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@ARTICLE{Lopez:179850,
author = {C. Lopez and N. Schleussner and S. H. Bernhart and K.
Kleinheinz and S. Sungalee and H. L. Sczakiel and H.
Kretzmer and U. H. Toprak$^*$ and S. Glaser and R. Wagener
and O. Ammerpohl and S. Bens and M. Giefing and J. C. G.
Sanchez and G. Apic and D. Hubschmann$^*$ and M. Janz and M.
Kreuz and A. Mottok and J. M. Muller and J. Seufert$^*$ and
S. Hoffmann and J. O. Korbel and R. B. Russell and R. Schule
and L. Trumper and W. Klapper and B. Radlwimmer$^*$ and P.
Lichter$^*$ and R. Kuppers$^*$ and M. Schlesner$^*$ and S.
Mathas and R. Siebert},
title = {{F}ocal structural variants revealed by whole genome
sequencing disrupt the histone demethylase {KDM}4{C} in {B}
cell lymphomas.},
journal = {Haematologica},
volume = {108},
number = {2},
issn = {0390-6078},
address = {Pavia},
publisher = {Ferrata Storti Foundation},
reportid = {DKFZ-2022-00924},
pages = {543-554},
year = {2023},
note = {2023 Feb 1;108(2):543-554},
abstract = {Histone methylation-modifiers, like EZH2 and KMT2D, are
recurrently altered in B-cell lymphomas. To comprehensively
describe the landscape of alterations affecting genes
encoding histone methylation-modifiers in lymphomagenesis we
investigated whole genome and transcriptome data of 186
mature B-cell lymphomas sequenced in the ICGC MMML-Seq
project. Besides confirming common alterations of KMT2D
$(47\%$ of cases), EZH2 $(17\%),$ SETD1B $(5\%),$ PRDM9
$(4\%),$ KMT2C $(4\%),$ and SETD2 $(4\%)$ also identified by
prior exome or RNAseq studies, we here unravel KDM4C in
chromosome 9p24, encoding a histone demethylase, to be
recurrently altered. Focal structural variation was the main
mechanism of KDM4C alterations, which was independent from
9p24 amplification. We identified KDM4C alterations also in
lymphoma cell lines including a focal homozygous deletion in
a classical Hodgkin lymphoma cell line. By integrating
RNAseq and genome sequencing data we predict KDM4C
structural variants to result in loss-of-function. By
functional reconstitution studies in cell lines, we provide
evidence that KDM4C can act as tumor suppressor. Thus, we
show that identification of structural variants in whole
genome sequencing data adds to the comprehensive description
of the mutational landscape of lymphomas and, moreover,
establish KDM4C as putative tumor suppressive gene
recurrently altered in subsets of B-cell derived lymphomas.},
cin = {B240 / B087 / HD01 / B060 / ED01},
ddc = {610},
cid = {I:(DE-He78)B240-20160331 / I:(DE-He78)B087-20160331 /
I:(DE-He78)HD01-20160331 / I:(DE-He78)B060-20160331 /
I:(DE-He78)ED01-20160331},
pnm = {312 - Funktionelle und strukturelle Genomforschung
(POF4-312)},
pid = {G:(DE-HGF)POF4-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:35522148},
doi = {10.3324/haematol.2021.280005},
url = {https://inrepo02.dkfz.de/record/179850},
}