therefore postulated that fluorescence in situ hybridization (FISH) with probes from this region might enhance current strategies for identifying high-risk patients at diagnosis. In a blinded comparative pilot study of 19 Wilms tumor samples from 18 patients with favorable histology, FISH and DNA polymorphism analysis yielded concordant results in 14 cases, either retention (n = 6) or loss (n = 8) of chromosome arm 16q markers. Discordant findings in 4 of the 5 remaining cases resulted from detection of LOH, but no loss by FISH. Two of these cases, directly comparable at marker D16S422, appeared to have tumor-specific uniparental disomy, in that 2 copies of D16S422 and the 16 centromere were evident, despite LOH. In 2 other cases, the discrepancies could be explained by LOH confined to loci distal to the D16S422 locus. In the fifth case, FISH detected 2 distinct populations of tumor cells, one characterized by normal diploidy and the other by monosomy 16, whereas DNA polymorphism analysis failed to indicate LOH altogether. Thus, FISH confirmed the presence of allelic loss (hence, the possible location of biologically important tumor suppressor genes) on the distal long arm of chromosome 16 in cases of favorable-histology Wilms tumor, with the advantages of technical simplicity, successful analysis of samples that were otherwise uninformative by analysis of DNA polymorphisms, and the addition of internal controls for chromosomal aneusomy. We suggest that combined analysis of the chromosome 16q region in Wilms tumor by FISH and DNA polymorphism analysis would improve evaluations to identify high-risk patients who might benefit from alternative therapy. FAU - Shearer, P D AU - Shearer PD AD - Department of Hematology/Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. FAU - Valentine, M B AU - Valentine MB FAU - Grundy, P AU - Grundy P FAU - DeCou, J M AU - DeCou JM FAU - Banavali, S D AU - Banavali SD FAU - Komuro, H AU - Komuro H FAU - Green, D M AU - Green DM FAU - Beckwith, J B AU - Beckwith JB FAU - Look, A T AU - Look AT LA - eng GR - CA21765/CA/NCI NIH HHS/United States GR - CA71907/CA/NCI NIH HHS/United States PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Cancer Genet Cytogenet JT - Cancer genetics and cytogenetics JID - 7909240 RN - 0 (DNA, Neoplasm) SB - IM MH - Child MH - Child, Preschool MH - *Chromosome Deletion MH - *Chromosomes, Human, Pair 16 MH - DNA, Neoplasm/analysis MH - Female MH - Homozygote MH - Humans MH - *In Situ Hybridization, Fluorescence MH - Infant MH - Kidney Neoplasms/*genetics MH - Loss of Heterozygosity MH - Male MH - Polymorphism, Genetic MH - Wilms Tumor/*genetics EDAT- 1999/12/22 00:00 MHDA- 1999/12/22 00:01 CRDT- 1999/12/22 00:00 PHST- 1999/12/22 00:00 [pubmed] PHST- 1999/12/22 00:01 [medline] PHST- 1999/12/22 00:00 [entrez] AID - S016546089900093X [pii] AID - 10.1016/s0165-4608(99)00093-x [doi] PST - ppublish SO - Cancer Genet Cytogenet. 1999 Dec;115(2):100-5. doi: 10.1016/s0165-4608(99)00093-x.