Database Query Results : Selenium, , Risk

Se, Selenium: Click to Expand ⟱
Features: micronutrient
Naturally occurring element. Selenium is incorporated into selenoproteins, such as glutathione peroxidases (GPxs) and thioredoxin reductases (TrxRs), which play critical roles in protecting cells from oxidative damage.
Involved in GPx, TrxR, ans Selenoprotien P which protect normal cells from oxidative stress.
Important in Thyroid hormone metabolism, immune system regulation, reproductive health, and Brain and heart protection.

-recommended daily allowance (RDA) for selenium is about 55 µg/day for adults. (upper tolerance 400ug/day)
-One Brazil nut may contain 50-300ug/nut

Sodium selenite (Na₂SeO₃) is a selenium compound with well-documented anticancer and chemopreventive properties
-Oxidation state: +4 (selenite form of selenium)
-Type: Inorganic selenium compound (water-soluble)

-Sodium selenite generates reactive oxygen species (ROS) selectively in tumor cells.
-Induces cytochrome c release, caspase-3 activation, and DNA fragmentation.
-Reduces VEGF expression and endothelial cell migration.
-Blocks cell division at G2/M phase
-Suppresses MMP-2 and MMP-9 activity
-Activates p53
-Inhibits NF-κB
-PI3K/Akt/mTOR Suppression
-Inactivation of Thioredoxin/Glutathione systems
-NRF2 inhibition in cancer cell might be connected with O2 level

Narrow therapeutic window:
-Low micromolar (≤5 µM) → anticancer
-High (>10 µM) → toxic to normal cells

Some Selenium Supplements use Sodium Selenite as the active ingredient.
- NOW Foods Selenium, Nature's Bounty Selenium, etc

Other common form is Selenomethionine, as it is better absorbed (found in brazil nuts), but might be less effective?
| Category                             | Role in cancer                                                                                  |
| -------------------------------- | ----------------------------------------------------------------------------------------------- |
| Sodium Selenium (selenite)       | Direct cytotoxic redox poison                                                                   |
| Selenium (organic / nutritional) | **Redox buffer & immune modulator** (generally *anti-therapy* when oxidative stress is desired) |
| SeNPs                            | Tunable redox-signaling anticancer platform                                                     |

Selenium (Organic / Nutritional) — Cancer-Relevant Pathways
Rank Pathway / Target Axis Direction Primary Effect Notes / Cancer Relevance Ref
1 Selenoprotein antioxidant systems (GPX1–4, TXNRD) ↑ antioxidant capacity ROS buffering Dietary selenium increases glutathione peroxidase and thioredoxin reductase activity, lowering oxidative stress (ref)
2 Glutathione redox cycling (GSH/GSSG) ↑ GSH recycling Redox homeostasis Selenium supports GPX-mediated peroxide detoxification and preserves cellular GSH pools (ref)
3 Ferroptosis suppression (GPX4 axis) ↓ ferroptosis susceptibility Lipid peroxide detoxification GPX4 is a selenoprotein; adequate selenium suppresses lipid peroxidation and ferroptotic death (ref)
4 NRF2 antioxidant response ↔ / ↑ (supportive) Stress adaptation Selenium status influences NRF2 target gene expression indirectly via redox tone (ref)
5 DNA damage prevention / repair environment ↓ oxidative DNA damage Genomic stability Selenium sufficiency reduces oxidative DNA lesions and supports repair capacity (ref)
6 p53 redox regulation ↔ stabilized (context-dependent) Checkpoint fidelity Redox balance maintained by selenium supports normal p53 signaling rather than triggering apoptosis (ref)
7 NF-κB inflammatory signaling ↓ chronic activation Anti-inflammatory bias Selenium supplementation suppresses NF-κB activation under inflammatory/oxidative conditions (ref)
8 Immune competence (T-cell, NK-cell function) ↑ immune function Improved immune surveillance Selenium supports cytotoxic lymphocyte activity and cytokine balance (ref)
9 Angiogenesis signaling (VEGF) ↔ / mild ↓ Vascular normalization Nutritional selenium does not strongly inhibit angiogenesis but may modestly reduce VEGF under stress (ref)
10 PI3K–AKT survival signaling ↔ (homeostatic) Cell survival maintenance Unlike selenite or SeNPs, organic selenium does not directly suppress PI3K–AKT at nutritional doses (ref)
11 Autophagy (baseline maintenance) ↔ Cellular homeostasis Selenium supports basal autophagy via redox balance but does not drive cytotoxic autophagy (ref)
12 Cancer risk modulation (epidemiologic) ↓ risk in deficient populations Prevention (not treatment) Protective effects are context-dependent; excess selenium may be neutral or adverse in replete populations (ref)


