Genistein (soy isoflavone) / ROS Cancer Research Results

GEN, Genistein (soy isoflavone): Click to Expand ⟱
Features: Estrogen-like activity
Genistein is a naturally occurring isoflavone predominantly found in soy products.
It binds estrogen receptors (with relative preference for ERβ over ERα), inhibits certain tyrosine kinases, and modulates PI3K/AKT, NF-κB, MAPK, and cell-cycle pathways in preclinical cancer models. It is also reported to influence angiogenesis and epigenetic regulation. Oral exposure produces conjugated metabolites (glucuronides/sulfates), and free genistein plasma levels are typically much lower than many in-vitro µM concentrations.
-soy isoflavone
Anticancer effects through several mechanisms:
-Modulation of Hormone Activity: can bind to estrogen receptors(hormone-dependent cancers like breast and prostate cancer).
-Inhibition of Cell Proliferation:- -inducing cell cycle arrest.
-Induction of Apoptosis:- by influencing pro- and anti-apoptotic regulators.
-Anti-inflammatory and Antioxidant Effects:-antioxidant properties help to neutralize ROS
-Anti-angiogenic Activity:may also inhibit tumor angiogenesis

Key Cellular Signaling Pathways Involved
-Estrogen Receptor Signaling: interacting with estrogen receptors (ERα and ERβ)
-PI3K/Akt/mTOR Pathway:inhibits this pro-survival pathway, leading to reduced cell growth
-MAPK/ERK Pathway: can contribute to cell cycle arrest.
-NF-κB Pathway:may downregulate NF-κB, supporting a reduction in tumor-promoting inflammation.
-Wnt/β-catenin Pathway: involved in cell proliferation, differentiation, and oncogenic transformation.

Dosages often ranging from approximately 40 mg to 100 mg per day for potential therapeutic effects. Genistein has limited bioavailability when ingested as part of the diet. Efforts to enhance its absorption include the use of specific formulations, such as those that combine genistein with other compounds or utilize novel delivery systems.

Genistein — a naturally occurring polyphenolic isoflavone and phytoestrogen found predominantly in soybeans and soy-derived foods, usually present in plants as glycosides that are hydrolyzed to the biologically active aglycone. It is formally classified as a dietary isoflavone, selective estrogen-receptor modulator-like phytochemical, and experimental anticancer agent. Standard abbreviations include GEN and G. Genistein preferentially engages estrogen receptor beta at lower concentrations, but can also activate estrogen receptor alpha as exposure increases; therefore, its biological effects are strongly dependent on dose, tissue, receptor expression, hormonal environment, and life stage. It is also widely used experimentally as a protein-tyrosine-kinase inhibitor, although many laboratory kinase effects require concentrations exceeding typical free systemic exposure after oral intake.

Primary mechanisms (ranked):

  1. Context-dependent estrogen-receptor modulation, with relative preference for ERβ but clinically relevant potential for ERα activation at sufficient exposure.
  2. Inhibition of receptor and non-receptor tyrosine-kinase signaling, including EGFR-associated pathways, with downstream suppression of PI3K/AKT/mTOR and MAPK signaling in responsive models.
  3. Cell-cycle checkpoint activation and growth arrest through cyclin/CDK regulation, p21 induction, and frequently G2/M accumulation.
  4. Topoisomerase II interference and DNA-damage signaling at higher concentrations, contributing to checkpoint activation and apoptosis but also creating a potential genotoxicity constraint.
  5. Intrinsic apoptosis through mitochondrial dysfunction, altered BAX/BCL-2 balance, cytochrome-c release, and caspase activation.
  6. Suppression of NF-κB, STAT3, inflammatory mediators, and tumor-supportive survival transcription.
  7. Epigenetic modulation involving DNMTs, HDACs, histone acetylation, and re-expression of selected tumor-suppressor genes.
  8. Suppression of angiogenesis, epithelial–mesenchymal transition, invasion, and cancer-stem-cell phenotypes through VEGF/HIF-1α, MMP, Hedgehog/GLI, Wnt/β-catenin, and related pathways.
  9. Context-dependent redox modulation: antioxidant and cytoprotective effects are common at nutritional or lower exposure, whereas mitochondrial ROS generation and pro-oxidant cytotoxicity can occur at higher experimental concentrations.
  10. Potential chemo- and radiosensitization through survival-signaling suppression, cell-cycle redistribution, DNA-damage interactions, and inhibition of treatment-induced NF-κB activation; evidence remains predominantly preclinical.

Bioavailability / PK relevance: Oral genistein undergoes extensive intestinal and hepatic glucuronidation and sulfation. Circulating total genistein may reach micromolar concentrations after concentrated preparations, but most is conjugated; pharmacologically active free aglycone concentrations are generally substantially lower. Absorption varies with food matrix, glycoside hydrolysis, intestinal microbiota, dose, formulation, and enterohepatic recycling. Nanoparticle, lipid, phospholipid, and other delivery systems can increase experimental exposure but are not established oncology treatments.

