دورية أكاديمية
أعرض في EDS

Therapy-induced APOBEC3A drives evolution of persistent cancer cells.

التفاصيل البيبلوغرافية
العنوان: Therapy-induced APOBEC3A drives evolution of persistent cancer cells.
المؤلفون: Isozaki H; Massachusetts General Hospital Cancer Center, Boston, MA, USA. hisozaki@mgh.harvard.edu.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. hisozaki@mgh.harvard.edu., Sakhtemani R; Massachusetts General Hospital Cancer Center, Boston, MA, USA.; Broad Institute of MIT and Harvard, Cambridge, MA, USA., Abbasi A; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Nikpour N; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Stanzione M; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Oh S; Department of Biological Chemistry, Center for Epigenetics and Metabolism, Chao Family Comprehensive Cancer Center, School of Medicine, University of California Irvine, Irvine, CA, USA., Langenbucher A; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Monroe S; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Su W; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Cabanos HF; Massachusetts General Hospital Cancer Center, Boston, MA, USA.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA., Siddiqui FM; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Phan N; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Jalili P; Department of Biological Chemistry, Center for Epigenetics and Metabolism, Chao Family Comprehensive Cancer Center, School of Medicine, University of California Irvine, Irvine, CA, USA., Timonina D; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Bilton S; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Gomez-Caraballo M; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Archibald HL; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Nangia V; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Dionne K; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Riley A; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Lawlor M; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Banwait MK; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Cobb RG; Massachusetts General Hospital Cancer Center, Boston, MA, USA., Zou L; Massachusetts General Hospital Cancer Center, Boston, MA, USA.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.; Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC, USA., Dyson NJ; Massachusetts General Hospital Cancer Center, Boston, MA, USA.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA., Ott CJ; Massachusetts General Hospital Cancer Center, Boston, MA, USA.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.; Broad Institute of MIT and Harvard, Cambridge, MA, USA., Benes C; Massachusetts General Hospital Cancer Center, Boston, MA, USA.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA., Getz G; Massachusetts General Hospital Cancer Center, Boston, MA, USA.; Broad Institute of MIT and Harvard, Cambridge, MA, USA.; Department of Pathology, Massachusetts General Hospital, Boston, MA, USA.; Department of Pathology, Harvard Medical School, Boston, MA, USA., Chan CS; Department of Medicine, Rutgers Robert Wood Johnson Medical School and Center for Systems and Computational Biology, Rutgers Cancer Institute, New Brunswick, NJ, USA., Shaw AT; Massachusetts General Hospital Cancer Center, Boston, MA, USA.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA., Gainor JF; Massachusetts General Hospital Cancer Center, Boston, MA, USA.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA., Lin JJ; Massachusetts General Hospital Cancer Center, Boston, MA, USA.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA., Sequist LV; Massachusetts General Hospital Cancer Center, Boston, MA, USA.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA., Piotrowska Z; Massachusetts General Hospital Cancer Center, Boston, MA, USA.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA., Yeap BY; Massachusetts General Hospital Cancer Center, Boston, MA, USA.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA., Engelman JA; Massachusetts General Hospital Cancer Center, Boston, MA, USA.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA., Lee JJ; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA., Maruvka YE; Faculty of Biotechnology and Food Engineering, Lorey Loki Center for Life Science and Engineering, Technion, Haifa, Israel., Buisson R; Department of Biological Chemistry, Center for Epigenetics and Metabolism, Chao Family Comprehensive Cancer Center, School of Medicine, University of California Irvine, Irvine, CA, USA.; Department of Pharmaceutical Sciences, School of Pharmacy & Pharmaceutical Sciences, University of California Irvine, Irvine, CA, USA., Lawrence MS; Massachusetts General Hospital Cancer Center, Boston, MA, USA. mslawrence@mgh.harvard.edu.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. mslawrence@mgh.harvard.edu.; Broad Institute of MIT and Harvard, Cambridge, MA, USA. mslawrence@mgh.harvard.edu., Hata AN; Massachusetts General Hospital Cancer Center, Boston, MA, USA. ahata@mgh.harvard.edu.; Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. ahata@mgh.harvard.edu.
المصدر: Nature [Nature] 2023 Aug; Vol. 620 (7973), pp. 393-401. Date of Electronic Publication: 2023 Jul 05.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 0410462 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-4687 (Electronic) Linking ISSN: 00280836 NLM ISO Abbreviation: Nature Subsets: MEDLINE
أسماء مطبوعة: Publication: Basingstoke : Nature Publishing Group
Original Publication: London, Macmillan Journals ltd.
مواضيع طبية MeSH: Cytidine Deaminase*/deficiency , Cytidine Deaminase*/drug effects , Cytidine Deaminase*/genetics , Cytidine Deaminase*/metabolism , Lung Neoplasms*/drug therapy , Lung Neoplasms*/genetics , Lung Neoplasms*/metabolism , Lung Neoplasms*/pathology, Humans ; DNA Breaks, Double-Stranded ; Genomic Instability ; Molecular Targeted Therapy ; Mutation ; Drug Resistance, Neoplasm
مستخلص: Acquired drug resistance to anticancer targeted therapies remains an unsolved clinical problem. Although many drivers of acquired drug resistance have been identified 1-4 , the underlying molecular mechanisms shaping tumour evolution during treatment are incompletely understood. Genomic profiling of patient tumours has implicated apolipoprotein B messenger RNA editing catalytic polypeptide-like (APOBEC) cytidine deaminases in tumour evolution; however, their role during therapy and the development of acquired drug resistance is undefined. Here we report that lung cancer targeted therapies commonly used in the clinic can induce cytidine deaminase APOBEC3A (A3A), leading to sustained mutagenesis in drug-tolerant cancer cells persisting during therapy. Therapy-induced A3A promotes the formation of double-strand DNA breaks, increasing genomic instability in drug-tolerant persisters. Deletion of A3A reduces APOBEC mutations and structural variations in persister cells and delays the development of drug resistance. APOBEC mutational signatures are enriched in tumours from patients with lung cancer who progressed after extended responses to targeted therapies. This study shows that induction of A3A in response to targeted therapies drives evolution of drug-tolerant persister cells, suggesting that suppression of A3A expression or activity may represent a potential therapeutic strategy in the prevention or delay of acquired resistance to lung cancer targeted therapy.
(© 2023. The Author(s), under exclusive licence to Springer Nature Limited.)
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معلومات مُعتمدة: R01 CA137008 United States CA NCI NIH HHS; R01 CA164273 United States CA NCI NIH HHS; R01 CA249291 United States CA NCI NIH HHS; P50 CA265826 United States CA NCI NIH HHS; K08 CA197389 United States CA NCI NIH HHS; R37 CA252081 United States CA NCI NIH HHS; U01 CA220323 United States CA NCI NIH HHS; P30 CA062203 United States CA NCI NIH HHS
المشرفين على المادة: EC 3.5.4.5 (APOBEC3A protein, human)
EC 3.5.4.5 (Cytidine Deaminase)
تواريخ الأحداث: Date Created: 20230705 Date Completed: 20230814 Latest Revision: 20240202
رمز التحديث: 20240202
مُعرف محوري في PubMed: PMC10804446
DOI: 10.1038/s41586-023-06303-1
PMID: 37407818
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-4687
DOI:10.1038/s41586-023-06303-1