Risk, Risk: Click to Expand ⟱
Source:
Type:
Risk: by definition reduces risk of disease or cancer.
Down Target direction of risk indicates lower cancer risk.
ChemoPreventive also mean lower cancer risk. But for Chemopreventive an up arrow indicates more preventive. 
Cancer Risk Impact Score (CRIS)
CRIS scale:
–5 = very strong risk reduction
–4 = strong risk reduction
–3 = moderate risk reduction
–2 = modest risk reduction
–1 = weak / context-dependent
0 = neutral




CRIS Exposure / Compound Evidence Cancers Notes




-5 Exercise (overall)
VStrong Hum BC, CRC, Endo, PCa, Liv






-5 Aerobic + resistance VStrong Hum Broad inc + mort






-4 Aerobic exercise (mod–vig) VStrong Hum BC, CRC, Endo






-4 Resistance training (alone) Strong Hum BC, CRC






-3 High-intensity interval training Mod–Strong Hum BC, CRC






-2 NEAT / low-intensity activity Moderate Hum CRC






-5 Cruciferous vegetable pattern Strong Hum Lung, CRC, BC, PCa






-5 Sunlight exposure (physiologic) Strong Hum CRC, BC, PCa






-4 Fasting (metabolic pattern)
Strong Mech + Hum BC, CRC, PCa 






-4 Curcumin
Hum + Pre GI, BC, PCa






-4 Sulforaphane
Hum + Pre Lung, CRC, BC






-4 PEITC
Hum + Pre Lung, CRC, PCa






-4 EGCG (tea matrix)
Strong Hum GI, PCa, BC






-4 Lycopene
Strong Hum PCa






-4 Apigenin
Pre + Diet Hum BC, PCa, CRC 






-4 Luteolin
Pre + Diet Hum Lung, CRC, BC 






-4 Kaempferol
Diet Hum Ov, Panc, Lung






-4 Fisetin
Pre + Early Hum CRC, PCa, Mel






-4 Ellagic acid → Urolithin A
Hum (microbiome) CRC, PCa, BC






-3 Omega-3 (EPA/DHA)
Strong Hum CRC, BC






-3 Vitamin D3 (supp)
Obs + RCT CRC, BC






-3 Garlic (allicin)
Mod Hum GI






-3 Mushroom beta-glucans
Hum adjunct GI, BC






-3 Melatonin
Hum + Mech BC, PCa






-3 Coffee (whole)
Strong Hum Liv, Endo






-2 Quercetin
Limited Hum Lung, CRC






-2 Resveratrol
Limited Hum CRC, BC






-2 I3C / DIM
Mod Hum BC, Cerv






-2 Thymoquinone
Early Hum BC, CRC






-2 Beta-carotene (food)
Hum Lung






-1 Vitamin K2 (MK-4/7)
Limited Hum Liv, PCa






-1 Boron
Obs PCa, Lung






0 Vitamin C (oral)
Strong Hum —






0 Genistein (soy)
Strong Hum BC, PCa






0 Selenium (diet)
Mixed Hum PCa






0 Capsaicin
Mixed Gastric






+2 Vitamin E (alpha only)
Strong RCT PCa






+2 Green tea extract (high-dose)
Case reports Liv






+4 Beta-carotene (supplement)
Strong RCT Lung (smokers)






+5 Alcohol (ethanol)
Strong Hum BC, Liv, Eso







Evidence
Hum        human data
VStrong    very strong
Strong     strong
Mod        moderate
Obs        observational
Pre        preclinical
RCT        randomized controlled trial
Mech       mechanistic
Adjunct    adjunct clinical use


Scientific Papers found: Click to Expand⟱
4496- Se,    Selenium status and survival from colorectal cancer in the European prospective investigation of cancer and nutrition
- Analysis, CRC, NA
Risk↝, Higher levels of Se showed non-significant inverse associations with reduction in both CRC and overall mortality
OS↑, We found no major association of Se status markers with survival after CRC diagnosis, but an association of SELENOP with overall mortality.

