Improved Identification of von Hippel-Lindau Gene Alterations in Clear Cell Renal Tumors
Purpose: To provide a comprehensive, thorough analysis of somatic mutation and promoter hypermethylation of the von Hippel-Lindau ( VHL ) gene in the cancer genome, unique to clear cell renal cancer (ccRCC). Identify relationships between the prevalence of VHL gene alterations and alteration subtype...
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| Published in | Clinical cancer research Vol. 14; no. 15; pp. 4726 - 4734 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Association for Cancer Research
01.08.2008
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 1078-0432 1557-3265 |
| DOI | 10.1158/1078-0432.CCR-07-4921 |
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| Abstract | Purpose: To provide a comprehensive, thorough analysis of somatic mutation and promoter hypermethylation of the von Hippel-Lindau ( VHL ) gene in the cancer genome, unique to clear cell renal cancer (ccRCC). Identify relationships between the prevalence of VHL gene alterations and alteration subtypes with patient and tumor characteristics.
Experimental Design: As part of a large kidney cancer case-control study conducted in Central Europe, we analyzed VHL mutations and promoter methylation in 205 well-characterized, histologically confirmed patient tumor biopsies using a combination
of sensitive, high-throughput methods (endonuclease scanning and Sanger sequencing) and analysis of 11 CpG sites in the VHL promoter.
Results: We identified mutations in 82.4% of cases, the highest VHL gene mutation prevalence reported to date. Analysis of 11 VHL promoter CpG sites revealed that 8.3% of tumors were hypermethylated and all were mutation negative. In total, 91% of ccRCCs
exhibited alteration of the gene through genetic or epigenetic mechanisms. Analysis of patient and tumor characteristics revealed
that certain mutation subtypes were significantly associated with Fuhrman nuclear grade, metastasis, node positivity, and
self-reported family history of RCC.
Conclusion: Detection of VHL gene alterations using these accurate, sensitive, and practical methods provides evidence that the vast majority of histologically
confirmed ccRCC tumors possess genetic or epigenetic alteration of the VHL gene and support the hypothesis that VHL alteration is an early event in ccRCC carcinogenesis. These findings also indicate that VHL molecular subtypes can provide a sensitive marker of tumor heterogeneity among histologically similar ccRCC cases for etiologic,
prognostic, and translational studies. |
|---|---|
| AbstractList | Purpose: To provide a comprehensive, thorough analysis of somatic mutation and promoter hypermethylation of the von Hippel-Lindau ( VHL ) gene in the cancer genome, unique to clear cell renal cancer (ccRCC). Identify relationships between the prevalence of VHL gene alterations and alteration subtypes with patient and tumor characteristics.
Experimental Design: As part of a large kidney cancer case-control study conducted in Central Europe, we analyzed VHL mutations and promoter methylation in 205 well-characterized, histologically confirmed patient tumor biopsies using a combination
of sensitive, high-throughput methods (endonuclease scanning and Sanger sequencing) and analysis of 11 CpG sites in the VHL promoter.
Results: We identified mutations in 82.4% of cases, the highest VHL gene mutation prevalence reported to date. Analysis of 11 VHL promoter CpG sites revealed that 8.3% of tumors were hypermethylated and all were mutation negative. In total, 91% of ccRCCs
exhibited alteration of the gene through genetic or epigenetic mechanisms. Analysis of patient and tumor characteristics revealed
that certain mutation subtypes were significantly associated with Fuhrman nuclear grade, metastasis, node positivity, and
self-reported family history of RCC.
