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Blood, Vol. 93 No. 12 (June 15), 1999:
pp. 4347-4353
Hypermethylation of the DAP-Kinase CpG Island Is a Common
Alteration in B-Cell Malignancies
Rachel A. Katzenellenbogen,
Stephen B. Baylin, and
James G. Herman
From The Johns Hopkins Comprehensive Cancer Center, Baltimore, MD.
Death-associated protein kinase (DAP-Kinase) is a novel
serine/threonine kinase whose expression is required for  interferon-induced apoptosis. A previous study suggested that
DAP-Kinase expression may be lost epigenetically in cancer cell lines,
because treatment of several nonexpressing cell lines with
5-aza-2'-deoxycytidine resulted in the expression of DAP-Kinase.
Using methylation-specific polymerase chain reaction (MSP), we examined
the DAP-Kinase CpG island for hypermethylation in cancer. Normal
lymphocytes and lymphoblastoid cell lines are unmethylated in the
5' CpG island of DAP-Kinase. However, in primary tumor samples,
all Burkitt's lymphomas and 84% of the B-cell non-Hodgkin's
lymphomas were hypermethylated in the DAP-Kinase CpG island. In
contrast, none of the T-cell non-Hodgkin's lymphoma samples and 15%
or less of leukemia samples examined had hypermethylated DAP-Kinase
alleles. U937, an unmethylated, DAP-Kinase-expressing leukemia cell
line, was treated with interferon and underwent apoptosis; however,
Raji, a fully methylated, DAP-Kinase nonexpressing Burkitt's lymphoma
cell line, only did so when treated with 5-aza-2'-deoxycytidine
followed by interferon. Our findings in cell lines and primary
tumors suggest that hypermethylation of the DAP-Kinase gene and loss of
interferon-mediated apoptosis may be important in the development
of B-cell malignancies and may provide a promising biomarker for
B-cell-lineage lymphomas.
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