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.
%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
}