Chemotherapy induced DNA damage response: Convergence of drugs and pathways
Open accessAbstract
Chemotherapeutics target rapidly dividing cancer cells by directly or indirectly inducing DNA damage. Upon recognizing DNA damage, cells initiate a variety of signaling pathways collectively referred to as the DNA damage response (DDR). Interestingly, the pathways used to elicit this response are as varied as the types of DNA damage induced. However, the activation of these various pathways has similar results including DNA repair, suppression of global general translation, cell cycle arrest and, ultimately, either cell survival or cell death. This review will focus on a series of chemotherapy-induced DNA lesions and highlight recent advances in our understanding of the DDR, the DNA repair pathways it activates and the cellular consequences of these converging pathways.
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Traditional chemotherapeutics directly or indirectly induce DNA damage, thereby initiating DNA damage response (DDR) to repair lesions.
“As traditional chemotherapeutics directly or indirectly induce DNA damage, thereby initiating DNA damage response (DDR) to repair lesions (90), it has been postulated that these repair mechanisms could increase conversion of rAAV genome into dsDNA (91), or divert DDR proteins that would otherwise impede dsDNA production (92).”
From Immunomodulation in Administration of RAAV: Preclinical and Clinical Adjuvant Pharmacotherapies (2021) · cites this paper as [90]
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- Authors
- Woods, D., & Turchi, J. J.
- Affiliations
- Indiana University School of Medicine (US)
- Indiana University Indianapolis (US)
- Corresponding author
- Turchi, John J.
- ORCID
- Turchi, John J.
- Venue
- Cancer Biology & Therapy
- Publisher
- Informa UK Limited
- Published
- 2013-05
- Volume
- 14
- Issue
- 5
- Pages
- 379-389
- ISSN
- 1538-4047 (ISSN-L)
- 1555-8576
- PMC
- PMC3672181
- OpenAlex
- W2050142910
- Cited by
- 296
- References
- 82
- Citations by year
- 2026: 20 · 2025: 23 · 2024: 34 · 2023: 38 · 2022: 32 · 2021: 31 · 2020: 23 · 2019: 15 · 2018: 17 · 2017: 12 · 2016: 18 · 2015: 19 · 2014: 9 · 2013: 4
- FWCI
- 1.57
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- Cancer Biology & Therapy (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- IUScholarWorks (Indiana University) (submittedVersion, cc-by-nc)
- Funders
- National Institutes of Health
- National Cancer Institute (CA82741, R01CA082741)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer therapeutics and mechanisms
- Keywords
- DNA damage response, chemotherapy, DNA damage, DNA repair pathways, cell cycle arrest, cell death, DNA lesions, tumor cell killing
- MeSH terms
- Antineoplastic Agents, Cell Cycle, Cell Survival, Cisplatin, DNA Damage, Humans, Signal Transduction, Cell Death
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