4711- Se,    Association of selenium status and blood glutathione concentrations in blacks and whites
- Human, Nor, NA
Risk↓, Selenium deficiency has been linked with increased cancer risk and, in some studies, selenium supplementation was protective against certain cancers.
chemoP↑, Previous studies suggest that selenium chemoprevention may involve reduced oxidative stress through enhanced glutathione (GSH).
*GSH↑, selenium concentrations were associated with increased blood GSH concentration and GCL activity (P<0.05).

4714- Se,  SSE,  SeNPs,    Selenium in cancer management: exploring the therapeutic potential
- Review, Var, NA
Risk↓, Prolonged selenium deficiency has been conclusively linked to an elevated risk of various diseases, including but not limited to cancer, cardiovascular disease, inflammatory bowel disease, Keshan disease, and acquired immunodeficiency syndrome.
*BioAv↑, compounds such as selenite, selenate, and selenium-enriched amino acid analogs are more amenable to absorption, particularly when synergized by vitamins A, D and E
eff↝, Based on current research, selenium supplementation alone has not shown favorable results in prostate cancer treatment.
*ROS↓, It is a well-established fact that selenium demonstrates its anticancer capabilities primarily through its antioxidant attributes. These attributes help maintain the cellular redox balance and shield healthy cells from ROS
MMP↓, Sodium selenite, the most abundant inorganic selenium compound in nature, reduces mitochondrial membrane potential and enhances the antiproliferative and apoptosis-inducing effects of polyene paclitaxel on prostate cancer cell PC3
ROS↑, The above studies also suggest that ROS generation, upregulation of p53, and reduction of mitochondrial membrane potential play important roles in selenium-assisted anti-tumor processes.
P53↑,
*toxicity↓, selenium-containing nanoparticles an attractive avenue for research, with the potential to revolutionize cancer treatment by offering targeted, effective therapies with reduced toxicity.
TumCP↓, SeNPs effectively curbed the proliferation of these cancer cells by triggering a cascade of caspase-mediated apoptosis
Casp↑,
Apoptosis↑,

4722- Se,    The Yin and Yang of Nrf2-Regulated Selenoproteins in Carcinogenesis
- Review, Var, NA
Risk↓, Selenium deficiency is associated with a higher cancer risk making also this essential trace element a promising candidate for cancer prevention.
*NRF2↓, Selenium deficiency activates Nrf2 as does a TrxR1 knockout making a synergism between both systems plausible. Although this might hold true for healthy cells, the interplay may turn into the opposite in cancer cells
NRF2↑, The induction of the detoxifying and antioxidant enzymes by Nrf2 will make cancer cells chemoresistant and will protect them against oxidative damage.
*NRF2↓, Selenium exerts its effects mainly as part of selenoproteins with redox functions, and Nrf2 upregulates enzymes of the adaptive response.
OS↑, selenium, vitamin E, and β-carotene, called factor D, significantly reduced total mortality, total cancer mortality, and most significantly mortality from gastric cancer. selenium ... according to subsequent studies it appeared to have the most effic
eff↝, Considering age, the effect of factor D was much stronger in individuals younger than 55 but almost absent in subjects older than 55 years.
eff↝, selenium appears to prevent initiation of cancer in healthy cells at young age, in the elderly it may be harmful and rather support tumor growth of already initiated cells
NRF2↝, “dark” side of Nrf2. Its upregulation in cancer cells provides an advantage for these cells to grow and, in addition, makes them resistant against chemotherapy

4724- Se,    Chapter Four - Selenium in the Redox Regulation of the Nrf2 and the Wnt Pathway
- Review, Var, NA
Risk↓, Selenium deficiency is known to increase cancer risk by so far unclear mechanisms.
*selenoP↑, Selenium exerts its biological effects via selenocysteine as an integral part of selenoproteins.
other↝, A moderate Se deficiency activates the Nrf2 and the Wnt pathways
Risk↓, not only healthy cells but also malignant ones benefit from intact Keap1/Nrf2 signaling, making a dysregulated hydroperoxide signaling a plausible explanation for the increased cancer risk in selenium deficiency.

