Mechanisms of tandem duplication in the cancer genome.
Document Type
Article
Publication Date
1-1-2025
Publication Title
DNA repair
Keywords
JGM, Humans, Neoplasms, Gene Duplication, Genome, Human, Tandem Repeat Sequences, DNA Replication, Animals, Oncogenes
JAX Source
DNA Repair (Amst). 2025;145:103802.
Volume
145
First Page
103802
Last Page
103802
ISSN
1568-7856
PMID
39742573
DOI
https://doi.org/10.1016/j.dnarep.2024.103802
Grant
This work was supported by grant R35CA263813 (to R.S.), R01CA255705 to E.T.L and F.M., D.G. is supported by the ‘major grant’ award from the Fund for Innovation in Cancer Informatics
Abstract
Tandem duplications (TD) are among the most frequent type of structural variant (SV) in the cancer genome. They are characterized by a single breakpoint junction that defines the boundaries and the size of the duplicated segment. Cancer-associated TDs often increase oncogene copy number or disrupt tumor suppressor gene function, and thus have important roles in tumor evolution. TDs in cancer genomes fall into three classes, defined by the size of duplications, and are associated with distinct genetic drivers. In this review, we survey key features of cancer-related TDs and consider possible underlying mechanisms in relation to stressed DNA replication and the 3D organization of the S phase genome.
Recommended Citation
Scully R,
Glodzik D,
Menghi F,
Liu E,
Zhang C.
Mechanisms of tandem duplication in the cancer genome. DNA Repair (Amst). 2025;145:103802.