Date Fruit Extract / ROS Cancer Research Results

DFE, Date Fruit Extract: Click to Expand ⟱
Features:
Dates (the fruit of Phoenix dactylifera) have been increasingly studied for their potential anticancer and cancer-preventive properties, mainly due to their rich phytochemical content and strong antioxidant activity.
Dates contain a broad spectrum of bioactive compounds linked to cancer prevention:
-Phenolic acids – e.g., ferulic acid, gallic acid, caffeic acid, and p-coumaric acid
-Flavonoids – e.g., quercetin, luteolin, apigenin
-Carotenoids – e.g., β-carotene, lutein
-Tannins, saponins, and sterols
-Dietary fiber and polysaccharides
These compounds have antioxidant, anti-inflammatory, and antiproliferative effects.

Date fiber and polyphenols foster beneficial gut bacteria (e.g., Bifidobacterium, Lactobacillus) that produce short-chain fatty acids (SCFAs), which protect the colon and may lower colon cancer risk.

Date Fruit Extract — a non-standardized botanical extract prepared from the edible fruit pulp of Phoenix dactylifera L., including cultivars such as Ajwa, Medjool, Hallawi, Sukkari, and others. It is classified as a complex food-derived phytochemical mixture rather than a single defined drug or active pharmaceutical ingredient. The standard abbreviation is DFE. Principal constituents vary substantially with cultivar, ripeness, processing, and extraction solvent, but commonly include phenolic acids such as gallic, ferulic, caffeic, protocatechuic, and p-coumaric acids; flavonoids such as quercetin, luteolin, apigenin, catechin, and epicatechin derivatives; carotenoids; condensed tannins; polysaccharides; and dietary fiber. Date fruit, date seed, leaf, pollen, and nanoparticle preparations are compositionally distinct and should not be treated as interchangeable with fruit-pulp extract.

Primary mechanisms (ranked):

  1. Induction of mitochondrial apoptosis in susceptible cancer cells, involving mitochondrial membrane depolarization, BAX/BCL-2 imbalance, caspase activation, and DNA fragmentation.
  2. Suppression of cancer-cell proliferation through cell-cycle arrest, with reported accumulation in G1 or G2/M phases depending on the extract, concentration, and tumor model.
  3. Redox modulation, including antioxidant protection in normal tissues but concentration-dependent ROS and mitochondrial ROS elevation in some cancer-cell models.
  4. Modulation of p53-associated stress and apoptotic signaling in responsive tumor cells.
  5. Anti-inflammatory activity through suppression of NF-κB-associated inflammatory signaling and inflammatory mediators, although direct tumor-specific evidence is limited.
  6. Secondary modulation of PI3K/AKT and related survival signaling, reported inconsistently and not established as a universal mechanism.
  7. Potential suppression of migration, clonogenic survival, angiogenic signaling, and tumor growth in selected preclinical models.
  8. Indirect colon-health effects through fermentable fiber and polyphenol interactions with the gut microbiota and production of short-chain fatty acids.

Bioavailability / PK relevance: No clinically validated pharmacokinetic profile exists for DFE as a standardized anticancer agent. Its polyphenols undergo incomplete intestinal absorption, extensive phase-II conjugation, microbial metabolism, and rapid systemic clearance. Consequently, circulating concentrations of individual parent compounds are generally much lower than concentrations used for direct cancer-cell cytotoxicity. Local gastrointestinal exposure and microbial metabolites may be more biologically relevant than systemic exposure after ordinary date consumption.

In-vitro vs systemic exposure relevance: Most antiproliferative studies use crude solvent fractions at tens to hundreds of micrograms per millilitre. These concentrations cannot be directly equated with plasma exposure after eating dates or taking an unstandardized extract. Extract-specific cytotoxic effects may reflect concentrated mixtures, solvent-selective enrichment, or interactions among multiple constituents. Common in-vitro exposures probably exceed achievable systemic concentrations from dietary intake.

