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Characterization of Camptothecin-induced Genomic Changes in the Camptothecin-resistant T-ALL-derived Cell Line CPT-K5
Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avis › Tidsskriftartikel › Forskning › peer review
Dokumenter
- 91.full
Forlagets udgivne version, 899 KB, PDF-dokument
DOI
- https://doi.org/10.21873/cgp.20068
Forlagets udgivne version
- Institut for Klinisk Medicin - Blodsygdomme
- Institut for Molekylærbiologi og Genetik - Neurobiologi
- DANDRITE - Nissen Group
- Institut for Molekylærbiologi og Genetik - Strukturel Biologi
- Institut for Molekylærbiologi og Genetik
- Institut for Molekylærbiologi og Genetik - Genom stabilitet og teknologi
- Institut for Klinisk Medicin - Patologi
Acquisition of resistance to topoisomerase I (TOP1)-targeting camptothecin (CPT) derivatives is a major clinical problem. Little is known about the underlying chromosomal and genomic mechanisms. We characterized the CPT-K5 cell line expressing mutant CPT-resistant TOP1 and its parental T-cell derived acute lymphoblastic leukemia CPT-sensitive RPMI-8402 cell line by karyotyping and molecular genetic methods, including subtractive oligo-based array comparative genomic hybridization (soaCGH) analysis. Karyotyping revealed that CPT-K5 cells had acquired additional structural aberrations and a reduced modal chromosomal number compared to RPMI-8402. soaCGH analysis identified vast copy number alterations and >200 unbalanced DNA breakpoints distributed unevenly across the chromosomal complement in CPT-K5. In addition, the short tandem repeat alleles were found to be highly different between CPT-K5 and its parental cell line. We identified copy number alterations affecting genes important for maintaining genome integrity and reducing CPT-induced DNA damage. We show for the first time that short tandem repeats are targets for TOP1 cleavage, that can be differentially stimulated by CPT.
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Cancer Genomics & Proteomics |
| Vol/bind | 15 |
| Nummer | 2 |
| Sider (fra-til) | 91-114 |
| Antal sider | 24 |
| ISSN | 1109-6535 |
| DOI | |
| Status | Udgivet - 3 mar. 2018 |
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