Abstract:
:The p16INK4 gene, encoding a cyclin-dependent kinase inhibitor, is frequently methylated in colorectal cancer, and a side-specific methylation frequency was suggested. To clarify the frequency of real loss of tumor suppressor function dependent on anatomical localization, we investigated 43 primary colorectal carcinomas by determining aberrant promoter methylation using methylation-specific PCR. In addition, we evaluated the p16INK4 protein expression immunohistochemically. P16INK4 methylation was found in 18 of 43 (41.9%) cases. Fourteen of 43 cases (32.6%) were negative for p16INK4 protein, whereas 10 of these 14 cases showed methylation of the promoter region of the p16INK4 gene. Methylation of the promoter region was significantly correlated with loss of p16INK4 protein (p<0.01). P16INK4 tumor suppressor inactivation was significantly correlated with proximal location (p=0.031 for methylation and p=0.028 for immunostaining). The groups characterized by tumors with and without aberrant promoter methylation or loss of p16INK4 immunostaining showed no significant difference in either Dukes' stage and grade or age and gender. This is further evidence that p16INK4 methylation causes gene silencing. Loss of p16INK4 tumor suppressor function in colorectal tumors was associated with proximal location in the gut.
journal_name
Int J Oncoljournal_title
International journal of oncologyauthors
Schneider-Stock R,Boltze C,Peters B,Höpfner T,Meyer F,Lippert H,Roessner Akeywords:
subject
Has Abstractpub_date
2003-10-01 00:00:00pages
1009-13issue
4eissn
1019-6439issn
1791-2423journal_volume
23pub_type
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