ArticleSmall GTPases2017
KRas, ROS and the initiation of pancreatic cancer.
Article in Small GTPases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 79 citations in OpenAlex.
- PRDX4 expression potentially links redox adaptation to oncogenic signaling and tumor progression in pancreatic ductal adenocarcinoma.Translational oncology · 2026Article
- Review
- Rosindol: A fluorogen for the quantitative measurement of reactive oxygen species in living cells.bioRxiv : the preprint server for biology · 2026Article
- Combined assessment of stromal tumor infiltrating lymphocytes and tumor peroxiredoxin 4 expression improved prognostic stratification in postoperative pancreatic cancer patients.Diagnostic pathology · 2026Article
- Downregulation of Sod2 increases atypical flat lesions and dysplasia to advance pancreatic ductal adenocarcinoma.Molecular cancer · 2025Article
- Article
- The Impact of Peroxiredoxin 3 on Molecular Testing, Diagnosis, and Prognosis in Human Pancreatic Ductal Adenocarcinoma.Cancers · 2025Article
- Assessment of the Nutraceutical Properties of Wild Strawberry (Fragaria vesca L.) Extracts on Human Colorectal Cell Lines.Molecular nutrition & food research · 2025Article
- Targeted mitochondrial therapy for pancreatic cancer.Translational oncology · 2025Review
- Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025Review
- EGFR-targeting RNase A-cetuximab antibody-drug conjugate induces ROS-mediated apoptosis to overcome drug resistance in KRAS mutant cancer cells.Scientific reports · 2025Article
- Physical Activity and Incident Pancreatic Cancer: Results From the UK Biobank Prospective Cohort.Cureus · 2025Article
- Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer.Current issues in molecular biology · 2024Review
- Inhibition of the PI3K/AKT/mTOR pathway in pancreatic cancer: is it a worthwhile endeavor?Therapeutic advances in medical oncology · 2024Review
- Iron-Dependent Cell Death: A New Treatment Approach against Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2023Review
- Crosstalk of ferroptosis regulators and tumor immunity in pancreatic adenocarcinoma: novel perspective to mRNA vaccines and personalized immunotherapy.Apoptosis : an international journal on programmed cell death · 2023Article
- Senescence program and its reprogramming in pancreatic premalignancy.Cell death & disease · 2023Review
- Zooming in and out of ferroptosis in human disease.Frontiers of medicine · 2023Review
- Circulating gamma-glutamyl transpeptidase and risk of pancreatic cancer: A prospective cohort study in the UK Biobank.Cancer medicine · 2023Article
- Overview of Cancer Metabolism and Signaling Transduction.International journal of molecular sciences · 2022Review
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
Oncogenic mutations of KRAS are the most frequent driver mutations in pancreatic cancer. Expression of an oncogenic allele of KRAS leads to metabolic changes and altered cellular signaling that both can increase the production of intracellular reactive oxygen species (ROS). Increases in ROS have been shown to drive the formation and progression of pancreatic precancerous lesions by upregulating survival and growth factor signaling. A key issue for precancerous and cancer cells is to keep ROS at levels where they are beneficial for tumor development and progression, but below the threshold that leads to induction of senescence or cell death. In KRas-driven neoplasia aberrantly increased ROS levels are therefore balanced by an upregulation of antioxidant genes.
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.