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@ARTICLE{Li:163800,
author = {Y. Li and N. D. Roberts and J. A. Wala and O. Shapira and
S. E. Schumacher and K. Kumar and E. Khurana and S. Waszak
and J. O. Korbel and J. E. Haber and M. Imielinski and
PCAWGStructuralVariationWorkingGroup and J. Weischenfeldt
and R. Beroukhim and P. J. Campbell and PCAWGConsortium},
title = {{P}atterns of somatic structural variation in human cancer
genomes.},
journal = {Nature},
volume = {578},
number = {7793},
issn = {1476-4687},
address = {London [u.a.]},
publisher = {Nature Publ. Group52462},
reportid = {DKFZ-2020-02053},
pages = {112 - 121},
year = {2020},
note = {siehe Correction: DKFZ Autoren affiliiert im PCAWG
Consortium: https://inrepo02.dkfz.de/record/265691 /
https://doi.org/10.1038/s41586-022-05597-x},
abstract = {A key mutational process in cancer is structural variation,
in which rearrangements delete, amplify or reorder genomic
segments that range in size from kilobases to whole
chromosomes1-7. Here we develop methods to group, classify
and describe somatic structural variants, using data from
the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium
of the International Cancer Genome Consortium (ICGC) and The
Cancer Genome Atlas (TCGA), which aggregated whole-genome
sequencing data from 2,658 cancers across 38 tumour
types8. Sixteen signatures of structural variation emerged.
Deletions have a multimodal size distribution, assort
unevenly across tumour types and patients, are enriched in
late-replicating regions and correlate with inversions.
Tandem duplications also have a multimodal size
distribution, but are enriched in early-replicating
regions-as are unbalanced translocations. Replication-based
mechanisms of rearrangement generate varied chromosomal
structures with low-level copy-number gains and frequent
inverted rearrangements. One prominent structure consists of
2-7 templates copied from distinct regions of the genome
strung together within one locus. Such cycles of templated
insertions correlate with tandem duplications, and-in liver
cancer-frequently activate the telomerase gene TERT. A wide
variety of rearrangement processes are active in cancer,
which generate complex configurations of the genome upon
which selection can act.},
keywords = {Gene Rearrangement: genetics / Genetic Variation / Genome,
Human: genetics / Genomics / Humans / Mutagenesis,
Insertional / Neoplasms: genetics / Telomerase: genetics /
TERT protein, human (NLM Chemicals) / Telomerase (NLM
Chemicals)},
cin = {B370 / B330 / B240 / HD01 / B080 / B060 / B062 / B360 /
B260 / BE01 / B063 / B087 / W610 / W190 / B066},
ddc = {500},
cid = {I:(DE-He78)B370-20160331 / I:(DE-He78)B330-20160331 /
I:(DE-He78)B240-20160331 / I:(DE-He78)HD01-20160331 /
I:(DE-He78)B080-20160331 / I:(DE-He78)B060-20160331 /
I:(DE-He78)B062-20160331 / I:(DE-He78)B360-20160331 /
I:(DE-He78)B260-20160331 / I:(DE-He78)BE01-20160331 /
I:(DE-He78)B063-20160331 / I:(DE-He78)B087-20160331 /
I:(DE-He78)W610-20160331 / I:(DE-He78)W190-20160331 /
I:(DE-He78)B066-20160331},
pnm = {312 - Functional and structural genomics (POF3-312)},
pid = {G:(DE-HGF)POF3-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:32025012},
pmc = {pmc:PMC7025897},
doi = {10.1038/s41586-019-1913-9},
url = {https://inrepo02.dkfz.de/record/163800},
}