Quantitative Methylation-Specific Polymerase Chain Reaction Gene Patterns in Urine Sediment Distinguish Prostate Cancer Patients From Control Subjects
Aberrant promoter hypermethylation of several known or putative tumor suppressor genes occurs frequently during the pathogenesis of prostate cancers and is a promising marker for cancer detection. We sought to develop a test for prostate cancer based on a quantitative methylation-specific polymerase...
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| Published in | Journal of clinical oncology Vol. 23; no. 27; pp. 6569 - 6575 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Baltimore, MD
American Society of Clinical Oncology
20.09.2005
Lippincott Williams & Wilkins |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Aberrant promoter hypermethylation of several known or putative tumor suppressor genes occurs frequently during the pathogenesis of prostate cancers and is a promising marker for cancer detection. We sought to develop a test for prostate cancer based on a quantitative methylation-specific polymerase chain reaction (QMSP) of multiple genes in urine sediment DNA.
We tested urine sediment DNA for aberrant methylation of nine gene promoters (p16INK4a, p14(ARF), MGMT, GSTP1, RARbeta2, CDH1 [E-cadherin], TIMP3, Rassf1A, and APC) from 52 patients with prostate cancer and 21 matched primary tumors by quantitative fluorogenic real-time polymerase chain reaction. We also analyzed urine sediments from 91 age-matched individuals without any history of genitourinary malignancy as controls.
Promoter hypermethylation of at least one of the genes studied was detected in urine samples from all 52 prostate cancer patients. Urine samples from the 91 controls without evidence of genitourinary cancer revealed no methylation of the p16, ARF, MGMT, and GSTP1 gene promoters, whereas methylation of RARbeta2, TIMP3, CDH1, Rassf1A, and APC was detected at low levels.
Overall, methylation found in urine samples matched the methylation status in the primary tumor. A combination of only four genes (p16, ARF, MGMT, and GSTP1) would theoretically allow us to detect 87% of prostate cancers with 100% specificity. Our data support further development of the noninvasive QMSP assay in urine DNA for early detection and surveillance of prostate cancer. |
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| AbstractList | Aberrant promoter hypermethylation of several known or putative tumor suppressor genes occurs frequently during the pathogenesis of prostate cancers and is a promising marker for cancer detection. We sought to develop a test for prostate cancer based on a quantitative methylation-specific polymerase chain reaction (QMSP) of multiple genes in urine sediment DNA.PURPOSEAberrant promoter hypermethylation of several known or putative tumor suppressor genes occurs frequently during the pathogenesis of prostate cancers and is a promising marker for cancer detection. We sought to develop a test for prostate cancer based on a quantitative methylation-specific polymerase chain reaction (QMSP) of multiple genes in urine sediment DNA.We tested urine sediment DNA for aberrant methylation of nine gene promoters (p16INK4a, p14(ARF), MGMT, GSTP1, RARbeta2, CDH1 [E-cadherin], TIMP3, Rassf1A, and APC) from 52 patients with prostate cancer and 21 matched primary tumors by quantitative fluorogenic real-time polymerase chain reaction. We also analyzed urine sediments from 91 age-matched individuals without any history of genitourinary malignancy as controls.PATIENTS AND METHODSWe tested urine sediment DNA for aberrant methylation of nine gene promoters (p16INK4a, p14(ARF), MGMT, GSTP1, RARbeta2, CDH1 [E-cadherin], TIMP3, Rassf1A, and APC) from 52 patients with prostate cancer and 21 matched primary tumors by quantitative fluorogenic real-time polymerase chain reaction. We also analyzed urine sediments from 91 age-matched individuals without any history of genitourinary malignancy as controls.Promoter hypermethylation of at least one of the genes studied was detected in urine samples from all 52 prostate cancer patients. Urine samples from the 91 controls without evidence of genitourinary cancer revealed no methylation of the p16, ARF, MGMT, and GSTP1 gene promoters, whereas methylation of RARbeta2, TIMP3, CDH1, Rassf1A, and APC was detected at low levels.RESULTSPromoter hypermethylation of at least one of the genes studied was detected in urine samples from all 52 prostate cancer patients. Urine samples from the 91 controls without evidence of genitourinary cancer revealed no methylation of the p16, ARF, MGMT, and GSTP1 gene promoters, whereas methylation of RARbeta2, TIMP3, CDH1, Rassf1A, and APC was detected at low levels.Overall, methylation found in urine samples matched the methylation status in the primary tumor. A combination of only four genes (p16, ARF, MGMT, and GSTP1) would theoretically allow us to detect 87% of prostate cancers with 100% specificity. Our data support further development of the noninvasive QMSP assay in urine DNA for early detection and surveillance of prostate cancer.CONCLUSIONOverall, methylation found in urine samples matched the methylation status in the primary tumor. A combination of only four genes (p16, ARF, MGMT, and GSTP1) would theoretically allow us to detect 87% of prostate cancers with 100% specificity. Our data support further development of the noninvasive QMSP assay in urine DNA for early detection and surveillance of prostate cancer. Aberrant promoter hypermethylation of several known or putative tumor suppressor genes occurs frequently during the pathogenesis of prostate cancers and is a promising marker for cancer detection. We sought to develop a test for prostate cancer based on a quantitative methylation-specific polymerase chain reaction (QMSP) of multiple genes in urine sediment