ArticleCancer medicine2025
Molecular Mechanisms of Synergistic Effect of PRIMA-1
Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Unbiased assessment of APR-246 responsive p53 mutants in ovarian cancer.Cell death discovery · 2026Article
- Synergistic anticancer and antibacterial effects of novel regimens of phytopolyphenols and repurposing drugs on cultured cells.Oncology research · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundThe toxicity and drug resistance associated with oxaliplatin (L-OHP) limit its long-term use for colorectal cancer (CRC) patients. p53 mutation is a common genetic trait of CRC. PRIMA-1
methodsCell viability was assessed with Cell Counting Kit-8 (CCK-8) assay and combination index (CI) was calculated using The Chou-Talalay method. We also employed wound healing assay and colony formation assay to determine the effect of L-OHP, PRIMA-1
resultsOur findings showed heightened cytotoxicity and inhibition of migration, and colony formation in CRC cells treated with both drugs, irrespective of p53 status, presenting a promising avenue for addressing L-OHP resistance and toxicity. RNA-seq analysis revealed differential responses between p53-wide type HCT116 and p53-mutant DLD-1 cells, with pathway alterations implicated in tumorigenesis. WGCNA identified key modules and hub genes associated with combination therapy response. In vivo studies demonstrated enhanced efficacy of combined therapy over PRIMA-1
conclusionsIn summary, our research reveals the differential molecular mechanisms of combined PRIMA-1
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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.