Clinical evidence status: Preclinical. Evidence consists primarily of cell-culture studies, limited animal experiments, compositional studies, and small human dietary studies evaluating metabolic, inflammatory, or gastrointestinal outcomes. No randomized controlled oncology trial has established DFE as a cancer treatment, adjunctive anticancer therapy, radiosensitizer, or chemotherapy sensitizer. Date fruit and date-derived extracts are not approved by Health Canada, the FDA, or the EMA as anticancer drugs.

Safety and deployment: Whole dates are conventional foods and are generally well tolerated, but they contain substantial carbohydrate and sugar and may require portion control in people with impaired glycemic regulation. Extracts may differ markedly from the food in concentration, solvent residues, composition, and contaminant risk. Clinical interaction data with chemotherapy, anticoagulants, endocrine therapies, or targeted agents are inadequate. DFE should not be assumed to protect normal tissue selectively or improve anticancer treatment efficacy without direct combination studies.

Date Fruit Extract Mechanistic Profile

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Mitochondrial apoptosis MMP ↓; BAX ↑; BCL-2 ↓; caspase-3 ↑; apoptosis ↑ Apoptotic injury often ↓ in oxidative-damage models R, G Programmed cancer-cell death Best-supported direct anticancer mechanism, but demonstrated mainly with concentrated Ajwa or solvent-fraction extracts in vitro.
2 Cell-cycle control Proliferation ↓; G1 or G2/M arrest ↑ (model-dependent) ↔ G Cytostasis Cell-cycle phase varies by tumor line, cultivar, solvent fraction, concentration, and exposure duration.
3 ROS and mitochondrial oxidative stress ROS ↑; mitochondrial ROS ↑ (dose-dependent) ROS ↓; lipid peroxidation ↓; antioxidant capacity ↑ P, R Context-dependent redox modulation Cancer-cell pro-oxidant activity has been reported, while antioxidant protection predominates in normal-tissue injury models. Tumor selectivity is not clinically established.
4 p53 stress response p53 ↑; apoptotic signaling ↑ (model-dependent) ↔ R, G Stress-mediated growth suppression Reported in selected models and should not be generalized to p53-deficient or mutant-p53 tumors.
5 NF-κB inflammatory signaling NF-κB-associated survival and inflammation ↓ (limited evidence) Inflammatory signaling ↓ R, G Anti-inflammatory modulation More consistently supported in inflammatory or tissue-injury systems than in direct oncology experiments.
6 PI3K and AKT survival signaling PI3K/AKT ↓ (context-dependent) ↔ or AKT support ↑ in injury models R, G Survival-pathway suppression Not consistently measured across DFE studies and may partly reflect activities of individual phenolic constituents.
7 Clonogenic survival and tumor growth Colony formation ↓; tumor-cell burden ↓ in limited models ↔ G Long-term growth inhibition Evidence is substantially weaker than for established anticancer agents and remains extract-specific.
8 Migration and invasion Migration ↓; invasion-related signaling possibly ↓ ↔ G Potential antimetastatic activity Limited mechanistic data; MMP and epithelial-mesenchymal transition effects require further confirmation.
9 Angiogenic signaling VEGF-associated signaling possibly ↓ ↔ G Potential angiogenesis suppression Sparse evidence and not established as a primary effect of fruit-pulp extract.
10 NRF2 antioxidant response NRF2 modulation mixed (context-dependent) NRF2 and antioxidant enzymes ↑ R, G Secondary cytoprotective response NRF2 activation may protect normal tissues but could theoretically support antioxidant resistance in some cancers. Direct DFE tumor data are insufficient to define the net effect.
11 Gut microbiota and short-chain fatty acids Indirect colon-environment modulation Beneficial bacterial growth ↑; fermentation products ↑ G Local gastrointestinal and metabolic effect Human dietary evidence supports microbiota and bowel-environment effects more strongly than systemic anticancer activity.
12 Clinical Translation Constraint Effective exposure uncertain; extract composition heterogeneous Food-level tolerance generally favorable G Limits clinical interpretation Major constraints include cultivar and solvent variability, absent extract standardization, low systemic polyphenol exposure, high in-vitro concentrations, limited animal oncology evidence, and no controlled cancer trials.

