ArticleJapanese journal of cancer research : Gann2002
Cloning of the 5' upstream region of the rat p16 gene and its role in silencing.
Article in Japanese journal of cancer research : Gann, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 25 citations in OpenAlex.
- Why Does DNA Methylation Accumulate at CpG Loci?: Sequential Analysis ofActa histochemica et cytochemica · 2026Article
- Review
- Methylation of the BIN1 gene promoter CpG island associated with breast and prostate cancer.Journal of carcinogenesis · 2007Article
- Whole-genome analyses of loss of heterozygosity and methylation analysis of four tumor-suppressor genes in N-methyl-N'-nitro-N-nitrosoguanidine-induced rat stomach carcinomas.Cancer science · 2005Article
- Aberrant methylations in cancer cells: where do they come from?Cancer science · 2005Review
- Promoter hypermethylation of DAP-kinase is associated with poor survival in primary biliary tract carcinoma patients.Cancer science · 2004Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypermethylation of the 5' upstream region (5' region) of the human p16(CDKN2A) (p16) gene is known to cause silencing, which is involved in a wide range of human cancers. For the rat p16 gene, its 5' region has not been cloned, and it is uncertain whether surrogate use of exon 1 alpha is adequate for analysis of p16 silencing. In this study, we observed that methylation analysis of exon 1 alpha gave false positive results in three samples of normal rat mammary epithelia and in two of six primary mammary carcinomas. Therefore, we determined the nucleotide sequence of the 5' region of the rat p16 gene. To confirm that methylation status of the 5' region is correlated with p16 expression, the methylation status was analyzed by bisulfite sequencing and methylation-specific PCR in three samples of normal mammary glands, six samples of mammary carcinomas and four cell lines. The 5' region was demethylated in all of the three normal and six carcinoma samples that fully expressed p16. On the other hand, the 5' region was highly methylated in the 3Y1 cell line, which lacked p16 expression, but without deletion. These results showed that the methylation status of the 5' region was more closely correlated with p16 expression than that of the exon 1 alpha and analysis of the methylation status is useful in examining p16 silencing in various rat tumors.
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