4744- Se,  Chemo,  antiOx,    Ingestion of selenium and other antioxidants during prostate cancer radiotherapy: A good thing?
- Review, Pca, NA
Risk↓, A large body of epidemiological evidence, including observational, trials, and randomized controlled clinical trials, support the proposition that selenium may prevent prostate cancer in humans
chemoP↑, This systematic review provides the first evidence that antioxidant supplementation during chemotherapy holds potential for reducing dose-limiting toxicities.

4492- Se,    Selenium in cancer prevention: a review of the evidence and mechanism of action
- Review, Var, NA
Risk↓, Since as early as the 1960s geographical studies have shown a consistent trend for populations with low Se intakes to have higher cancer mortality rates
AntiCan↑, Interventions with Sehave shown benefit in reducing the risk of cancer incidence and mortality in all cancers combined, and specifically in liver, prostate, colo-rectal and lung cancers.
*selenoP↑, data showing an effect of selenoprotein genotype on cancer risk implies that selenoproteins are indeed implicated
TumMeta↓, There is some evidence that Se may affect not only cancer risk but also progression and metastasis.
*DNAdam↓, Supplementation of the diet of sexually-intact elderly male dogs with Se, as selenomethionine or high-Se yeast, at 3 or 6 ug/kg body weight per d for 7 months was found to reduce DNA damage and up-regulate epithelial cell apoptosis in their prostate
OS↑, significant secondary end-point effects of 50% lower total cancer mortality and 37% lower total cancer incidence were found, with fewer prostate, colo–rectal and lung cancers(200 ug Se (as Se-enriched yeast)/d
*ROS↓, ability of Se in selenoproteins to reduce oxidative stress is relevant to its anti-cancer effects.

1691- Se,    The influence of selenium and selenoprotein gene variants on colorectal cancer risk
- Analysis, CRC, NA
Risk↓, Low intake of the micronutrient selenium (Se) has been implicated as a risk factor in CRC

1692- Se,    Association of Selenoprotein and Selenium Pathway Genotypes with Risk of Colorectal Cancer and Interaction with Selenium Status
- Analysis, CRC, NA
Risk↓, study suggests that SNPs in the Se pathway alone or in combination with suboptimal Se status may contribute to CRC development.

1693- Se,    Prediagnostic selenium status, selenoprotein gene variants and association with breast cancer risk in a European cohort study
- Analysis, BC, NA
Risk↓, Selenium (Se) may help prevent breast cancer (BC) development.
other∅, Higher Se status does not appear to be associated with BC risk, although activity of the selenoenzyme GPX3 may be inversely associated with premenopausal BC risk, and SNPs in the Se pathway alone or in combination with suboptimal Se status may influe

1695- Se,    Serum Selenium Concentration as a Potential Diagnostic Marker for Early-Stage Colorectal Cancer: A Comparative Study
- Trial, CRC, NA
Risk↓, Selenium deficiency is an established risk factor for colorectal cancer. It is believed that selenium supplementation and eating fish or foods rich in selenium and folic acid are factors modifying the incidence and development of colorectal cancer.
selm↑, Colorectal cancer patients had significantly lower serum selenium concentration than the comparison patients (67.24±15.55 μg/L vs 78.81±12.93 μg/L; P<0.001), and selenium concentration was below the reference range in a high percentage of colorectal
Dose↓, Mean selenium concentration differed significantly between both groups; 67.24±15.55 μg/L in the study group vs 78.81±12.93 μg/L in the comparison group (Figure 1; P<0.001). Selenium concentrations in the CRC patients were seldom within the reference
antiOx↑, Selenium has a strong antioxidant effect, although its excess causes toxic effects.
Dose↑, Therefore, selenium supplementation can be justified in people whose microelement concentration is in the lowest tertile (≤105.2 ng/mL)
Dose↝, arod et al showed that selenium supplementation in the Polish population should be considered in people with serum selenium concentration below 70 μg/L, with the aim of maintaining the concentration in the range of 70–90 μg/L

1698- Se,    Association between Dietary Zinc and Selenium Intake, Oxidative Stress-Related Gene Polymorphism, and Colorectal Cancer Risk in Chinese Population - A Case-Control Study
- Human, CRC, NA
Risk↓, Intake of selenium was found to be inversely associated with CRC risk, while zinc was not associated with CRC risk.

