Research Radartracking 1,762 published studies · 471 human · 11 safety signals · 58 clinical trials · 44 cancer pages · updated Sep 2026Open the Research Map →
Educational only, not medical advice. OncoForge makes no claim that Selenium (Stand-alone) treats, prevents, or cures any condition, beyond what the linked studies show. Evidence levels vary; effects may not translate to people, and some compounds can cause harm. Always coordinate with your oncology team.
Key Takeaway
Cofactor for selenoenzymes (GPx, TrxR) that buffers redox stress; certain selenium metabolites (e.g., methylselenol) can push p53-mediated apoptosis. Clinical signals are context-dependent—benefit is more likely when correcting deficiency; indiscriminate high-dose use can be harmful.
Selenium incorporates into glutathione peroxidases (GPx) and thioredoxin reductases (TrxR), lowering peroxides and stabilizing redox signaling. Pro-apoptotic selenium metabolites (methylselenol) enhance p53 transactivation, DNA damage responses, and caspase cleavage, selectively stressing tumor cells with impaired antioxidant reserve. In adjunct settings, selenium may reduce chemo/radiotoxicity and modulate immunity; prevention data are mixed and strongly moderated by baseline selenium status and chemical form.
Targets & pathways
Curated mechanistic targets reported for this agent — how it may act on cells, not proof of a clinical effect.
Vitamin E: Antioxidant in lung, but caution prostate.
Overlapping mechanisms
Redox: Overlaps vitamin E/sulforaphane; status ceiling.
p53: Redundant inducers; monitor genotox.
Safety & interactions
Severity and how well-established each signal is are shown separately. Verify everything with your oncologist or pharmacist — absence here does not mean safe.
Risk categories
SelenosisDeficiency WorsenVitamin E Interaction
Potential interactions
platinum_chemoMonitorLowTheoreticalPotential antagonism; time separately.
What has been studied, and how strong it is, by topic. A dashed cell means no studies were found for that combination — a gap, not evidence of no effect. Open a row to see its studies.
This is a narrative review examining the potential role of selenium in glioblastoma. The authors summarize evidence that selenium, an essential micronutrient, has antioxidative and anti-cancer properties, may be deficient in patients with brain malignancies, and could influence glioblastoma biology through selenoprotein-mediated redox regulation, effects on angiogenesis, brain edema, and interactions in the tumor microenvironment.
Studied with: radiochemotherapy, surgery.
Key findings
Latest investigations suggest micronutrients such as selenium may have positive effects relevant to glioblastoma management and to limitations of surgery and radiochemotherapy.
Selenium is described as an essential micronutrient with anti-oxidative and anti-cancer properties.
There is evidence of selenium deficiency in patients suffering from brain malignancies according to the authors.
Selenium, via selenoproteins, modulates metabolic pathways and regulates redox homeostasis.
Selenium impacts interactions in the tumor microenvironment among tumor cells, tumor-associated cells, and immune cells, with implications for angiogenesis, brain edema, and glioma-associated microglia/macrophages.
Limitations: Review article — no new primary experimental or clinical data presented in this abstract.; Abstract does not report clinical trial data, doses, safety, or therapeutic windows for selenium in glioblastoma.; Conclusions appear to synthesize prior studies; the strength and type (preclinical vs clinical) of that evidence are not detailed in the abstract.; Potential for publication or selection bias inherent to narrative reviews; systematic search and inclusion criteria are not described in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
This is a narrative review summarizing recent evidence on how diet influences colorectal cancer risk. The authors state that a Western diet (high in fat, red and processed meat) is associated with increased risk, whereas higher dietary fiber and some micronutrients (vitamin D, selenium, calcium, antioxidants) may have protective effects; diet-induced changes in the gut microbiota can either increase or decrease risk.
Key findings
Western diet characterized by high fat, red meat and processed meat intake is an important contributor to colorectal cancer risk.
High intake of dietary fiber may partially counteract the unfavorable effects of meat via reduced intestinal transit time, dilution of carcinogens, antioxidant provision, and increased production of protective fermentation products such as butyrate.
Some micronutrients (vitamin D, selenium, calcium, vitamins C and E) have been advocated to have protective effects against colorectal cancer.
Diet-induced modifications of the gut microbiota modulate colonic epithelial homeostasis and can produce either mutagenic/carcinogenic agents or protective compounds.
Modification of diet and lifestyle may modify colorectal cancer risk and, per the authors' statement, could prevent neoplasia in up to 50% of cases.
