Allelotype of pediatric rhabdomyosarcoma

Mike Visser; Carin Sijmons; Johannes Bras; Robert J. Arceci; Mark Godfried; Linda J. Valentijn; P. A. Voûte; Frank Baas

doi:10.1038/sj.onc.1201302

Allelotype of pediatric rhabdomyosarcoma

Mike Visser, Carin Sijmons, Johannes Bras, Robert J. Arceci, Mark Godfried, Linda J. Valentijn, P. A. Voûte, Frank Baas

Research output: Contribution to journal › Article › peer-review

85 Scopus citations

Abstract

An allelotype covering all autosomes was constructed for the embryonal form of childhood rhabdomyosarcoma (ERMS) in order to identify regions encompassing tumorsuppressor genes (TSG) involved in ERMS. Thusfar most studies were focussed on chromosome 11p15.5, which frequently shows loss of heterozygozity (LOH) in embryonal tumors like RMS and Wilms' tumor (WT). In this study we show that, besides LOH of chromosome 11p15.5 (72%), LOH of chromosome 16q was present in 54% of the tumors analysed. Delineation of these two regions shows that the smallest region of overlap (SRO) for chromosome 11 was between D11S988 and D11S922. This region, estimated to be 7 cM and 3-5 Mb, is also the location of the putative Wilms) tumor WT2 TSG. It contains several genes including IGF2 and potential tumorsuppressor genes like H19 and p57(kip2), which might contribute to the carcinogenesis of RMS. Analysis of chromosome 16q LOH defined the SRO between D16S752 and D16S413. LOH of chromosome 16 is also found in other tumors, including WT. Our data suggest that genes involved in the development of RMS and WT may not only be similar for chromosome 11 but also for chromosome 16.

Original language	English (US)
Pages (from-to)	1309-1314
Number of pages	6
Journal	Oncogene
Volume	15
Issue number	11
DOIs	https://doi.org/10.1038/sj.onc.1201302
State	Published - 1997
Externally published	Yes

Keywords

Alleotype
LOH, loss of heterozygosity
RMS
Rhabdomyosarcoma
SRD
TSG, tumor suppressor gene

ASJC Scopus subject areas

Molecular Biology
Genetics
Cancer Research

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10.1038/sj.onc.1201302

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@article{c6f671918a99458fbce083a9033972b3,

title = "Allelotype of pediatric rhabdomyosarcoma",

abstract = "An allelotype covering all autosomes was constructed for the embryonal form of childhood rhabdomyosarcoma (ERMS) in order to identify regions encompassing tumorsuppressor genes (TSG) involved in ERMS. Thusfar most studies were focussed on chromosome 11p15.5, which frequently shows loss of heterozygozity (LOH) in embryonal tumors like RMS and Wilms' tumor (WT). In this study we show that, besides LOH of chromosome 11p15.5 (72%), LOH of chromosome 16q was present in 54% of the tumors analysed. Delineation of these two regions shows that the smallest region of overlap (SRO) for chromosome 11 was between D11S988 and D11S922. This region, estimated to be 7 cM and 3-5 Mb, is also the location of the putative Wilms) tumor WT2 TSG. It contains several genes including IGF2 and potential tumorsuppressor genes like H19 and p57(kip2), which might contribute to the carcinogenesis of RMS. Analysis of chromosome 16q LOH defined the SRO between D16S752 and D16S413. LOH of chromosome 16 is also found in other tumors, including WT. Our data suggest that genes involved in the development of RMS and WT may not only be similar for chromosome 11 but also for chromosome 16.",

keywords = "Alleotype, LOH, loss of heterozygosity, RMS, Rhabdomyosarcoma, SRD, TSG, tumor suppressor gene",

author = "Mike Visser and Carin Sijmons and Johannes Bras and Arceci, {Robert J.} and Mark Godfried and Valentijn, {Linda J.} and Vo{\^u}te, {P. A.} and Frank Baas",