Conclusion: Detection of VHL gene alterations using these accurate, sensitive, and practical methods provides evidence that the vast majority of histologically
confirmed ccRCC tumors possess genetic or epigenetic alteration of the VHL gene and support the hypothesis that VHL alteration is an early event in ccRCC carcinogenesis. These findings also indicate that VHL molecular subtypes can provide a sensitive marker of tumor heterogeneity among histologically similar ccRCC cases for etiologic,
prognostic, and translational studies. To provide a comprehensive, thorough analysis of somatic mutation and promoter hypermethylation of the von Hippel-Lindau (VHL) gene in the cancer genome, unique to clear cell renal cancer (ccRCC). Identify relationships between the prevalence of VHL gene alterations and alteration subtypes with patient and tumor characteristics.PURPOSETo provide a comprehensive, thorough analysis of somatic mutation and promoter hypermethylation of the von Hippel-Lindau (VHL) gene in the cancer genome, unique to clear cell renal cancer (ccRCC). Identify relationships between the prevalence of VHL gene alterations and alteration subtypes with patient and tumor characteristics.As part of a large kidney cancer case-control study conducted in Central Europe, we analyzed VHL mutations and promoter methylation in 205 well-characterized, histologically confirmed patient tumor biopsies using a combination of sensitive, high-throughput methods (endonuclease scanning and Sanger sequencing) and analysis of 11 CpG sites in the VHL promoter.EXPERIMENTAL DESIGNAs part of a large kidney cancer case-control study conducted in Central Europe, we analyzed VHL mutations and promoter methylation in 205 well-characterized, histologically confirmed patient tumor biopsies using a combination of sensitive, high-throughput methods (endonuclease scanning and Sanger sequencing) and analysis of 11 CpG sites in the VHL promoter.We identified mutations in 82.4% of cases, the highest VHL gene mutation prevalence reported to date. Analysis of 11 VHL promoter CpG sites revealed that 8.3% of tumors were hypermethylated and all were mutation negative. In total, 91% of ccRCCs exhibited alteration of the gene through genetic or epigenetic mechanisms. Analysis of patient and tumor characteristics revealed that certain mutation subtypes were significantly associated with Fuhrman nuclear grade, metastasis, node positivity, and self-reported family history of RCC.RESULTSWe identified mutations in 82.4% of cases, the highest VHL gene mutation prevalence reported to date. Analysis of 11 VHL promoter CpG sites revealed that 8.3% of tumors were hypermethylated and all were mutation negative. In total, 91% of ccRCCs exhibited alteration of the gene through genetic or epigenetic mechanisms. Analysis of patient and tumor characteristics revealed that certain mutation subtypes were significantly associated with Fuhrman nuclear grade, metastasis, node positivity, and self-reported family history of RCC.Detection of VHL gene alterations using these accurate, sensitive, and practical methods provides evidence that the vast majority of histologically confirmed ccRCC tumors possess genetic or epigenetic alteration of the VHL gene and support the hypothesis that VHL alteration is an early event in ccRCC carcinogenesis. These findings also indicate that VHL molecular subtypes can provide a sensitive marker of tumor heterogeneity among histologically similar ccRCC cases for etiologic, prognostic, and translational studies.CONCLUSIONDetection of VHL gene alterations using these accurate, sensitive, and practical methods provides evidence that the vast majority of histologically confirmed ccRCC tumors possess genetic or epigenetic alteration of the VHL gene and support the hypothesis that VHL alteration is an early event in ccRCC carcinogenesis. These findings also indicate that VHL molecular subtypes can provide a sensitive marker of tumor heterogeneity among histologically similar ccRCC cases for etiologic, prognostic, and translational studies. Purpose: To provide a comprehensive, thorough analysis of somatic mutation and promoter hypermethylation of the von Hippel-Lindau (VHL) gene in the cancer genome, unique to clear cell renal cancer (ccRCC). Identify relationships between the prevalence of VHL gene alterations and alteration subtypes with patient and tumor characteristics. Experimental Design: As part of a large kidney cancer case-control study conducted in Central Europe, we analyzed VHL mutations and promoter methylation in 205 well-characterized, histologically confirmed patient tumor biopsies using a combination of sensitive, high-throughput methods (endonuclease scanning and Sanger sequencing) and analysis of 11 CpG sites in the VHL promoter. Results: We identified mutations in 82.4% of cases, the highest VHL gene mutation prevalence reported to date. Analysis of 11 VHL promoter CpG sites revealed that 8.3% of tumors were hypermethylated and all were mutation negative. In total, 91% of ccRCCs exhibited alteration of the gene through genetic or epigenetic mechanisms. Analysis of patient and tumor characteristics revealed that certain mutation subtypes were significantly associated with Fuhrman nuclear grade, metastasis, node positivity, and self-reported family history of RCC. Conclusion: Detection of VHL gene alterations using these accurate, sensitive, and practical methods provides evidence that the vast majority of histologically confirmed ccRCC tumors possess genetic or epigenetic