The DOI matches its Crossref record; 199 of the 199 references it cites were found in a registry or an index.
Targeting replication stress in cancer therapy
Open accessAbstract
Replication stress is a cause of genome instability in cancer cells. This Review discusses strategies to increase replicative stress by inhibiting the checkpoint kinases that coordinate DNA damage response and cell cycle, as well as combination strategies with other targeted therapies. Replication stress is a major cause of genomic instability and a crucial vulnerability of cancer cells. This vulnerability can be therapeutically targeted by inhibiting kinases that coordinate the DNA damage response with cell cycle control, including ATR, CHK1, WEE1 and MYT1 checkpoint kinases. In addition, inhibiting the DNA damage response releases DNA fragments into the cytoplasm, eliciting an innate immune response. Therefore, several ATR, CHK1, WEE1 and MYT1 inhibitors are undergoing clinical evaluation as monotherapies or in combination with chemotherapy, poly[ADP-ribose]polymerase (PARP) inhibitors, or immune checkpoint inhibitors to capitalize on high replication stress, overcome therapeutic resistance and promote effective antitumour immunity. Here, we review current and emerging approaches for targeting replication stress in cancer, from preclinical and biomarker development to clinical trial evaluation.
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Metadata
- Authors
- da Costa, A. A. B. A., Chowdhury, D., Shapiro, G. I., D’Andrea, A. D., & Konstantinopoulos, P. A.
- Venue
- Nature Reviews Drug Discovery
- Published
- 2022-10-06
- Volume
- 22
- Issue
- 1
- Pages
- 38-58
- ISSN
- 1474-1776 (ISSN-L)
- 1474-1784
- OpenAlex
- W4302424483
- Cited by
- 359
- References
- 199
- FWCI
- 5.57
- Type
- journal article
- Language
- en
- Open access
- green
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- da Costa, A. A. B. A., Chowdhury, D., Shapiro, G. I., D’Andrea, A. D., & Konstantinopoulos, P. A. (2023). Targeting replication stress in cancer therapy. Nature Reviews Drug Discovery. https://doi.org/10.1038/s41573-022-00558-5
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