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@ARTICLE{Bormann:136018,
author = {F. Bormann$^*$ and M. Rodríguez-Paredes$^*$ and F.
Lasitschka and D. Edelmann$^*$ and T. Musch$^*$ and A.
Benner$^*$ and Y. Bergman and S. Dieter$^*$ and C. Ball$^*$
and H. Glimm$^*$ and H. G. Linhart$^*$ and F. Lyko$^*$},
title = {{C}ell-of-{O}rigin {DNA} {M}ethylation {S}ignatures {A}re
{M}aintained during {C}olorectal {C}arcinogenesis.},
journal = {Cell reports},
volume = {23},
number = {11},
issn = {2211-1247},
address = {Maryland Heights, MO},
publisher = {Cell Press},
reportid = {DKFZ-2018-00718},
pages = {3407 - 3418},
year = {2018},
note = {DKFZ-ZMBH-Allianz},
abstract = {Colorectal adenomas are precursor lesions of colorectal
cancers and represent clonal amplifications of single cells
from colonic crypts. DNA methylation patterns specify
cell-type identity during cellular differentiation and,
therefore, provide opportunities for the molecular analysis
of tumors. We have now analyzed DNA methylation patterns in
colorectal adenomas and identified three biologically
defined subclasses that describe different intestinal crypt
differentiation stages. Importantly, colorectal carcinomas
could be classified into the same methylation subtypes,
reflecting their shared cell types of origin with adenomas.
Further data analysis also revealed significantly reduced
overall survival for one of the subtypes. Our results
provide a concept for understanding the methylation patterns
observed in colorectal cancer and provide opportunities for
tumor subclassification and patient stratification.},
cin = {A130 / C060 / G911 / L301},
ddc = {570},
cid = {I:(DE-He78)A130-20160331 / I:(DE-He78)C060-20160331 /
I:(DE-He78)G911-20160331 / I:(DE-He78)L301-20160331},
pnm = {311 - Signalling pathways, cell and tumor biology
(POF3-311)},
pid = {G:(DE-HGF)POF3-311},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:29898408},
doi = {10.1016/j.celrep.2018.05.045},
url = {https://inrepo02.dkfz.de/record/136018},
}