ReviewClinics (Sao Paulo, Brazil)2018
DNA repair pathways and cisplatin resistance: an intimate relationship.
Review in Clinics (Sao Paulo, Brazil), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 258 papers, 1 of them a synthesis that pooled it.
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
258 citing papers in PubMed, 1 synthesis or guideline pooled it, 439 citations in OpenAlex.
- Genetic polymorphisms and platinum-induced hematological toxicity: a systematic review.Frontiers in pharmacology · 2024Pooled it
- Transcription remodeling and stalling by cisplatin-induced interstrand crosslinks.Nature chemical biology · 2026Article
- Integrated stress response activation in combination PG3 and cisplatin-treatedbioRxiv : the preprint server for biology · 2026Article
- Article
- Immunohistochemical expression of JAK2, STAT3, POLH, UBE2T, and REV7 in serous ovarian carcinoma: clinicopathological associations and co-expression patterns.Journal of molecular histology · 2026Article
- DNA Polymerase Beta Catalytic and Fidelity Mutations Drive Platinum-Specific Drug Sensitivity.Cancers · 2026Article
- Translational control by RPL22L1-specific ribosomes enhances DNA repair and chemoresistance.Nature communications · 2026Article
- The Dual Role of Human UDP-Glucuronosyltransferase-Mediated Metabolism in Tumor Drug Resistance: Mechanisms and Prospects.International journal of molecular sciences · 2026Review
- HMGB2 Impacts Cisplatin-Induced DNA Adduct Processing in Chemoresistant Ovarian Cancer Cells.Genes · 2026Article
- IDO1 Silencing Enhances Cisplatin Sensitivity in Gastric Cancer Cells via Modulation of Apoptosis and Oxidative Stress.Current issues in molecular biology · 2026Article
- A kinetically inert platinum antitumor agent overcomes mutant p53-driven chemoresistance via oxidative stress-mediated DNA damage.Medical oncology (Northwood, London, England) · 2026Article
- Mechanisms of resistance in small cell lung cancer.Chinese medical journal · 2026Review
- The role of oxidative stress and antioxidant therapy in cisplatin neurotoxicity: preclinical evidence in the last decade.Archives of toxicology · 2026Review
- Development and Characterization of a Guar Gum Bionanocomposite Loaded with Biogenic Selenium Nanoparticles and Its Cytotoxic Evaluation.Gels (Basel, Switzerland) · 2026Article
- A Cisplatin-Based Prodrug Inhibits Nucleotide Excision Repair Independently of Chromatin Accessibility to Overcome Resistance.Biomolecules · 2026Article
- Navigating the Genetic Risk of Chemotherapy-Induced Hearing Loss in the Stria Vascularis.Clinical pharmacology and therapeutics · 2026Review
- Combining 5-ALA-PDT with berbamine as an in vitro multimodal therapy approach against bladder cancer cells.Scientific reports · 2026Article
- Treatment strategies for locally advanced and metastatic urothelial carcinoma based on molecular profiles: A Review.Histology and histopathology · 2026Review
- Discovery of Two Structurally Distinct Classes of Inhibitors Targeting the Nuclease MUS81 and Enhancing Efficacy of Chemotherapy in Cancer Cells.Journal of medicinal chemistry · 2026Article
- HMGB1 Assists in Overcoming Cisplatin Resistance in Chemoresistant Human Ovarian Cancer Cells.Molecular carcinogenesis · 2026Article
198 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
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The main goal of chemotherapeutic drugs is to induce massive cell death in tumors. Cisplatin is an antitumor drug widely used to treat several types of cancer. Despite its remarkable efficiency, most tumors show intrinsic or acquired drug resistance. The primary biological target of cisplatin is genomic DNA, and it causes a plethora of DNA lesions that block transcription and replication. These cisplatin-induced DNA lesions strongly induce cell death if they are not properly repaired or processed. To counteract cisplatin-induced DNA damage, cells use an intricate network of mechanisms, including DNA damage repair and translesion synthesis. In this review, we describe how cisplatin-induced DNA lesions are repaired or tolerated by cells and focus on the pivotal role of DNA repair and tolerance mechanisms in tumor resistance to cisplatin. In fact, several recent clinical findings have correlated the tumor cell status of DNA repair/translesion synthesis with patient response to cisplatin treatment. Furthermore, these mechanisms provide interesting targets for pharmacological modulation that can increase the efficiency of cisplatin chemotherapy.
Indexed as
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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.