%0 Journal Article %1 Feinberg06 %A Feinberg, Andrew P %A Ohlsson, Rolf %A Henikoff, Steven %D 2006 %J Nat. Rev. Genet. %K Animals Chemoprevention Chromatin DNA_Methylation Disease_Progression Epigenesis,_Genetic Gene_Silencing Genes,_Tumor_Suppressor Genomic_Imprinting Humans Models,_Genetic Mutation Neoplasms,_genetics Risk Stem_Cells,_cytology/metabolism %N 1 %P 21-33 %R 10.1038/nrg1748 %T The epigenetic progenitor origin of human cancer. %U http://dx.doi.org/10.1038/nrg1748 %V 7 %X Cancer is widely perceived as a heterogeneous group of disorders with markedly different biological properties, which are caused by a series of clonally selected genetic changes in key tumour-suppressor genes and oncogenes. However, recent data suggest that cancer has a fundamentally common basis that is grounded in a polyclonal epigenetic disruption of stem/progenitor cells, mediated by 'tumour-progenitor genes'. Furthermore, tumour cell heterogeneity is due in part to epigenetic variation in progenitor cells, and epigenetic plasticity together with genetic lesions drives tumour progression. This crucial early role for epigenetic alterations in cancer is in addition to epigenetic alterations that can substitute for genetic variation later in tumour progression. Therefore, non-neoplastic but epigenetically disrupted stem/progenitor cells might be a crucial target for cancer risk assessment and chemoprevention.

@article{Feinberg06, abstract = {Cancer is widely perceived as a heterogeneous group of disorders with markedly different biological properties, which are caused by a series of clonally selected genetic changes in key tumour-suppressor genes and oncogenes. However, recent data suggest that cancer has a fundamentally common basis that is grounded in a polyclonal epigenetic disruption of stem/progenitor cells, mediated by {'}tumour-progenitor genes{'}. Furthermore, tumour cell heterogeneity is due in part to epigenetic variation in progenitor cells, and epigenetic plasticity together with genetic lesions drives tumour progression. This crucial early role for epigenetic alterations in cancer is in addition to epigenetic alterations that can substitute for genetic variation later in tumour progression. Therefore, non-neoplastic but epigenetically disrupted stem/progenitor cells might be a crucial target for cancer risk assessment and chemoprevention.}, added-at = {2010-01-26T20:35:53.000+0100}, author = {Feinberg, Andrew P and Ohlsson, Rolf and Henikoff, Steven}, biburl = {https://www.bibsonomy.org/bibtex/284535cab7d2c2d351a0277ac4bfdaf5c/denilw}, doi = {10.1038/nrg1748}, file = {article:../Cancer/The epigenetic progenitor origin of human cancer.pdf:pdf}, institution = {Department of Medicine, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, Maryland 21205, USA. afeinberg@jhu.edu}, interhash = {52a4c072a39830e2ec7567a233b879a2}, intrahash = {84535cab7d2c2d351a0277ac4bfdaf5c}, journal = {Nat. Rev. Genet.}, keywords = {Animals Chemoprevention Chromatin DNA_Methylation Disease_Progression Epigenesis,_Genetic Gene_Silencing Genes,_Tumor_Suppressor Genomic_Imprinting Humans Models,_Genetic Mutation Neoplasms,_genetics Risk Stem_Cells,_cytology/metabolism}, month = Jan, number = 1, owner = {denilw}, pages = {21-33}, pii = {nrg1748}, pmid = {16369569}, timestamp = {2010-01-26T20:35:57.000+0100}, title = {The epigenetic progenitor origin of human cancer.}, url = {http://dx.doi.org/10.1038/nrg1748}, volume = 7, year = 2006 }