2006
DOI: 10.1016/j.canlet.2005.08.034
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DAPK promotor methylation is an early event in colorectal carcinogenesis

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Cited by 58 publications
(37 citation statements)
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“…Numerous studies report a significant correlation of alteration of protein expressions in tumor surrounding benign tissues of several cancers with different stages of metastatic disease or local progression. In their molecular behavior the adjacent benign tissues seem to act like malignant tissue [18][19][20][21].…”
Section: Discussionmentioning
confidence: 99%
“…Numerous studies report a significant correlation of alteration of protein expressions in tumor surrounding benign tissues of several cancers with different stages of metastatic disease or local progression. In their molecular behavior the adjacent benign tissues seem to act like malignant tissue [18][19][20][21].…”
Section: Discussionmentioning
confidence: 99%
“…Loss of DAPK activity leads to protection from interferon-␥-induced cell death, and overexpression of DAPK leads to apoptosis (30). The inactivation of DAPK by promoter hypermethylation has also been suggested to play an important role in the early steps of tumor progression to colorectal carcinoma (32). Thus, downregulation of calmodulin may contribute to colorectal tumorigenesis via inactivation of DAPK.…”
Section: Discussionmentioning
confidence: 99%
“…(ii) Second, the cancer cell can silence or lose a downstream proapoptotic partner of the receptor. As an example, death-associated protein kinase 1(figure 3B), a proapoptotic partner of UNC5B, is silenced by hypermethylation of its promoter in CRC 80. (iii) Third, an autocrine production of ligand can be selected by the tumour, that is, the cancer cell or the associated stroma, and this would keep the receptor fooled in an occupied state (figure 2A).…”
Section: Therapeutic Perspectives Linked To Dependence Receptorsmentioning
confidence: 99%