1700- Se,    Metabolism of Selenium, Selenocysteine, and Selenoproteins in Ferroptosis in Solid Tumor Cancers
- Review, Var, NA
Dose↝, In humans, the optimal range of Se in the serum is around 125 μg/L
Risk↑, Additionally, serum Se levels > 150 μg/L were associated with a modest increase in cancer mortality among adults in the United States.
Dose↝, same study also noticed a rise in cancer mortality with serum Se levels below 130 μg/L, which could be considered optimal
Risk↓, other side of the curve, inadequate amounts of Se or Se deficiency are also linked to an elevated risk of several diseases.

1701- Se,    An Assessment of Serum Selenium Concentration in Women with Ovarian Cancer
- Human, Ovarian, NA
Risk↓, The mean concentration of selenium was lower among diseased ones than among controls (53.31 μg/L vs. 78.99 μg/L). A decrease in selenium concentration was noticed with the advancement of ovarian cancer.
Risk↓, a clear relationship between low selenium concentration and the occurrence of ovarian cancer was found
Dose∅, average concentration of selenium in the SELECT and Nutritional Prevention of Cancer Trial was approximately 135 [47] and 114 µg/L [75], respectively.

1702- Se,    Supplemental Selenium May Decrease Ovarian Cancer Risk in African-American Women
- Human, Ovarian, NA
Risk↓, Women with the highest intakes of supplemental selenium (>20 μg/d) had an ∼30% lower risk of ovarian cancer than those with no supplemental intake
eff∅, There was also no association of dietary or supplemental zinc or copper intake with ovarian cancer.

1703- Se,    An Assessment of Serum Selenium Concentration in Women with Endometrial Cancer
- Study, EC, NA
Risk↓, The mean concentration of selenium was lower in patients with endometrial cancer than in healthy controls (60.63 µg/L (0.77 µmol/L) vs. 78.74 µg/L (0.99 µmol/L), respectively). strong correlation between lower selenium levels and the incidence of EC
selm↝, A strong correlation between the level of selenium in the blood serum and the risk of endometrial cancer indicates that patients with low levels should be a candidate group requiring appropriate preventive examinations.

1704- Se,    Prospective study of toenail selenium levels and cancer among women
- Study, Var, NA
Risk∅, No inverse association was observed between selenium levels in toenails and cancer risk

2140- Se,    Selenium Exposure and Cancer Risk: an Updated Meta-analysis and Meta-regression
- Review, Var, NA
Risk↓, High selenium exposure- It decreased the risk of breast cancer, lung cancer, esophageal cancer, gastric cancer and prostate cancer, but it was not associated with colorectal cancer, bladder cancer and skin cancer.
antiOx↑, The major positive effect may be contributed by the antioxidant function of GPxs and selenoprotein P
eff↑, High selenium exposure could decrease cancer risk, especially high plasma/serum selenium and toenail selenium.
eff↝, High selenium exposure may have dissimilar effects on specific types of cancer.

2141- Se,    Selenium and cancer risk: Wide-angled Mendelian randomization analysis
- Review, NA, NA
Dose↝, Nonetheless, a nutrition survey in US people indicated that a trivial proportion of the population had serum levels of selenium >170 ng/mL
Risk↝, Evidence on the association between selenium and cancer risk is inconclusive

2142- Se,    A U-shaped association between selenium intake and cancer risk
- Review, NA, NA
*Risk↝, We observed a U-shaped association between selenium intake and cancer risk.
Dose↝, A safe intake ranged from 110.8 to 124.4 µg/day (mean 117.8 µg/day).
*Risk↓, individuals with the lowest intake (i.e., 27.8–77.2 µg/day) were associated with an increased risk of cancer (ie higher levels means lower risk)

