ReviewOncogene2003
Cisplatin: mode of cytotoxic action and molecular basis of resistance.
Review in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,325 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
1,325 citing papers in PubMed, 3,295 citations in OpenAlex.
- Control of Gemcitabine Activity With Blue and Red Light.Chemistry (Weinheim an der Bergstrasse, Germany) · 2026Article
- Role of the MDM2/p53 axis in regulating cisplatin response in tumor cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Unraveling the Mechanisms of Chemoresistance in Gastric Cancer: Insights and Emerging Research Strategies.Current oncology reports · 2026Review
- Pt(iv) scaffold effects on nucleolar stress and DNA damage response pathways.RSC chemical biology · 2026Article
- Targeting fibroblast activation suppresses chemotherapy-induced pro-invasive remodeling of the extracellular matrix.bioRxiv : the preprint server for biology · 2026Article
- Unveiling Distinct Developmental and Cellular Impacts of Cisplatin on Zebrafish (Methods and protocols · 2026Article
- Metabolomic Analysis of Intracellular Amino Acid Profile Differences Between Cisplatin-Resistant and Cisplatin- Sensitive CALU-1 Lung Cancer Cells.Cell biochemistry and biophysics · 2026Article
- Autophagy as a therapeutic target for cisplatin-resistant gastric cancer.Genes & diseases · 2026Review
- The role of KIAA1467 in breast cancer: insights from pan-cancer and single-cell sequencing analysis.Translational cancer research · 2026Article
- 10-HDA Suppresses the Growth of Gastric Cancer Cells Through Inducing Apoptosis and G0/G1 Cell Cycle Arrest.Nutrients · 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
- Nanocarrier-based delivery of Pt(IV) compounds for chemoimmunotherapy and theranostics: Advances, challenges, and prospects.Acta pharmaceutica Sinica. B · 2026Review
- Oncogenic EGFR rewires STING-TBK1 signalosomes to license DNA damage tolerance in NSCLC.The EMBO journal · 2026Article
- Evaluation of the Cytotoxic and Antimigratory Activity Induced by [Pt(1-hexyl-1International journal of molecular sciences · 2026Article
- Role of circular RNAs in regulating toxicity induced by cancer therapies.Genes & diseases · 2026Review
- Oxidative stress-driven mRedox biology · 2026Article
- Intercalation Favors DNA Covalent Photobinding in Photoresponsive Dual PDT/PCT Bimetallic Assemblies.Journal of chemical information and modeling · 2026Article
- Integrated Evaluation of the Synergistic Antitumor Effects of Thymoquinone and Docetaxel in Ovarian Cancer Cells: Apoptosis, Oxidative Stress, and 3D Spheroid Responses.Biomedicines · 2026Article
- Spatiotemporal organisation of residual disease in mouse and human BRCA1-deficient mammary tumours and breast cancer.Nature communications · 2026Article
1,265 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
1 author at 1 institution in 1 country.
Funding
Abstract
Cisplatin is one of the most potent antitumor agents known, displaying clinical activity against a wide variety of solid tumors. Its cytotoxic mode of action is mediated by its interaction with DNA to form DNA adducts, primarily intrastrand crosslink adducts, which activate several signal transduction pathways, including those involving ATR, p53, p73, and MAPK, and culminate in the activation of apoptosis. DNA damage-mediated apoptotic signals, however, can be attenuated, and the resistance that ensues is a major limitation of cisplatin-based chemotherapy. The mechanisms responsible for cisplatin resistance are several, and contribute to the multifactorial nature of the problem. Resistance mechanisms that limit the extent of DNA damage include reduced drug uptake, increased drug inactivation, and increased DNA adduct repair. Origins of these pharmacologic-based mechanisms, however, are at the molecular level. Mechanisms that inhibit propagation of the DNA damage signal to the apoptotic machinery include loss of damage recognition, overexpression of HER-2/neu, activation of the PI3-K/Akt (also known as PI3-K/PKB) pathway, loss of p53 function, overexpression of antiapoptotic bcl-2, and interference in caspase activation. The molecular signature defining the resistant phenotype varies between tumors, and the number of resistance mechanisms activated in response to selection pressures dictates the overall extent of cisplatin resistance.
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.