note = "Funding Information: Thanks to Darryl Hake and Lisa Adams for assistance at RMS xenografts and Lilianne Wijnaendts for collecting tissue samples and help with the statistical analysis and Prof Dr A Westerveld, Dr Mannens and Drs M Alders for their comments on this manuscript. This work was supported by the Dutch Cancer Society, by the Foundation of Pediatric Cancer Research and by the Phi Beta Psi Sorority.",

year = "1997",

doi = "10.1038/sj.onc.1201302",

language = "English (US)",

volume = "15",

pages = "1309--1314",

journal = "Oncogene",

issn = "0950-9232",

publisher = "Nature Publishing Group",

number = "11",

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TY - JOUR

T1 - Allelotype of pediatric rhabdomyosarcoma

AU - Visser, Mike

AU - Sijmons, Carin

AU - Bras, Johannes

AU - Arceci, Robert J.

AU - Godfried, Mark

AU - Valentijn, Linda J.

AU - Voûte, P. A.

AU - Baas, Frank

N1 - Funding Information: Thanks to Darryl Hake and Lisa Adams for assistance at RMS xenografts and Lilianne Wijnaendts for collecting tissue samples and help with the statistical analysis and Prof Dr A Westerveld, Dr Mannens and Drs M Alders for their comments on this manuscript. This work was supported by the Dutch Cancer Society, by the Foundation of Pediatric Cancer Research and by the Phi Beta Psi Sorority.

PY - 1997

Y1 - 1997

N2 - An allelotype covering all autosomes was constructed for the embryonal form of childhood rhabdomyosarcoma (ERMS) in order to identify regions encompassing tumorsuppressor genes (TSG) involved in ERMS. Thusfar most studies were focussed on chromosome 11p15.5, which frequently shows loss of heterozygozity (LOH) in embryonal tumors like RMS and Wilms' tumor (WT). In this study we show that, besides LOH of chromosome 11p15.5 (72%), LOH of chromosome 16q was present in 54% of the tumors analysed. Delineation of these two regions shows that the smallest region of overlap (SRO) for chromosome 11 was between D11S988 and D11S922. This region, estimated to be 7 cM and 3-5 Mb, is also the location of the putative Wilms) tumor WT2 TSG. It contains several genes including IGF2 and potential tumorsuppressor genes like H19 and p57(kip2), which might contribute to the carcinogenesis of RMS. Analysis of chromosome 16q LOH defined the SRO between D16S752 and D16S413. LOH of chromosome 16 is also found in other tumors, including WT. Our data suggest that genes involved in the development of RMS and WT may not only be similar for chromosome 11 but also for chromosome 16.

AB - An allelotype covering all autosomes was constructed for the embryonal form of childhood rhabdomyosarcoma (ERMS) in order to identify regions encompassing tumorsuppressor genes (TSG) involved in ERMS. Thusfar most studies were focussed on chromosome 11p15.5, which frequently shows loss of heterozygozity (LOH) in embryonal tumors like RMS and Wilms' tumor (WT). In this study we show that, besides LOH of chromosome 11p15.5 (72%), LOH of chromosome 16q was present in 54% of the tumors analysed. Delineation of these two regions shows that the smallest region of overlap (SRO) for chromosome 11 was between D11S988 and D11S922. This region, estimated to be 7 cM and 3-5 Mb, is also the location of the putative Wilms) tumor WT2 TSG. It contains several genes including IGF2 and potential tumorsuppressor genes like H19 and p57(kip2), which might contribute to the carcinogenesis of RMS. Analysis of chromosome 16q LOH defined the SRO between D16S752 and D16S413. LOH of chromosome 16 is also found in other tumors, including WT. Our data suggest that genes involved in the development of RMS and WT may not only be similar for chromosome 11 but also for chromosome 16.

KW - Alleotype

KW - LOH, loss of heterozygosity

KW - RMS

KW - Rhabdomyosarcoma

KW - SRD

KW - TSG, tumor suppressor gene

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DO - 10.1038/sj.onc.1201302

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SP - 1309

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JO - Oncogene

JF - Oncogene

IS - 11

ER -

Allelotype of pediatric rhabdomyosarcoma

Abstract

Keywords

ASJC Scopus subject areas

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