ReviewOncogene2003
Mechanisms of resistance to topoisomerase I-targeting drugs.
Review in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
62 citing papers in PubMed, 174 citations in OpenAlex.
- Trastuzumab deruxtecan in HER2-positive advanced gastric cancer: exploratory biomarker analysis of the randomized, phase 2 DESTINY-Gastric01 trial.Nature medicine · 2024Trial
- Antibody-Drug Conjugates in Lung Cancer: Promise, Progress, and Persistent Challenges.Current issues in molecular biology · 2026Review
- Recent advances in function-enhanced antibody-drug conjugates: Antibody optimization and payload combination.Acta pharmacologica Sinica · 2026Article
- Targeting the cancer metabolism-immunity interface: update and perspectives.Experimental hematology & oncology · 2026Review
- Metabolic drivers of genome instability in cancer: mechanisms and therapeutic opportunities.Experimental hematology & oncology · 2026Review
- Drug resistance to antibody-drug conjugates: mechanisms, challenges, and perspectives.Cancer biology & medicine · 2026Review
- FOXM1 induces therapy resistance and inhibits apoptosis in a variety of human cancers.Cell death & disease · 2026Review
- Mechanisms of resistance to antibody-drug conjugates in cancer: molecular barriers and pharmacological solutions.Cancer chemotherapy and pharmacology · 2025Review
- Resistance to antibody-drug conjugates: A review.Acta pharmaceutica Sinica. B · 2025Review
- In vitro evolution and whole genome analysis to study chemotherapy drug resistance in haploid human cells.Scientific reports · 2024Article
- Antibody-drug conjugates in breast cancer: overcoming resistance and boosting immune response.The Journal of clinical investigation · 2023Review
- Topoisomerase I poisons-induced autophagy: Cytoprotective, Cytotoxic or Non-protective.Autophagy reports · 2023Article
- Dual Topoisomerase I/II Inhibition-Induced Apoptosis and Necro-Apoptosis in Cancer Cells by a Novel Ciprofloxacin Derivative via RIPK1/RIPK3/MLKL Activation.Molecules (Basel, Switzerland) · 2022Article
- Article
- AKT inhibition sensitizes EVI1 expressing colon cancer cells to irinotecan therapy by regulating the Akt/mTOR axis.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- TDP1-independent pathways in the process and repair of TOP1-induced DNA damage.Nature communications · 2022Article
- Targeted Delivery of DNA Topoisomerase Inhibitor SN38 to Intracranial Tumors of Glioblastoma Using Sub-5 Ultrafine Iron Oxide Nanoparticles.Advanced healthcare materials · 2022Article
- DNA repair and cholesterol-mediated drug efflux induce dose-dependent chemoresistance in nutrient-deprived neuroblastoma cells.iScience · 2021Article
- Natural Compounds as Therapeutic Agents: The Case of Human Topoisomerase IB.International journal of molecular sciences · 2021Review
- Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA topoisomerases are a class of enzymes that alter the topology of DNA and are targets of several anticancer drugs. Camptothecins (CPTs) are a relatively new family of compounds that specifically target topoisomerase I (Top1). These compounds "poison" Top1 by binding to the Top1-DNA complex in a manner that prevents the religation of DNA. Topotecan and irinotecan are two CPTs that are approved for the treatment of a variety of malignancies, including colorectal, ovarian, and small cell lung cancers, as well as myeloid malignancies. Although CPTs have proven to be effective anticancer drugs, resistance is still a critical clinical problem. The mechanisms underlying de novo and acquired clinical resistance to CPTs and the newer classes of Top1 poisons are unclear. However, based on preclinical studies, it is likely that clinical resistance to these drugs is the result of: (1) inadequate accumulation of drug in the tumor, (2) resistance-conferring alterations in Top1, or (3) alterations in the cellular response to the Top1-CPT interaction. This review will focus on the current knowledge regarding mechanisms of resistance to CPTs and other Top1-targeting drugs.
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What OpenQuestion holds
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.