ReviewCancers2021
Platinum Complexes in Colorectal Cancer and Other Solid Tumors.
Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 80 citations in OpenAlex.
- Co-Exposure to Lunasin and Other Drugs as a Potential Chemopreventive Strategy Against Breast and Colon Cancers: A Review.International journal of molecular sciences · 2026Review
- Radiation-Associated Enteric-Type Urethral Adenocarcinoma 20 Years After Prostate Brachytherapy: A Case Treated With Neoadjuvant Gemcitabine-Cisplatin and Robot-Assisted Radical Cystectomy.IJU case reports · 2026Article
- Combinational studies of BOLD-100/KP1339 with established chemotherapeutics in gastrointestinal multicellular tumor spheroids.Cancer chemotherapy and pharmacology · 2026Article
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- Article
- Deciphering Pharmacological Targets of Plumbagin in Cisplatin-resistant Ovarian Cancer Model usingCurrent pharmaceutical design · 2026Article
- Integrative Evaluation ofMolecules (Basel, Switzerland) · 2025Article
- Colorectal Cancer at the Crossroads: The Good, the Bad, and the Future of Platinum-Based Drugs.Chemical reviews · 2025Review
- The SPINK Protein Family in Cancer: Emerging Roles in Tumor Progression, Therapeutic Resistance, and Precision Oncology.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Understanding microRNA-Mediated Chemoresistance in Colorectal Cancer Treatment.International journal of molecular sciences · 2025Review
- Identification of Penexanthone A as a Novel Chemosensitizer to Induce Ferroptosis by Targeting Nrf2 in Human Colorectal Cancer Cells.Marine drugs · 2024Article
- Synergistic Mechanisms of Selected Polyphenols in Overcoming Chemoresistance and Enhancing Chemosensitivity in Colorectal Cancer.Antioxidants (Basel, Switzerland) · 2024Review
- USP25 Elevates SHLD2-Mediated DNA Double-Strand Break Repair and Regulates Chemoresponse in Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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- Extracellular vesicles containing MFGE8 from colorectal cancer facilitate macrophage efferocytosis.Cell communication and signaling : CCS · 2024Article
- Baicalin enhances the chemotherapy sensitivity of oxaliplatin-resistant gastric cancer cells by activating p53-mediated ferroptosis.Scientific reports · 2024Article
- Effects of Reduced Extracellular Sodium Concentrations on Cisplatin Treatment in Human Tumor Cells: The Role of Autophagy.International journal of molecular sciences · 2024Article
- Strong apoptotic response of testis tumor cells following cisplatin treatment.International urology and nephrology · 2024Article
- Cytokine-armed dendritic cell progenitors for antigen-agnostic cancer immunotherapy.Nature cancer · 2024Article
- p53 deficiency mediates cisplatin resistance by upregulating RRM2 and crotonylation of RRM2Frontiers in molecular biosciences · 2024Article
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin is one of the most commonly used drugs for the treatment of various solid neoplasms, including testicular, lung, ovarian, head and neck, and bladder cancers. Unfortunately, the therapeutic efficacy of cisplatin against colorectal cancer is poor. Various mechanisms appear to contribute to cisplatin resistance in cancer cells, including reduced drug accumulation, enhanced drug detoxification, modulation of DNA repair mechanisms, and finally alterations in cisplatin DNA damage signaling preventing apoptosis in cancer cells. Regarding colorectal cancer, defects in mismatch repair and altered p53-mediated DNA damage signaling are the main factors controlling the resistance phenotype. In particular, p53 inactivation appears to be associated with chemoresistance and poor prognosis. To overcome resistance in cancers, several strategies can be envisaged. Improved cisplatin analogues, which retain activity in resistant cancer, might be applied. Targeting p53-mediated DNA damage signaling provides another therapeutic strategy to circumvent cisplatin resistance. This review provides an overview on the DNA repair pathways involved in the processing of cisplatin damage and will describe signal transduction from cisplatin DNA lesions, with special attention given to colorectal cancer cells. Furthermore, examples for improved platinum compounds and biochemical modulators of cisplatin DNA damage signaling will be presented in the context of colon cancer therapy.
Indexed as
Identifiers
What Socratic 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 Socratic graph.