AKT1 interacts with DHX9 to Mitigate R Loop–Induced Replication Stress in Ovarian Cancer
Author:
Affiliation:
1. 1Women's Malignancies Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
2. 2Functional Genomics Laboratory, National Center for Advancing Translational Sciences, NIH, Rockville, Maryland.
Abstract
Funder
National Cancer Institute
Publisher
American Association for Cancer Research (AACR)
Link
https://aacrjournals.org/cancerres/article-pdf/doi/10.1158/0008-5472.CAN-23-1908/3405418/can-23-1908.pdf
Reference75 articles.
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3. Participation of the ATR/CHK1 pathway in replicative stress targeted therapy of high-grade ovarian cancer;Gralewska;J Hematol Oncol,2020
4. Understanding and overcoming resistance to PARP inhibitors in cancer therapy;Dias;Nat Rev Clin Oncol,2021
5. Cell cycle checkpoints and beyond: Exploiting the ATR/CHK1/WEE1 pathway for the treatment of PARP inhibitor–resistant cancer;Gupta;Pharmacol Res,2022
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1. LncRNA DYNLRB2-AS1 promotes gemcitabine resistance of nasopharyngeal carcinoma by inhibiting the ubiquitination degradation of DHX9 protein;Drug Resistance Updates;2024-09
2. Combination Therapy Approach to Overcome the Resistance to PI3K Pathway Inhibitors in Gynecological Cancers;Cells;2024-06-19
3. AKTing on R Loops Makes for an ATRactive Target in Ovarian Cancer Therapy;Cancer Research;2024-03-15
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