Hypermethylation of ribosomal DNA in human breast carcinoma

Yan, Pearlly S.; Rodrí­guez, Francisco José Robles; Laux, Douglas; Perry, Martin R.; Standiford, Steven B.; Huang, Tim H.M.

doi:10.1054/bjoc.1999.0955

Cited by 40 publications

(39 citation statements)

References 9 publications

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“…An amplicon in the lanes denoted U represents amplification from unmethylated DNA and methylated DNA in the lanes denoted M, post-sodium bisulphite conversion subtype or growth characteristics, this was not the case for the DAP kinase gene CpG island, suggesting that these epigenetic changes do not represent random methylation errors. Finally in other tumour types, investigators have examined multiple CpG islands that are commonly methylated in cancer (Huang et al, 1999;Yan et al, 2000;Esteller et al, 2001). Collectively, these studies show common methylated CpG islands across different tumour types, others that show tumour-type specificity and still others where the methylation signature correlates with clinical parameters.…”

Section: Discussionmentioning

confidence: 99%

Loss of expression of the growth inhibitory gene GADD45γ, in human pituitary adenomas, is associated with CpG island methylation

et al. 2003

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Section: Discussionmentioning

confidence: 99%

Loss of expression of the growth inhibitory gene GADD45γ, in human pituitary adenomas, is associated with CpG island methylation

et al. 2003

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“…Cancer-associated hypermethylation occurs not only in genes with a known or likely role in carcinogenesis, but also in genes not implicated in cancer, such as, MYOD at its 5' CpG island (Issa, 2000). Hypermethylation of ribosomal DNA genes was found in breast cancer (Yan et al, 2000), but reports of cancer-associated hypermethylation of repeated sequences in human cancer are rare.…”

Section: Types Of Sequences Affected By Cancer-associated Hypermethylmentioning

confidence: 99%

DNA methylation in cancer: too much, but also too little

2002

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Cancer-associated DNA hypomethylation is as prevalent as cancer-linked hypermethylation, but these two types of epigenetic abnormalities usually seem to affect different DNA sequences. Much more of the genome is generally subject to undermethylation rather than overmethylation. Genomic hypermethylation in cancer has been observed most often in CpG islands in gene regions. In contrast, very frequent hypomethylation is seen in both highly and moderately repeated DNA sequences in cancer, including heterochromatic DNA repeats, dispersed retrotransposons, and endogenous retroviral elements. Also, unique sequences, including transcription control sequences, are often subject to cancer-associated undermethylation. The high frequency of cancer-linked DNA hypomethylation, the nature of the affected sequences, and the absence of associations with DNA hypermethylation are consistent with an independent role for DNA undermethylation in cancer formation or tumor progression. Increased karyotypic instability and activation of tumor-promoting genes by cis or trans effects, that might include altered heterochromatin-euchromatin interactions, may be important consequences of DNA hypomethylation which favor oncogenesis. The relationship of DNA hypomethylation to tumorigenesis is important to be considered in the light of cancer therapies involving decreasing DNA methylation. Inducing DNA hypomethylation may have short-term anticancer effects, but might also help speed tumor progression from cancer cells surviving the DNA demethylation chemotherapy.

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“…A third genomic strategy for identifying methylationsilenced genes in human cancer is CpG island microarrays, also known as differential methylation hybridization (DMH) (Yan et al, 2000). The DMH method utilizes hybridization of BstUI (methylation sensitive) digested DNA amplicons to a CpG island genomic DNA library.…”

Section: Identifying the Molecular Targets Of Gene Silencingmentioning

confidence: 99%