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[Cancer Research 59, 2302-2306, May 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 2302-2306, May 15, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

CpG Island Hypermethylation in Human Colorectal Tumors Is Not Associated with DNA Methyltransferase Overexpression1

Cindy A. Eads, Kathleen D. Danenberg, Kazuyuki Kawakami, Leonard B. Saltz, Peter V. Danenberg and Peter W. Laird2

Departments of Surgery [C. A. E., P. W. L.] and Biochemistry and Molecular Biology [C. A. E., K. D. D., K. K., P. V. D., P. W. L.], University of Southern California, School of Medicine, Norris Comprehensive Cancer Center, Los Angeles, California 90033, and Memorial Sloan Kettering Cancer Center, New York, New York 10021-6094 [L. B. S.]

The molecular basis of aberrant hypermethylation of CpG islands observed in a subset of human colorectal tumors is unknown. One potential mechanism is the up-regulation of DNA (cytosine-5)-methyltransferases. Recently, two new mammalian DNA methyltransferase genes have been identified, which are referred to as DNMT3A and DNMT3B. The encoded proteins differ from the predominant mammalian DNA methyltransferase DNMT1 in that they have a substantially higher ratio of de novo to maintenance methyltransferase activity. We have used a highly quantitative 5' nuclease fluorogenic reverse transcription-PCR method (TaqMan) to analyze the expression of all three DNA methyltransferase genes in 25 individual colorectal adenocarcinoma specimens and matched normal mucosa samples. In addition, we examined the methylation patterns of four CpG islands [APC, ESR1 (estrogen receptor), CDKN2A (p16), and MLH1] to determine whether individual tumors show a positive correlation between the level of DNA methyltransferase expression and the frequency of CpG island hypermethylation. All three methyltransferases appear to be up-regulated in tumors when RNA levels are normalized using either ACTB (ß-actin) or POLR2A (RNA pol II large subunit), but not when RNA levels are normalized with proliferation-associated genes, such as H4F2 (histone H4) or PCNA. The frequency or extent of CpG island hypermethylation in individual tumors did not correlate with the expression of any of the three DNA methyltransferases. Our results suggest that deregulation of DNA methyltransferase gene expression does not play a role in establishing tumor-specific abnormal DNA methylation patterns in human colorectal cancer.




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Cancer Res., August 1, 2000; 60(16): 4366 - 4371.
[Abstract] [Full Text]

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 Cancer Res.Home page
R. T. Cormier and W. F. Dove
Dnmt1N/+ Reduces the Net Growth Rate and Multiplicity of Intestinal Adenomas in C57BL/6-Multiple Intestinal Neoplasia (Min)/+ Mice Independently of p53 but Demonstrates Strong Synergy with the Modifier of Min 1AKR Resistance Allele
Cancer Res., July 1, 2000; 60(14): 3965 - 3970.
[Abstract] [Full Text]

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 Nucleic Acids ResHome page
C. A. Eads, K. D. Danenberg, K. Kawakami, L. B. Saltz, C. Blake, D. Shibata, P. V. Danenberg, and P. W. Laird
MethyLight: a high-throughput assay to measure DNA methylation
Nucleic Acids Res., April 15, 2000; 28(8): e32 - e.
[Abstract] [Full Text] [PDF]

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 J. Nutr.Home page
S.-W. Choi and J. B. Mason
Folate and Carcinogenesis: An Integrated Scheme1-3
J. Nutr., January 1, 2000; 130(2): 129 - 132.
[Abstract] [Full Text]

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 Proc. Natl. Acad. Sci. USAHome page
S. A. Kuismanen, M. T. Holmberg, R. Salovaara, P. Schweizer, L. A. Aaltonen, A. de la Chapelle, M. Nystrom-Lahti, and P. Peltomaki
Epigenetic phenotypes distinguish microsatellite-stable and -unstable colorectal cancers
PNAS, October 26, 1999; 96(22): 12661 - 12666.
[Abstract] [Full Text] [PDF]

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 J. Biol. Chem.Home page
N. Detich, S. Ramchandani, and M. Szyf
A Conserved 3'-Untranslated Element Mediates Growth Regulation of DNA Methyltransferase 1 and Inhibits Its Transforming Activity
J. Biol. Chem., June 29, 2001; 276(27): 24881 - 24890.
[Abstract] [Full Text] [PDF]


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