Medical Letter on the CDC & FDA

Data on cancer gene therapy discussed by K. Grønbaek and colleagues

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"Since several alterations are usually required for a cancer to fully develop, the malignant phenotype is determined by the compound status of tumor suppressor genes and oncogenes. Cancer genes may be changed by several mechanisms, which potentially alter the protein encoding nucleotide template, change the copy number of genes, or lead to increased gene transcription. Epigenetic alterations, which, by definition, comprise mitotically and meiotically heritable changes in gene expression that are not caused by changes in the primary DNA sequence, are increasingly being recognized for their roles in carcinogenesis. These epigenetic alterations may involve covalent modifications of amino acid residues in the histones around which the DNA is wrapped, and changes in the methylation status of cytosine bases (C) in the context of CpG dinucleotides within the DNA itself. Methylation of clusters of CpGs called 'CpG-islands' in the promoters of genes has been associated with heritable gene silencing. The present review will focus on how disruption of the epigenome can contribute to cancer. In contrast to genetic alterations, gene silencing by epigenetic modifications is potentially reversible. Treatment by agents that inhibit cytosine methylation and histone deacetylation can initiate chromatin decondensation, demethylation and reestablishment of gene transcription. Accordingly, in the clinical setting, DNA methylation and histone modifications are very attractive targets for the development and implementation of new therapeutic approaches," wrote K. Grønbaek and colleagues, .

The researchers concluded: "Many clinical trials are ongoing, and epigenetic therapy has recently been approved by the United States Food and Drug Administration (US FDA) for use in the treatment of myelodysplastic syndrome (MDS) and primary cutaneous T-cell lymphoma (CTCL)."

Grønbaek and colleagues published their study in APMIS (Epigenetic changes in cancer. APMIS, 2007;115(10):1039-59).

For additional information, contact K. Grønbaek, Rigshospitalet, Dept. of Hematology, Copenhagen, Denmark.

The publisher of the journal APMIS can be contacted at: Blackwell Munksgaard, 35 Norre Sogade, PO Box 2148, DK-1016 Copenhagen, Denmark.

Keywords: Denmark, Copenhagen, Biotechnology, Cancer Gene Therapy, Carcinogenesis, DNA Research, DNA Sequence Proteomics, Deoxyribonucleic Acid, FDA, Genetics, Genomics, Lymphoma Gene Therapy, Oncology, Protein Encoding, Proteomics, Treatment, Tumor Suppression, U.S. Food and Drug Administration.

This article was prepared by Medical Letter on the CDC & FDA editors from staff and other reports. Copyright 2008, Medical Letter on the CDC & FDA via NewsRx.com.