Trial reportScientific reports2014
No evident dose-response relationship between cellular ROS level and its cytotoxicity--a paradoxical issue in ROS-based cancer therapy.
Trial report in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 120 citations in OpenAlex.
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- Biofilm-Antagonist Ginger-Based 3D-Printable Photoresins for Complex Implant Designs Exhibiting Advanced Multifunctional Biomedical Applications.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Bioactive Artificial Cells as Autonomous Metabolic Actuators Enable Bidirectional Communication with Tumor Cells.Journal of the American Chemical Society · 2025Article
- Protective Effects ofJournal of microbiology and biotechnology · 2025Article
- Flavonoids Derived fromNutrients · 2025Article
- Identification and functional validation of ACSL1 as a biomarker regulating ferroptosis in nucleus pulposus cell.Bioscience reports · 2025Article
- Role of Oxidative Stress in the Occurrence, Development, and Treatment of Breast Cancer.Antioxidants (Basel, Switzerland) · 2025Review
- Redox-Sensitive Fluorescent Nanoparticles for Biovisualization of Malignant Tumors.Sovremennye tekhnologii v meditsine · 2025Article
- Differential Regulation of Wingless-Wnt/c-Jun N-Terminal Kinase Crosstalk via Oxidative Eustress in Primary and Metastatic Colorectal Cancer Cells.Biomedicines · 2024Article
- Oxidative stress is two-sided in the treatment of acute myeloid leukemia.Cancer medicine · 2024Review
- Unresolved questions regarding cellular cysteine sources and their possible relationships to ferroptosis.Advances in cancer research · 2024Review
- Iron-based metal-organic framework co-loaded with buthionine sulfoximine and oxaliplatin for enhanced cancer chemo-ferrotherapy via sustainable glutathione elimination.Journal of nanobiotechnology · 2023Article
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- Therapeutic Potential ofAntioxidants (Basel, Switzerland) · 2023Article
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- [Hypoxia promotes differentiation of human induced pluripotent stem cells into embryoid bodiesNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- The role of reactive oxygen species in the immunity induced by nano-pulse stimulation.Scientific reports · 2021Article
- Article
- Lactate dehydrogenases amplify reactive oxygen species in cancer cells in response to oxidative stimuli.Signal transduction and targeted therapy · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeting cancer via ROS-based mechanism has been proposed as a radical therapeutic approach. Cancer cells exhibit higher endogenous oxidative stress than normal cells and pharmacological ROS insults via either enhancing ROS production or inhibiting ROS-scavenging activity can selectively kill cancer cells. In this study, we randomly chose 4 cancer cell lines and primary colon or rectal cancer cells from 4 patients to test the hypothesis and obtained following paradoxical results: while piperlongumin (PL) and β-phenylethyl isothiocyanate (PEITC), 2 well-defined ROS-based anticancer agents, induced an increase of cellular ROS and killed effectively the tested cells, lactic acidosis (LA), a common tumor environmental factor that plays multifaceted roles in promoting cancer progression, induced a much higher ROS level in the tested cancer cells than PL and PEITC, but spared them; L-buthionine sulfoximine (L-BSO, 20 μM) depleted cellular GSH more effectively and increased higher ROS level than PL or PEITC but permitted progressive growth of the tested cancer cells. No evident dose-response relationship between cellular ROS level and cytotoxicity was observed. If ROS is the effecter, it should obey the fundamental therapeutic principle - the dose-response relationship. This is a major concern.
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.