DNA. We tested urine sediment DNA for aberrant methylation of nine gene promoters (p16INK4a, p14(ARF), MGMT, GSTP1, RARbeta2, CDH1 [E-cadherin], TIMP3, Rassf1A, and APC) from 52 patients with prostate cancer and 21 matched primary tumors by quantitative fluorogenic real-time polymerase chain reaction. We also analyzed urine sediments from 91 age-matched individuals without any history of genitourinary malignancy as controls. Promoter hypermethylation of at least one of the genes studied was detected in urine samples from all 52 prostate cancer patients. Urine samples from the 91 controls without evidence of genitourinary cancer revealed no methylation of the p16, ARF, MGMT, and GSTP1 gene promoters, whereas methylation of RARbeta2, TIMP3, CDH1, Rassf1A, and APC was detected at low levels. Overall, methylation found in urine samples matched the methylation status in the primary tumor. A combination of only four genes (p16, ARF, MGMT, and GSTP1) would theoretically allow us to detect 87% of prostate cancers with 100% specificity. Our data support further development of the noninvasive QMSP assay in urine DNA for early detection and surveillance of prostate cancer. |
| Author | David Sidransky Rui Henrique Ozlem Topaloglu Shahnaz Begum Eli Rosenbaum Wim Van Criekinge William H. Westra Mohammad Obaidul Hoque |
| Author_xml | – sequence: 1 givenname: Mohammad Obaidul surname: Hoque fullname: Hoque, Mohammad Obaidul organization: From the Department of Otolaryngology-Head and Neck Surgery, The Johns Hopkins School of Medicine; Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD; and Bioinformatics and Computational Genomics, Department of Molecular Biotechnology, Faculty of Agricultural and Applied Biological Sciences, Gent University, Gent, Belgium – sequence: 2 givenname: Ozlem surname: Topaloglu fullname: Topaloglu, Ozlem organization: From the Department of Otolaryngology-Head and Neck Surgery, The Johns Hopkins School of Medicine; Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD; and Bioinformatics and Computational Genomics, Department of Molecular Biotechnology, Faculty of Agricultural and Applied Biological Sciences, Gent University, Gent, Belgium – sequence: 3 givenname: Shahnaz surname: Begum fullname: Begum, Shahnaz organization: From the Department of Otolaryngology-Head and Neck Surgery, The Johns Hopkins School of Medicine; Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD; and Bioinformatics and Computational Genomics, Department of Molecular Biotechnology, Faculty of Agricultural and Applied Biological Sciences, Gent University, Gent, Belgium – sequence: 4 givenname: Rui surname: Henrique fullname: Henrique, Rui organization: From the Department of Otolaryngology-Head and Neck Surgery, The Johns Hopkins School of Medicine; Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD; and Bioinformatics and Computational Genomics, Department of Molecular Biotechnology, Faculty of Agricultural and Applied Biological Sciences, Gent University, Gent, Belgium – sequence: 5 givenname: Eli surname: Rosenbaum fullname: Rosenbaum, Eli organization: From the Department of Otolaryngology-Head and Neck Surgery, The Johns Hopkins School of Medicine; Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD; and Bioinformatics and Computational Genomics, Department of Molecular Biotechnology, Faculty of Agricultural and Applied Biological Sciences, Gent University, Gent, Belgium – sequence: 6 givenname: Wim surname: Van Criekinge fullname: Van Criekinge, Wim organization: From the Department of Otolaryngology-Head and Neck Surgery, The Johns Hopkins School of Medicine; Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD; and Bioinformatics and Computational Genomics, Department of Molecular Biotechnology, Faculty of Agricultural and Applied Biological Sciences, Gent University, Gent, Belgium – sequence: 7 givenname: William H. surname: Westra fullname: Westra, William H. organization: From the Department of Otolaryngology-Head and Neck Surgery, The Johns Hopkins School of Medicine; Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD; and Bioinformatics and Computational Genomics, Department of Molecular Biotechnology, Faculty of Agricultural and Applied Biological Sciences, Gent University, Gent, Belgium – sequence: 8 givenname: David surname: Sidransky fullname: Sidransky, David organization: From the Department of Otolaryngology-Head and Neck Surgery, The Johns Hopkins School of Medicine; Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD; and Bioinformatics and Computational Genomics, Department of Molecular Biotechnology, Faculty of Agricultural and Applied Biological Sciences, Gent University, Gent, Belgium |
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| Snippet | Aberrant promoter hypermethylation of several known or putative tumor suppressor genes occurs frequently during the pathogenesis of prostate cancers and is a... |
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| SubjectTerms | Adult Aged Aged, 80 and over Biological and medical sciences Biomarkers, Tumor - urine Case-Control Studies DNA Methylation DNA, Neoplasm - genetics DNA, Neoplasm - urine Gene Expression Regulation, Neoplastic Genes, Tumor Suppressor - physiology Humans Logistic Models Male Medical sciences Middle Aged Neoplasm Proteins - urine Nephrology. Urinary tract diseases Polymerase Chain Reaction - methods Probability Promoter Regions, Genetic Prostatic Neoplasms - genetics Prostatic Neoplasms - surgery Prostatic Neoplasms - urine Reference Values Sensitivity and Specificity Tumors Tumors of the urinary system Urinalysis Urinary tract. Prostate gland |
| Title | Quantitative Methylation-Specific Polymerase Chain Reaction Gene Patterns in Urine Sediment Distinguish Prostate Cancer Patients From Control Subjects |
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