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      Gene-promoter hypermethylation as a biomarker in lung cancer.

      Author(s): 1
      Publication date (Electronic):
      Journal: Nature reviews. Cancer
      Publisher: Springer Nature America, Inc

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          Abstract

          Silencing of genes by aberrant promoter hypermethylation is now recognized as a crucial component in cancer initiation and progression. Highly sensitive assays have been developed to assess gene-promoter methylation in biological fluids. The detection of methylated genes in sputum could lead to the development of a screening test to non-invasively identify early cancer in high-risk people.

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          Cancer epigenetics comes of age.

          P. A. Jones, P. W. Laird, Andrew Dimond … (1999)
          The discovery of numerous hypermethylated promoters of tumour-suppressor genes, along with a better understanding of gene-silencing mechanisms, has moved DNA methylation from obscurity to recognition as an alternative mechanism of tumour-suppressor inactivation in cancer. Epigenetic events can also facilitate genetic damage, as illustrated by the increased mutagenicity of 5-methylcytosine and the silencing of the MLH1 mismatch repair gene by DNA methylation in colorectal tumours. We review here current mechanistic understanding of the role of DNA methylation in malignant transformation, and suggest Knudson's two-hit hypothesis should now be expanded to include epigenetic mechanisms of gene inactivation.
          Article 0 comments Cited 337 times – based on 0 reviews     Review now
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            Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands.

            J G Herman, J Graff, S Myöhänen … (1996)
            Article 0 comments Cited 325 times – based on 0 reviews     Review now
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              Synergy of demethylation and histone deacetylase inhibition in the re-expression of genes silenced in cancer.

              E E Cameron, K E Bachman, S Myöhänen … (1999)
              Densely methylated DNA associates with transcriptionally repressive chromatin characterized by the presence of underacetylated histones. Recently, these two epigenetic processes have been dynamically linked. The methyl-CpG-binding protein MeCP2 appears to reside in a complex with histone deacetylase activity. MeCP2 can mediate formation of transcriptionally repressive chromatin on methylated promoter templates in vitro, and this process can be reversed by trichostatin A (TSA), a specific inhibitor of histone deacetylase. Little is known, however, about the relative roles of methylation and histone deacetylase activity in the stable inhibition of transcription on densely methylated endogenous promoters, such as those for silenced alleles of imprinted genes, genes on the female inactive X chromosome and tumour-suppressor genes inactivated in cancer cells. We show here that the hypermethylated genes MLH1, TIMP3 (TIMP3), CDKN2B (INK4B, p15) and CDKN2A (INK4, p16) cannot be transcriptionally reactivated with TSA alone in tumour cells in which we have shown that TSA alone can upregulate the expression of non-methylated genes. Following minimal demethylation and slight gene reactivation in the presence of low dose 5-aza-2'deoxycytidine (5Aza-dC), however, TSA treatment results in robust re-expression of each gene. TSA does not contribute to demethylation of the genes, and none of the treatments alter the chromatin structure associated with the hypermethylated promoters. Thus, although DNA methylation and histone deacetylation appear to act as synergistic layers for the silencing of genes in cancer, dense CpG island methylation is dominant for the stable maintenance of a silent state at these loci.
              Article 0 comments Cited 299 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Nat. Rev. Cancer
                Title: Nature reviews. Cancer
                Publisher: Springer Nature America, Inc
                ISSN: 1474-175X
                ISSN (Print): 1474-175X
                Publication date (Electronic): Sep 2004
                Volume: 4
                Issue: 9
                Affiliations
                [1 ] Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA. SBelinsk@lrri.org
                Article
                Publisher Item ID: nrc1432
                DOI: 10.1038/nrc1432
                PubMed ID: 15343277
                SO-VID: e178496e-4aba-4266-9d02-002172a809b4
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