Shama Virani1, Emily Light2, Lisa A Peterson3, Maureen A Sartor4, Jeremy M G Taylor2, Jonathan B McHugh5, Gregory T Wolf3, Laura S Rozek1,3. 1. Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, Michigan. 2. Department of Biostatistics, University of Michigan, School of Public Health, Ann Arbor, Michigan. 3. Department of Otolaryngology-Head and Neck Surgery, University of Michigan Medical School, Ann Arbor, Michigan. 4. Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan. 5. Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan.
Abstract
BACKGROUND: As cancer progresses, methylation patterns change to promote the tumorigenic phenotype. However, stability of methylation markers over time and the extent that biopsy samples are representative of larger tumor specimens are unknown. This information is critical for clinical use of such biomarkers. METHODS: Ninety-eight patients with tumor specimens from 2 timepoints were measured for DNA methylation in the promoter regions across 4 genes. RESULTS: There were no significant differences in overall methylation of CCNA1 (cyclin A1), NDN (necdin), deleted in colorectal carcinoma (DCC), and cluster of differentiation 1a (CD1A) within paired specimens (p values = .56, .17, .66, and .58, respectively). All genes showed strong correlations between paired specimens across time. Methylation was most consistent for CCNA1 and NDN over time. CONCLUSION: This report provides the first evidence that methylation markers measured in biopsy samples are representative of gene methylation in later specimens and suggests that biopsy markers could be representative biomarkers for use in defining personalized treatment utilizing epigenetic changes.
BACKGROUND: As cancer progresses, methylation patterns change to promote the tumorigenic phenotype. However, stability of methylation markers over time and the extent that biopsy samples are representative of larger tumor specimens are unknown. This information is critical for clinical use of such biomarkers. METHODS: Ninety-eight patients with tumor specimens from 2 timepoints were measured for DNA methylation in the promoter regions across 4 genes. RESULTS: There were no significant differences in overall methylation of CCNA1 (cyclin A1), NDN (necdin), deleted in colorectal carcinoma (DCC), and cluster of differentiation 1a (CD1A) within paired specimens (p values = .56, .17, .66, and .58, respectively). All genes showed strong correlations between paired specimens across time. Methylation was most consistent for CCNA1 and NDN over time. CONCLUSION: This report provides the first evidence that methylation markers measured in biopsy samples are representative of gene methylation in later specimens and suggests that biopsy markers could be representative biomarkers for use in defining personalized treatment utilizing epigenetic changes.
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