Limitations: This is a review article that does not present new primary data or original trial results.; The review summary includes broad prevention estimates (e.g., "up to 50%" prevented) that are not quantified here and may reflect underlying heterogeneity in the literature.; Dietary and microbiome effects are described as having opposing effects under different conditions, indicating complexity and potential heterogeneity across studies..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 103
Researchers measured tumor DNA S-phase fraction (SPF) as a marker of growth in 103 cases of invasive squamous cervical cancer and compared SPF (<14% vs ≥14%) with DNA ploidy, serum progesterone, serum estradiol, smoking and clinical/pathological factors. They report that aneuploidy, serum progesterone ≥2.6 nmol/l, and smoking were significantly associated with higher SPF (≥14%) after adjustment, with the progesterone and smoking associations driven by premenopausal women. The authors conclude increased tumor growth was associated with higher serum progesterone, smoking and aneuploidy in these patients.
Sample: 103 cases of squamous cervical cancer stage IB-IV; tumor growth measured by DNA S-phase fraction (SPF), dichotomized at 14%.
Aneuploidy was significantly associated with SPF ≥14% (odds ratio (OR) 10.0).
Serum progesterone ≥2.6 nmol/l was significantly associated with SPF ≥14% (OR 7.5).
Smoking was significantly associated with SPF ≥14% (OR 3.0).
The associations of serum progesterone and smoking with higher SPF were attributed to an increased risk among premenopausal women.
Limitations: Observational cross-sectional design — cannot establish causation, only association.; Abstract provides limited detail on adjustment covariates and analytic methods.; Timing of serum hormone measurements relative to menstrual cycle or treatment is not reported in the abstract.; Single-cohort sample of 103 patients; generalizability and potential for residual confounding not addressed in abstract..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed
What changed recently
The latest additions to Selenium (Stand-alone)'s evidence base, and anything that's been retracted.
Cancers where Selenium (Stand-alone) reported positive results
Where at least one study reported a positive result, shown with the full picture, not just the wins. Positive results are more likely to be published, and most of these are early lab or animal studies that may not translate to people. This reports what studies found, not what works.
Human evidence
Squamous cell carcinoma of the cervix1 positive1 human
Limitations: Observational cross-sectional design — cannot establish causation, only association.; Abstract provides limited detail on adjustment covariates and analytic methods.; Timing of serum hormone measurements relative to menstrual cycle or treatment is not reported in the abstract.; Single-cohort sample of 103 patients; generalizability and potential for residual confounding not addressed in abstract..
Limitations: Review article — no new primary experimental or clinical data presented in this abstract.; Abstract does not report clinical trial data, doses, safety, or therapeutic windows for selenium in glioblastoma.; Conclusions appear to synthesize prior studies; the strength and type (preclinical vs clinical) of that evidence are not detailed in the abstract.; Potential for publication or selection bias inherent to narrative reviews; systematic search and inclusion criteria are not described in the abstract..
Evidence at a glance: Selenium (Stand-alone) by cancer
A deterministic grade of what published studies report for each: strength of evidence, the reported direction, and the largest credible effect, strongest-evidence first. This summarizes findings; it is not a claim that anything works.
Squamous cell carcinoma of the cervix◐Human · observational▲Reported positive1 human
Human observational evidence only — no trials.
Largest credible effect: Aneuploidy (OR) 10 PMID 11268431 · odds ratios 3–10 across 3 studies
No human studies yet · No numeric effect sizes reported · Based on a single study.
Dose: as studied, not a recommendation
These are doses as studied or reported, never a recommendation. The right amount of Selenium (Stand-alone) depends on you, your other medicines, and your situation; decide it with your oncology team and pharmacist, not from a web page.
Ranges seen in adjunct / practice use: 55–200 mcg/day (po) With meals; status-guided, RDA 55 mcg (women)/70 mcg (men); adjunct 100-200 mcg/day; upper safe 400 mcg; test serum Se 70-150 mcg/L target..
Clinical trials studying Selenium (Stand alone)
0 ongoing · 1 completed · tracked from ClinicalTrials.gov. Recruiting is not the same as proven, and completed is not the same as positive — read the results. Not a recommendation.
Selenium (Stand-alone) is named in these protocols discussed online. Listed for transparency: being part of a protocol is not evidence that it works, and OncoForge does not endorse them.
Inclusion here is not an endorsement. OncoForge makes no claim beyond what the linked studies show. Discuss anything on this page with your oncology team before acting on it.