ReviewJournal of molecular biology2026
Targeting DNA Topoisomerase I for the Treatment of Cancer: Past, Present and Future.
Review in Journal of molecular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- RAD51C breast cancer-identified variants with attenuated homologous recombination function exhibit sensitivity to combined PARP1 and ATR inhibition.NAR cancer · 2026Article
- Molecular Determinants of Response and Rational Drug Combinations for Antibody-Drug Conjugates (ADCs) with Topoisomerase I (TOP1) Inhibitor Payloads.Journal of molecular biology · 2026Review
- Irinotecan plus temozolomide for pediatric relapsed or refractory solid tumors: a retrospective cohort study.Translational pediatrics · 2026Article
- Identifying potential binding sites for complex formation between Tyrosyl-DNA phosphodiesterase 1 and poly [ADP-ribose] polymerase 1.Physical chemistry chemical physics : PCCP · 2026Article
- Enhancing the Water Solubility and Efficacy of Anticancer Drugs Using Hydroxypropyl-β-Cyclodextrin.International journal of molecular sciences · 2026Review
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.
Funding
Abstract
As an enzyme that relaxes torsionally strained DNA, TOP1 is present in all nucleated human somatic cells. Even though this ubiquity makes TOP1 an unlikely anticancer drug target, six FDA-approved antineoplastic treatments, including two approved in the past five years, and a variety of experimental agents inhibit the TOP1 catalytic cycle. To provide insight into the continuing effort to develop TOP1-directed agents, here we briefly review the biology of TOP1, the cellular effects of stabilizing TOP1-DNA covalent complexes, mechanisms of resistance to TOP1 poisons, and strategies to overcome this resistance before describing efforts to develop TOP1 catalytic inhibitors as well as an exciting new generation of tumor targeting nanoparticles and antibody-drug conjugates that deliver TOP1-directed agents to cancers at high concentrations while sparing normal tissues. When paired with inhibitors of DNA damage response pathways, epigenetic therapies, or immune modulators, these new TOP1-directed agents promise to improve the therapy of a wide range of solid tumors.
Indexed as
Identifiers
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.