For every cell, there is a time to live and a time to die. It is apparent that cell life and death decisions are taken by individual cells based on their interpretation of physiological or non-physiological stimuli, or their own self-assessment of internal damage or changes in their environment. Apoptosis or programmed cell death is a key regulator of physiological growth control and regulation of tissue homoeostasis. One of the most important advances in cancer research in recent years is the recognition that cell death, mostly by apoptosis, is crucially involved in the regulation of tumour formation and also critically determines treatment response. The initiation and progression of cancer, traditionally seen as a genetic disease, is now realized to involve epigenetic abnormalities along with genetic alterations. The study of epigenetic mechanisms in cancer, such as DNA methylation, histone modifications and microRNA expression, has revealed a plethora of events that contribute to the neoplastic phenotype through stable changes in the expression of genes critical to cell death pathways. A better understanding of the epigenetic molecular events that regulate apoptosis, together with the reversible nature of epigenetic aberrations, should contribute to the emergence of the promising field of epigenetic therapy.
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September 2010
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Review Article|
September 20 2010
Epigenetic regulation of cell life and death decisions and deregulation in cancer
Nabil Hajji
;
Nabil Hajji
1
*Department of Experimental Medicine and Toxicology, Division of Investigative Science, Imperial College, London, U.K.
1To whom correspondence should be addressed (n.hajji@imperial.ac.uk)
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Bertrand Joseph
Bertrand Joseph
†Department of Oncology Pathology, Cancer Centrum Karolinska, Karolinska Institutet, Stockholm, Sweden
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Essays Biochem (2010) 48: 121–146.
Citation
Hans J. Lipps, Jan Postberg, Dean A. Jackson, Nabil Hajji, Bertrand Joseph; Epigenetic regulation of cell life and death decisions and deregulation in cancer. Essays Biochem 20 September 2010; 48 121–146. doi: https://doi.org/10.1042/bse0480121
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