alteration of the VHL gene and support the hypothesis that VHL alteration is an early event in ccRCC carcinogenesis. These findings also indicate that VHL molecular subtypes can provide a sensitive marker of tumor heterogeneity among histologically similar ccRCC cases for etiologic, prognostic, and translational studies. To provide a comprehensive, thorough analysis of somatic mutation and promoter hypermethylation of the von Hippel-Lindau (VHL) gene in the cancer genome, unique to clear cell renal cancer (ccRCC). Identify relationships between the prevalence of VHL gene alterations and alteration subtypes with patient and tumor characteristics. As part of a large kidney cancer case-control study conducted in Central Europe, we analyzed VHL mutations and promoter methylation in 205 well-characterized, histologically confirmed patient tumor biopsies using a combination of sensitive, high-throughput methods (endonuclease scanning and Sanger sequencing) and analysis of 11 CpG sites in the VHL promoter. We identified mutations in 82.4% of cases, the highest VHL gene mutation prevalence reported to date. Analysis of 11 VHL promoter CpG sites revealed that 8.3% of tumors were hypermethylated and all were mutation negative. In total, 91% of ccRCCs exhibited alteration of the gene through genetic or epigenetic mechanisms. Analysis of patient and tumor characteristics revealed that certain mutation subtypes were significantly associated with Fuhrman nuclear grade, metastasis, node positivity, and self-reported family history of RCC. Detection of VHL gene alterations using these accurate, sensitive, and practical methods provides evidence that the vast majority of histologically confirmed ccRCC tumors possess genetic or epigenetic alteration of the VHL gene and support the hypothesis that VHL alteration is an early event in ccRCC carcinogenesis. These findings also indicate that VHL molecular subtypes can provide a sensitive marker of tumor heterogeneity among histologically similar ccRCC cases for etiologic, prognostic, and translational studies. |
| Author | Laura S. Schmidt Vladimir Janout Paul Brennan Vsevolod Matveev Paolo Boffetta Gary F. Gerard Sunil Mahurkar Erich Jaeger Rayjean Hung Jeffrey A. Durocher Jorge R. Toro Marie Navratilova Neonilia Szeszenia-Dabrowska Yangu Shi Maria Merino Lee E. Moore Wong-Ho Chow Nathaniel Rothman Ivana Holcatova Dana Mates Anush Mukeria Sara Karami Frederic M. Waldman Vladimir Bencko Berton Zbar David Zaridze W. Marston Linehan Hellena Kollarova Michael L. Nickerson |
| AuthorAffiliation | 2 Comprehensive Cancer Center, University of California, San Francisco, San Francisco, California 14 University of Toronto, Ontario Canada 3 Institute of Carcinogenesis, Cancer Research Centre, Moscow, Russia 4 Department of Preventive Medicine, Faculty of Medicine, Palacky University, Olomouc, Czech Republic 8 Institute of Public Health, Bucharest, Romania 1 Transgenomic, Gaithersburg, Maryland 7 Department of Epidemiology, Institute of Occupational Medicine, Lodz, Poland 6 Department of Cancer Epidemiology and Genetics, Masaryk Memorial Cancer Institute, Brno, Czech Republic 10 Laboratory of Immunobiology, National Cancer Institute-Frederick, National Institutes of Health, Frederick, Maryland 12 Urologic Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 5 Institute of Hygiene and Epidemiology, Charles University, Prague, Czech Republic 11 Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, |
| AuthorAffiliation_xml | – name: 6 Department of Cancer Epidemiology and Genetics, Masaryk Memorial Cancer Institute, Brno, Czech Republic – name: 7 Department of Epidemiology, Institute of Occupational Medicine, Lodz, Poland – name: 14 University of Toronto, Ontario Canada – name: 10 Laboratory of Immunobiology, National Cancer Institute-Frederick, National Institutes of Health, Frederick, Maryland – name: 2 Comprehensive Cancer Center, University of California, San Francisco, San Francisco, California – name: 8 Institute of Public Health, Bucharest, Romania – name: 11 Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland – name: 4 Department of Preventive Medicine, Faculty of Medicine, Palacky University, Olomouc, Czech Republic – name: 5 Institute of Hygiene and Epidemiology, Charles University, Prague, Czech Republic – name: 13 National Cancer Institute, National Institutes of Health, Bethesda, Maryland – name: 12 Urologic Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland – name: 3 Institute of Carcinogenesis, Cancer Research Centre, Moscow, Russia – name: 1 Transgenomic, Gaithersburg, Maryland – name: 15 International Agency for Research on Cancer, Lyon, France – name: 9 Basic Research Program, SAIC, National Cancer Institute-Frederick, Frederick, Maryland |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/18676741$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Adenocarcinoma, Clear Cell - genetics Adenocarcinoma, Clear Cell - metabolism Carcinoma, Renal Cell - genetics Carcinoma, Renal Cell - metabolism Case-Control Studies CpG Islands DNA Methylation Female Gene Expression Profiling Gene Expression Regulation, Neoplastic Humans Kidney Neoplasms - metabolism Male Mutation Neoplasms - metabolism Promoter Regions, Genetic RCC Tumor Markers VHL Von Hippel-Lindau Tumor Suppressor Protein - genetics Von Hippel-Lindau Tumor Suppressor Protein - metabolism |
| Title | Improved Identification of von Hippel-Lindau Gene Alterations in Clear Cell Renal Tumors |
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