ReviewPharmacology & therapeutics2019
Schlafen 11 (SLFN11), a restriction factor for replicative stress induced by DNA-targeting anti-cancer therapies.
Review in Pharmacology & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
110 citing papers in PubMed, 165 citations in OpenAlex.
- DNA hypomethylation identifying clinical benefit subgroup of small-cell lung cancer: multi-omics analysis of a phase II trial with durvalumab plus olaparib as maintenance therapy.Journal for immunotherapy of cancer · 2026Trial
- Article
- Replication Stress Tolerance in Adult T-Cell Leukemia.Biomolecules · 2026Review
- Molecular Determinants of Response and Rational Drug Combinations for Antibody-Drug Conjugates (ADCs) with Topoisomerase I (TOP1) Inhibitor Payloads.Journal of molecular biology · 2026Review
- Schlafen 11 Is Overexpressed in Multiple Myeloma and Undergoes Nucleolar Translocation in Response to Bortezomib.Cancer research communications · 2026Article
- DNA replication stress and translational repression converge to drive CDK1- and caspase-dependent apoptosis in Ewing sarcoma.Oncogene · 2026Article
- The Influence of TDP1 Inhibitor Usnic Acid Derivative OL9-116 on the Effects of Topotecan in Human Cells.Current issues in molecular biology · 2026Article
- Ubiquitin-dependent recruitment of SLFN11 to chromatin is regulated by deubiquitinase (DUB) and RNF168.Research square · 2026Article
- Rapid Production of Recombinant Human SLFN14 Ribonuclease and Stoichiometric Analysis by Mass Photometry.Journal of visualized experiments : JoVE · 2026Article
- Schlafen 11 (SLFN11) overexpression and nucleolar localization in response to bortezomib in multiple myeloma.bioRxiv : the preprint server for biology · 2026Article
- RPA exhaustion activates SLFN11 to eliminate cells with heightened replication stress.Nature cell biology · 2026Article
- Targeting glycerophospholipid biosynthesis overcomes chemoresistance driven by SLFN11 loss in Ewing sarcoma.Cell death & disease · 2026Article
- Overcoming Therapeutic Resistance in Triple-Negative Breast Cancer: Targeting the Undrugged Kinome.International journal of molecular sciences · 2025Review
- Co-expression of CD30 and SLFN11 serves as a dual biomarker for the treatment of cutaneous T-cell lymphoma.NAR cancer · 2025Article
- Mechanistic insights into the monotherapy and combination potential of FEN1 inhibition in cancer therapy.Nucleic acids research · 2025Article
- The evolving landscape of antibody-drug conjugates (ADCs) for treatment of prostate cancer.NPJ precision oncology · 2025Review
- Ensemble model for neoadjuvant chemotherapy response prediction and treatment sensitivity in TNBC based on DNA replication stress signatures.Scientific reports · 2025Article
- PARP Inhibitors in Genitourinary Cancer: A New Paradigm Beyond Prostate Cancer.International journal of urology : official journal of the Japanese Urological Association · 2025Review
- CryoEM structure of the SLFN14 endoribonuclease reveals insight into RNA binding and cleavage.Nature communications · 2025Article
- Bimodal Genomic Approach Predicting Semaphorin 7A (SEMA7A) as Prognostic Biomarker in Adrenocortical Carcinoma.Cancers · 2025Article
50 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Schlafen 11 (SLFN11) sensitizes cells to a broad range of anti-cancer drugs including platinum derivatives (cisplatin and carboplatin), inhibitors of topoisomerases (irinotecan, topotecan, doxorubicin, daunorubicin, mitoxantrone and etoposide), DNA synthesis inhibitors (gemcitabine, cytarabine, hydroxyurea and nucleoside analogues), and poly(ADPribose) polymerase (PARP) inhibitors (olaparib, rucaparib, niraparib and talazoparib). In spite of their different primary mechanisms of action, all these drugs damage DNA during S-phase, activate the intra-S-phase checkpoint and induce replication fork slowing and stalling with single-stranded DNA segments coated with replication protein A. Such situation with abnormal replication forks is known as replication stress. SLFN11 irreversibly blocks replication in cells under replication stress, explaining why SLFN11-positive cells are markedly more efficiently killed by DNA-targeting drugs than SLFN11-negative cells. SLFN11 is inactivated in ~50% of cancer cell lines and in a large fraction of tumors, and is linked with the native immune, interferon and T-cells responses, implying the translational relevance of measuring SLFN11 expression as a predictive biomarker of response and resistance in patients. SLFN11 is also a plausible epigenetic target for reactivation by inhibitors of histone deacetylases (HDAC), DNA methyltransferases (DNMT) and EZH2 histone methyltransferase and for combination of these epigenetic inhibitors with DNA-targeting drugs in cells lacking SLFN11 expression. In addition, resistance due to lack of SLFN11 expression in tumors is a potential indication for cell-cycle checkpoint inhibitors in combination with DNA-targeting therapies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.