ArticleScientific reports2025
L-Ascorbic acid preferentially kills KRAS mutant pancreatic cancer cells through DNA damage.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed.
- KRAS signaling networks, mutational heterogeneity, and emerging therapeutic strategies for cancer treatment.Biomarker research · 2026Review
- Beyond redox: vitamin C in signaling, epigenetic regulation and protein modification-relevance to cancer therapy.Clinical epigenetics · 2026Review
- The Influence of Vitamin C on Stromal and Epithelial Cells of the Pancreas in Malignant and Benign/Inflammatory Pancreatic Diseases: Protocol for a Scoping Review.JMIR research protocols · 2026Article
- A Comprehensive Review of Vitamin C for Cancer Therapy: Anti-Tumor Mechanisms and Nano-Formulation Strategies.International journal of nanomedicine · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Pancreatic cancer (PC) is a worldwide leading cause of cancer-related death. Despite recent progress using immunotherapy with checkpoint inhibitors or targeted agents in various solid tumors, these approaches have not been successful in PC. Therefore, there is an urgent unmet need for the development of novel therapeutics for these difficult-to-treat patients. We hypothesized that high-dose L-ascorbic acid (AA) could disrupt redox homeostasis and selectively inhibit the viability of PC cells harboring KRAS mutations; thus, we investigated the molecular mechanism of AA cytotoxicity in PC cell lines (Hs 700T, BxPC-3, HPAC, HPAF-II, PANC-1, SU.86.86, and Hs 766T) and patient-derived cells (PDCs; PR11-043T and PR11-077T)), identifying a subset of patients who may benefit from AA therapy and opening an avenue for further clinical development. In this preclinical study, we found that AA efficiently inhibited the growth of KRAS G12D-mutant PC cells. Mechanistically, this was due to selective glycolysis inhibition via GAPDH inactivation and DNA damage, in PC cell lines harboring KRAS G12D. We also showed that AA synergizes with the DNA-damaging agent AZD6738 in PC cells and AA induces an enhanced DNA damage response in BRCA mutant PC cells, as confirmed in PC PDCs having with KRAS G12D or BRCA1/2 mutation. This study showed the antitumor activity of AA in PC cells and PDCs, indicating that KRAS G12D identifies an attractive subset of PC cells for treatment using AA and novel agents targeting key molecules involved the DNA damaging pathway. In addition, DNA damage response (DDR)-defective cell subsets, including germline BRCA1/2 mutants, may be potential candidates for this novel approach, which provides new insights for future clinical development.
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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.