Chih-Yung Yang1, Ju-Yu Tseng2, Chian-Feng Chen3, Teh-Ying Chou4, Hong-Wei Gao5, Chia-Ling Hua3, Chi-Hung Lin1,2,3,6, Jen-Kou Lin6,7, Jeng-Kai Jiang8,9. 1. Department of Education and Research, Taipei City Hospital, Taipei, Taiwan. 2. Institute of Microbiology and Immunology, National Yang-Ming University, Taipei, Taiwan. 3. VYM Genome Research Center, National Yang-Ming University, Taipei, Taiwan. 4. Department of Pathology, Taipei Veterans General Hospital, Taipei, Taiwan. 5. Department of Pathology, Tri-Service General Hospital, Taipei, Taiwan. 6. School of Medicine, National Yang-Ming University, Taipei, Taiwan. 7. Division of Colon & Rectal Surgery, Department of Surgery, Taipei Veterans General Hospital, Pei-Tou, Taipei, 11217, Taiwan. 8. School of Medicine, National Yang-Ming University, Taipei, Taiwan. jkjiang@vghtpe.gov.tw. 9. Division of Colon & Rectal Surgery, Department of Surgery, Taipei Veterans General Hospital, Pei-Tou, Taipei, 11217, Taiwan. jkjiang@vghtpe.gov.tw.
Abstract
PURPOSE: Colorectal polyps are generally believed to be the precursors of colorectal cancers (CRC); however, the proportion and speed of progression differed widely in different subsets of polyps. Using microarray-based comparative genomic hybridization (aCGH) platform and CD133 immunostaining, we characterized colon polyps according to their association with CRC that developed in the same individual. PATIENTS AND METHODS: aCGH was performed to unveil genomic changes in 18 cancer-synchronous polyps (CSP), and 9 cancer-preceding polyps (CPP), together with their corresponding cancers and 16 cases of incidental polyps (IP), were examined for comparison. aCGH profiles were analyzed to determine the clonal relationship (CR) between the paired adenoma and carcinoma. CD133 expressions in each subset of polyps were quantified by immunohistochemistry (IHC) staining. RESULTS: Progressive genomic changes were observed from IP, CSP/CPP to CRC; they encompass an entire chromosomal region in IP and sub-chromosomal region in CSP/CPP and CRC. CR analyses demonstrated that 50 % of CSP and 67 % of CPP were clonally related to the concurrent or later developed carcinomas, respectively. The CD133 expression levels were significantly higher in CSP/CPP than those in IP (P < 0.0001) and even higher in CSP/CPP that were clonally related to their corresponding carcinomas than CSP/CPP that were unrelated (P < 0.05). CONCLUSIONS: There were more genomic changes in CSP/CPP than IP; more than half of the CSP/CPP were clonally related to the corresponding carcinomas. Genomic changes at sub-chromosomal regions and/or high CD133 expression were associated with CSP/CPP and highlighted their carcinogenic potential.
PURPOSE:Colorectal polyps are generally believed to be the precursors of colorectal cancers (CRC); however, the proportion and speed of progression differed widely in different subsets of polyps. Using microarray-based comparative genomic hybridization (aCGH) platform and CD133 immunostaining, we characterized colon polyps according to their association with CRC that developed in the same individual. PATIENTS AND METHODS: aCGH was performed to unveil genomic changes in 18 cancer-synchronous polyps (CSP), and 9 cancer-preceding polyps (CPP), together with their corresponding cancers and 16 cases of incidental polyps (IP), were examined for comparison. aCGH profiles were analyzed to determine the clonal relationship (CR) between the paired adenoma and carcinoma. CD133 expressions in each subset of polyps were quantified by immunohistochemistry (IHC) staining. RESULTS: Progressive genomic changes were observed from IP, CSP/CPP to CRC; they encompass an entire chromosomal region in IP and sub-chromosomal region in CSP/CPP and CRC. CR analyses demonstrated that 50 % of CSP and 67 % of CPP were clonally related to the concurrent or later developed carcinomas, respectively. The CD133 expression levels were significantly higher in CSP/CPP than those in IP (P < 0.0001) and even higher in CSP/CPP that were clonally related to their corresponding carcinomas than CSP/CPP that were unrelated (P < 0.05). CONCLUSIONS: There were more genomic changes in CSP/CPP than IP; more than half of the CSP/CPP were clonally related to the corresponding carcinomas. Genomic changes at sub-chromosomal regions and/or high CD133 expression were associated with CSP/CPP and highlighted their carcinogenic potential.
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