%0 Journal Article %1 Sawan08 %A Sawan, Carla %A Vaissière, Thomas %A Murr, Rabih %A Herceg, Zdenko %D 2008 %J Mutat. Res. %K Chromatin_Assembly_and_Disassembly DNA_Methylation Epigenesis,_Genetic Gene_Silencing Histones,_metabolism Humans Models,_Genetic Mutation Neoplasms,_genetics Protein_Processing,_Post-Translational %N 1-2 %P 1-13 %R 10.1016/j.mrfmmm.2008.03.002 %T Epigenetic drivers and genetic passengers on the road to cancer. %U http://dx.doi.org/10.1016/j.mrfmmm.2008.03.002 %V 642 %X Cancer is traditionally viewed as a primarily genetic disorder, however it is now becoming accepted that cancer is also a consequence of abnormal epigenetic events. Genetic changes and aneuploidy are associated with alterations in DNA sequence, and they are a hallmark of the malignant process. Epigenetic alterations are universally present in human cancer and result in heritable changes in gene expression and chromatin structure over many cell generations without changes in DNA sequence, leading to functional consequences equivalent to those induced by genetic alterations. Importantly, intriguing evidence emerged suggesting that epigenetic changes may precede and provoke genetic changes. In this scenario, epigenetic events are primary events while genetic changes (such as mutations) may simply be a consequence of disrupted epigenetic states. This fact may explain why many genetic screens proved to be limited with regard to cancer causality and pathogenesis. Aberrant epigenetic events affect multiple genes and cellular pathways in a non-random fashion and this can predispose to induction and accumulation of genetic changes in the course of tumour initiation and progression. These considerations are critical for a better understanding of tumourigenesis and molecular events underlying the acquisition of drug resistance, as well as development of novel strategies for cancer therapy and prevention.

@article{Sawan08, abstract = {Cancer is traditionally viewed as a primarily genetic disorder, however it is now becoming accepted that cancer is also a consequence of abnormal epigenetic events. Genetic changes and aneuploidy are associated with alterations in DNA sequence, and they are a hallmark of the malignant process. Epigenetic alterations are universally present in human cancer and result in heritable changes in gene expression and chromatin structure over many cell generations without changes in DNA sequence, leading to functional consequences equivalent to those induced by genetic alterations. Importantly, intriguing evidence emerged suggesting that epigenetic changes may precede and provoke genetic changes. In this scenario, epigenetic events are primary events while genetic changes (such as mutations) may simply be a consequence of disrupted epigenetic states. This fact may explain why many genetic screens proved to be limited with regard to cancer causality and pathogenesis. Aberrant epigenetic events affect multiple genes and cellular pathways in a non-random fashion and this can predispose to induction and accumulation of genetic changes in the course of tumour initiation and progression. These considerations are critical for a better understanding of tumourigenesis and molecular events underlying the acquisition of drug resistance, as well as development of novel strategies for cancer therapy and prevention.}, added-at = {2010-01-26T20:35:53.000+0100}, author = {Sawan, Carla and Vaissi{\`{e}}re, Thomas and Murr, Rabih and Herceg, Zdenko}, biburl = {https://www.bibsonomy.org/bibtex/29363f9997a79406600959a6331063bf4/denilw}, doi = {10.1016/j.mrfmmm.2008.03.002}, file = {article:../Cancer Epigenetics/Epigenetic drivers and genetic passengers on the road to cancer.pdf:pdf}, institution = {International Agency for Research on Cancer, 150 Cours Albert Thomas, Rhone-Alpes, 69008 Lyon, France.}, interhash = {6aeff85728ce108938541ca2648199c7}, intrahash = {9363f9997a79406600959a6331063bf4}, journal = {Mutat. Res.}, keywords = {Chromatin_Assembly_and_Disassembly DNA_Methylation Epigenesis,_Genetic Gene_Silencing Histones,_metabolism Humans Models,_Genetic Mutation Neoplasms,_genetics Protein_Processing,_Post-Translational}, month = Jul, number = {1-2}, owner = {denilw}, pages = {1-13}, pii = {S0027-5107(08)00061-4}, pmid = {18471836}, timestamp = {2010-01-26T20:36:03.000+0100}, title = {Epigenetic drivers and genetic passengers on the road to cancer.}, url = {http://dx.doi.org/10.1016/j.mrfmmm.2008.03.002}, volume = 642, year = 2008 }