DAPK promotor methylation is an early event in colorectal carcinogenesis

Cancer Lett. 2006 Aug 18;240(1):69-75. doi: 10.1016/j.canlet.2005.08.034. Epub 2005 Oct 24.


Death-associated protein kinase (DAPK) is frequently inactivated by promotor hypermethylation in various human cancers. At present, little is known about the significance of DAPK inactivation in colorectal carcinogenesis. We therefore, investigated macrodissected samples of 22 formalin-fixed and paraffin-embedded T1-carcinomas showing normal colon mucosa, intraepithelial neoplasia and carcinoma tissue on the same slice. Dissected carcinoma areas showed a higher frequency of DAPK promotor methylation (81.2%) compared to intraepithelial neoplasia (68.2%). Colon mucosa adjacent to intraepithelial neoplasia or carcinoma showed DAPK promotor methylation in only two of eight cases (25%). We suggest that DAPK promotor hypermethylation may play an important role in the early steps of tumor progression in colorectal carcinoma.

Publication types

  • Comparative Study

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Apoptosis Regulatory Proteins / genetics
  • Apoptosis Regulatory Proteins / metabolism*
  • Biomarkers, Tumor / metabolism*
  • Calcium-Calmodulin-Dependent Protein Kinases / genetics
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
  • Carcinoma in Situ / enzymology*
  • Carcinoma in Situ / genetics
  • Carcinoma in Situ / pathology
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / metabolism*
  • Colorectal Neoplasms / enzymology*
  • Colorectal Neoplasms / genetics
  • Colorectal Neoplasms / pathology
  • DNA Methylation*
  • Death-Associated Protein Kinases
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Gene Silencing
  • Humans
  • Immunohistochemistry
  • Male
  • Middle Aged
  • Promoter Regions, Genetic*


  • Apoptosis Regulatory Proteins
  • Biomarkers, Tumor
  • Death-Associated Protein Kinases
  • Calcium-Calmodulin-Dependent Protein Kinases