Trial reportProstate cancer and prostatic diseases2013
Pharmacodynamic study of disulfiram in men with non-metastatic recurrent prostate cancer.
Trial report in Prostate cancer and prostatic diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03323346 (Phase II Open Labeled Trial of Disulfiram With Copper in Metastatic Breast Cancer), which is not on this map. Cited by 36 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.
Phase II Open Labeled Trial of Disulfiram With Copper in Metastatic Breast Cancer
Who cites it
36 citing papers in PubMed, 59 citations in OpenAlex.
- Effect of Disulfiram and Copper Plus Chemotherapy vs Chemotherapy Alone on Survival in Patients With Recurrent Glioblastoma: A Randomized Clinical Trial.JAMA network open · 2023Trial
- Proteome-wide association study of prostate cancer risk across populations.Nature communications · 2025Article
- Lung cancer chemo-interception by sulfasalazine and disulfiram codelivered using a nano self-emulsifying drug delivery system in mice.Carcinogenesis · 2025Article
- Hyperbranched Polyethyleneimine-Coordinated Copper(II) Metallopolymers with Preferential Targeting to Prostate Cancer Cells.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Drug Sensitivity Testing in Osteosarcoma: A Case Report.Current oncology (Toronto, Ont.) · 2025Article
- CuET overcomes regorafenib resistance by inhibiting epithelial-mesenchymal transition through suppression of the ERK pathway in hepatocellular carcinoma.Translational oncology · 2024Article
- Cuproptosis, the novel type of oxidation-induced cell death in thoracic cancers: can it enhance the success of immunotherapy?Cell communication and signaling : CCS · 2024Review
- Co-delivery of a tumor microenvironment-responsive disulfiram prodrug and CuONanoscale advances · 2023Article
- Cuproptosis: mechanisms and links with cancers.Molecular cancer · 2023Review
- Transcription factor p8 regulates autophagy in response to disulfiram via PI3K/mTOR/p70S6K signaling pathway in pancreatic cancer cells.Human cell · 2022Article
- Mouse pharmacokinetics and metabolism of the phenylurea thiocarbamate NSC 161128.Cancer chemotherapy and pharmacology · 2022Article
- Overcoming Drug Resistance in Advanced Prostate Cancer by Drug Repurposing.Medical sciences (Basel, Switzerland) · 2022Review
- Recent progress in DNA methyltransferase inhibitors as anticancer agents.Frontiers in pharmacology · 2022Review
- Repurposing Disulfiram for Targeting of Glioblastoma Stem Cells: An In Vitro Study.Biomolecules · 2021Article
- Modulation of Intracellular Copper Levels as the Mechanism of Action of Anticancer Copper Complexes: Clinical Relevance.Biomedicines · 2021Review
- Article
- Disulfiram: a novel repurposed drug for cancer therapy.Cancer chemotherapy and pharmacology · 2021Review
- Repurposing old drugs as new inhibitors of the ubiquitin-proteasome pathway for cancer treatment.Seminars in cancer biology · 2021Review
- Disulfiram as a Therapeutic Agent for Metastatic Malignant Melanoma-Old Myth or New Logos?Cancers · 2020Review
- Dithiocarbamate prodrugs activated by prostate specific antigen to target prostate cancer.Bioorganic & medicinal chemistry letters · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundPreclinical drug screens identified disulfiram as a potent in vitro inhibitor of prostate cancer (PCa) cell growth. Although many mechanisms for its anticancer activity have been proposed, tumor suppressor gene re-expression through promoter demethylation emerged as one of the more plausible.
methodsWe conducted an open-label, dose escalation trial of disulfiram in men with non-metastatic recurrent PCa after local therapy. Dose escalation occurred if a demethylating 'response' (that is, 10% decrease in peripheral blood mononuclear cell (PBMC) global 5-methyl cytosine (5(me)C) content) was observed in <3 patients in cohort 1. Cohorts 1 and 2 received disulfiram 250 mg and 500 mg daily, respectively. The primary end point was the proportion of subjects with a demethylation response. Secondary end points included the rate of PSA progression at 6 months, changes in PSA doubling time and safety/tolerability.
resultsChanges in global 5(me)C content were observed in two of nine patients (22.2%) in cohort 1 and 3 of 10 (30.0%) in cohort 2. Only five subjects were on trial for 6 months, all were in cohort 1 and all had PSA progression by 6 months. No changes in PSA kinetics were observed in either cohort. Disulfiram was poorly tolerated with six patients experiencing grade 3 adverse events (three per cohort). Three of the responders displayed pretreatment instability in their 5(me)C content.
conclusionsA minority of patients had transient global PBMC demethylation changes. Instability in 5(me)C may limit the reproducibility of these findings, limiting our ability to confirm our hypothesis. Given the toxicities and no clinical benefits, further development of disulfiram should not be pursued in this population.
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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.