4485- Se,    Selenium stimulates the antitumour immunity: Insights to future research
- Review, NA, NA
*antiOx↑, At nutritional low doses, selenium, depending on its form, may act as an antioxidant, protecting against oxidative stress, supporting cell survival and growth, thus, plays a chemo-preventive role
chemoPv↑,
ROS↑, at supra-nutritional higher pharmacological doses, selenium acts as pro-oxidant inducing redox signalling and cell death
Imm↑, selenium stimulates the immune system against cancer
selenoP↑, anti-oxidant through selenoproteins
*IL2↑, consumption of Se-enriched foods (200 μg per serving for 3 days) increases the levels of interleukin IL-2, IL-4, IL-5, IL-13 and IL-22, indicating an activated Th2-type response
*IL4↑,
*TNF-α↓, taking selenised yeast (300 μg.day−1) downregulates the gene expression of tumour necrosis factor (TNF)α and transforming growth factor (TGF)β; thus, consequently inhibit the epithelial-to-mesenchymal transition (EMT) in non-malignant prostate tissue
*TGF-β↓,
*EMT↓,
Risk↓, immune-enhancing effects of Se may reduce the risk of cancer
*GPx↑, chemo-preventive effects of Se are mainly mediated by the anti-oxidant function of selenoenzymes such as GPxs and TXNRDs [68] because Se supplementation increases both GPx1 and GPx4 activity in humans
*TrxR↑,

4486- Se,  Chit,    Selenium-Modified Chitosan Induces HepG2 Cell Apoptosis and Differential Protein Analysis
- in-vitro, Liver, HepG2
Apoptosis↑, selenium-modified chitosan (SMC)can induce HepG2 cell apoptosis with the cell cycle arrested in the S and G2/M phases
TumCCA↑,
MMP↓, gradual disruption of mitochondrial membrane potential
Bcl-2↓, reduce the expression of Bcl2, and improve the expression of Bax, cytochrome C, cleaved caspase 9, and cleaved caspase 3
BAX↑,
cl‑Casp9↑,
cl‑Casp3↑,
Risk↓, Relevant research suggests that an inverse relationship exists between selenium intake and cancer incidence, and selenium levels are usually lower in cancer patients.
*BioAv↑, favorable biocompatibility, good bioadhesivness, and low toxicity.
*toxicity↑,
TumCG↓, Studies have found that water-soluble chitosan can significantly inhibit the growth of liver cancer cells in a dose-dependent manner
AntiTum↑, SMC has been proved to possess stronger antitumor functions and lower toxicity in cancer patients
ROS↑, SMC induced A549 cell apoptosis via a reactive oxygen species–mediated mitochondrial apoptosis pathway, which upregulated Bax and downregulated Bcl2, promoted cytochrome C release from mitochondria to cytoplasm, and activated cleaved caspase 3
Cyt‑c↑,
Fas↑, upregulating the expression levels of Fas, FasL, and Fadd,
FasL↑,
FADD↑,

4495- Se,    Selenium status is associated with colorectal cancer risk in the European prospective investigation of cancer and nutrition cohort
- Study, CRC, NA
Risk↓, Higher Se concentrations were associated with a non-significant lower CRC risk
Dose↝, The findings indicate that Se status is suboptimal in many Europeans and suggest an inverse association between CRC risk and higher serum Se status, which is more evident in women.


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 23

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   NRF2↑, 1,   NRF2↝, 1,   ROS↑, 3,   selenoP↑, 1,  

Metal & Cofactor Biology ⓘ

selm↑, 1,   selm↝, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,  

Cell Death ⓘ

Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   cl‑Casp3↑, 1,   cl‑Casp9↑, 1,   Cyt‑c↑, 1,   FADD↑, 1,   Fas↑, 1,   FasL↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,   other∅, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Migration ⓘ

TumCP↓, 1,   TumMeta↓, 1,  

Immune & Inflammatory Signaling ⓘ

Imm↑, 1,  

Drug Metabolism & Resistance ⓘ

Dose↓, 1,   Dose↑, 1,   Dose↝, 6,   Dose∅, 1,   eff↑, 1,   eff↝, 4,   eff∅, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   chemoP↑, 2,   chemoPv↑, 1,   OS↑, 3,   Risk↓, 21,   Risk↑, 1,   Risk↝, 2,   Risk∅, 1,  
Total Targets: 42

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GPx↑, 1,   GSH↑, 1,   NRF2↓, 2,   ROS↓, 2,   selenoP↑, 2,   TrxR↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,  

Migration ⓘ

TGF-β↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL2↑, 1,   IL4↑, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,  

Functional Outcomes ⓘ

Risk↓, 1,   Risk↝, 1,   toxicity↓, 1,   toxicity↑, 1,  
Total Targets: 18

Scientific Paper Hit Count for: Risk, Risk
23 Selenium
1 Selenite (Sodium)
1 Selenium NanoParticles
1 Chemotherapy
1 Anti-oxidants
1 chitosan
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

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