TSF: P: 0–30 min    R: 30 min–3 hr    G: >3 hr
ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






ROS">Copper (ionic / nano)
+++↓[Fe][F]ROS-dominant






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






ROS">Alpha-lipoic acid (ALA)
±↑[D][M]NRF2-dominant






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






ROS">Quercetin
±↑/↓[D][Fe]NRF2-dominant






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
4454- DFE,    Cytostatic and Anti-tumor Potential of Ajwa Date Pulp against Human Hepatocellular Carcinoma HepG2 Cells
- in-vitro, Liver, HepG2
ROS↑, MMP↓, TumCCA↑, Apoptosis↑, selectivity↑, MMP↓, TumCCA↑,
4456- DFE,    Induction of apoptosis and cell cycle arrest by ethyl acetate fraction of Phoenix dactylifera L. (Ajwa dates) in prostate cancer cells
- in-vitro, Pca, PC3
TumCD↑, MMP↓, mt-ROS↑, Apoptosis↑, TumCCA↑,
6663- DFE,    Nutraceuticals of Phoenix dactylifera L.: Physicochemistry, Nutritional Value and Therapeutic Potential
- Review, Nor, NA - Review, AD, NA
*antiOx↑, *Inflam↓, *AntiBio↑, *AntiDiabetic↑, *AntiCan↑, *AntiArt↑, *neuroP↑, *hepatoP↑, *GastroP↑, *other↝, *cardioP↑, *cognitive↑, *ROS↓, *memory↑, *other↝, *SOD↑, *Catalase↑, *GSH↑, *GA↑, *Catechins↑, *FA↑, *QC↑, Api↑, *CA↑, *Imm↑, *Phen↑, *IL1β↓, *TGF-β↓, *COX1↓, *COX2/PTGS2↓, TumCP↓, Casp3↑, TumMeta↓, *GutMicro↑,
6668- DFE,  AgNPs,    Saponin-Derived Silver Nanoparticles from Phoenix dactylifera (Ajwa Dates) Exhibit Broad-Spectrum Bioactivities Combating Bacterial Infections
- in-vitro, Lung, A549
*AntiBio↑, antiOx↑, TumCD↑, ROS↑, DNAdam↑, *Catalase↑, *GPx↑, *SOD↑, *ROS↓,
4445- SeNPs,  DFE,    A comparative study on the hepatoprotective effect of selenium-nanoparticles and dates flesh extract on carbon tetrachloride induced liver damage in albino rats
- in-vivo, LiverDam, NA
*hepatoP↑, *antiOx↑, *AntiCan↑, *BioAv↑, *toxicity↓, *ROS↓, *MDA↓, *ALAT↓, *Albumin↑, *GSH↑, *SOD↑, *RenoP↑,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   ROS↑, 2,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 3,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 2,   Casp3↑, 1,   TumCD↑, 2,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 3,  

Migration(tgid=13) ⓘ

TumCP↓, 1,   TumMeta↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

selectivity↑, 1,  

Ingredients & Constituents(tgid=25) ⓘ

Api↑, 1,  
Total Targets: 13

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiArt↑, 1,   AntiBio↑, 2,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Catalase↑, 2,   GPx↑, 1,   GSH↑, 2,   MDA↓, 1,   ROS↓, 3,   SOD↑, 3,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 2,  

Migration(tgid=13) ⓘ

TGF-β↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GastroP↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 1,   COX2/PTGS2↓, 1,   IL1β↓, 1,   Imm↑, 1,   Inflam↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   Albumin↑, 1,   GutMicro↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   AntiDiabetic↑, 1,   cardioP↑, 1,   cognitive↑, 1,   hepatoP↑, 2,   memory↑, 1,   neuroP↑, 1,   RenoP↑, 1,   toxicity↓, 1,  

Ingredients & Constituents(tgid=25) ⓘ

CA↑, 1,   Catechins↑, 1,   FA↑, 1,   GA↑, 1,   Phen↑, 1,   QC↑, 1,  
Total Targets: 37

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
5 Date Fruit Extract
1 Silver-NanoParticles
1 Selenium NanoParticles
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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:371  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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