In-vitro vs systemic exposure relevance: Many anticancer studies use approximately 10–100 µM genistein, with pronounced apoptosis, topoisomerase inhibition, or G2/M arrest often occurring at 25–100 µM. These concentrations commonly exceed sustained free-genistein exposure achievable through soy foods or conventional oral supplementation. Lower nanomolar-to-low-micromolar concentrations may still modulate estrogen receptors and transcription, meaning hormonal activity may occur at exposures below those required for direct cytotoxicity.

Clinical evidence status: Extensive preclinical evidence; several small phase I–II or presurgical randomized human studies, principally in prostate and bladder cancer, have evaluated tissue biomarkers and short-term safety. Some studies reported modulation of PSA-related, inflammatory, epigenetic, proliferation, or kinase biomarkers, but consistent tumor regression, recurrence reduction, progression-free survival, or overall-survival benefit has not been demonstrated. Genistein is not an established or approved anticancer therapy and should be classified as an investigational preventive or adjunctive agent rather than a cancer treatment. Particular caution is warranted in estrogen-sensitive disease, during endocrine therapy, with concentrated supplements, and where thyroid function or medication absorption is clinically important.

Genistein Mechanistic Profile

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Estrogen receptor signaling ERβ signaling ↑; ERα signaling ↑ or ↔ (dose-dependent) (context-dependent) Estrogen-responsive transcription ↑ (dose-dependent) P, R, G Hormonal and transcriptional modulation Relative ERβ preference is not absolute. ERα activation becomes important with higher concentrations and in ERα-dominant tissues; tumor effects may therefore be antiproliferative, neutral, or proliferative depending on receptor balance and exposure.
2 Protein tyrosine kinase and EGFR signaling Tyrosine phosphorylation ↓; EGFR signaling ↓ (dose-dependent) Growth-factor signaling ↓ (high concentration only) P, R Mitogenic signaling suppression Genistein is commonly used experimentally as a broad tyrosine-kinase inhibitor, but selectivity is limited and many effects occur above nutritional systemic exposure.
3 PI3K AKT mTOR survival axis PI3K ↓; AKT phosphorylation ↓; mTOR signaling ↓ ↔ or ↓ (model-dependent) R, G Reduced survival, growth, and treatment resistance A recurrent downstream mechanism across prostate, breast, bladder, pancreatic, and other experimental cancer systems.
4 Cell-cycle checkpoints p21 ↑; cyclin B1 and CDK1 activity ↓; G2/M arrest ↑ Cell-cycle progression ↓ (high concentration only) G Cytostasis and checkpoint activation G2/M arrest is common, although G0/G1 or S-phase effects occur depending on cell type, exposure, and concurrent DNA damage.
5 Topoisomerase II and DNA damage Topoisomerase II function ↓; DNA strand breaks ↑; checkpoint signaling ↑ (high concentration only) Genotoxic stress ↑ (high concentration only) P, R, G DNA-damage-associated arrest and cell death This mechanism may contribute to anticancer activity but is also a safety constraint because topoisomerase II poisoning can produce chromosomal damage rather than selective tumor toxicity.
6 Mitochondrial apoptosis BAX and BCL-2 ratio ↑; mitochondrial membrane potential ↓; cytochrome c ↑; caspases ↑; apoptosis ↑ Apoptosis ↔ or ↓ at lower exposure; ↑ (high concentration only) R, G Programmed cell death Usually follows suppression of survival signaling, cell-cycle disruption, mitochondrial stress, or DNA damage.
7 NF-κB and inflammatory signaling IKK activity ↓; NF-κB activation ↓; COX-2 ↓; inflammatory cytokines ↓ Inflammatory signaling ↓ R, G Anti-inflammatory and anti-survival transcription May reduce tumor-promoting inflammation and treatment-induced survival signaling without constituting a tumor-selective cytotoxic mechanism.
8 STAT3 signaling STAT3 phosphorylation ↓; survivin ↓; BCL-2 ↓ ↔ or ↓ (model-dependent) R, G Reduced survival and stemness Reported particularly in pancreatic, prostate, breast, and other constitutively STAT3-active models.
9 Epigenetic regulation DNMT activity ↓; HDAC activity ↓; histone acetylation ↑; tumor-suppressor expression ↑ Epigenetic transcription ↔ or altered (context-dependent) G Epigenetic reprogramming Effects vary by dose and locus. Human presurgical studies demonstrate gene-expression and methylation changes but do not establish clinical anticancer efficacy.
10 Hedgehog GLI and cancer stemness SMO ↓; GLI1 ↓; CD44 ↓; stemness ↓; EMT ↓ ↔ G Reduced cancer-stem-cell phenotype Supported mainly by cell and xenograft studies using breast and prostate cancer models.
11 Wnt beta-catenin and EMT β-catenin signaling ↓; Snail ↓; Slug ↓; migration ↓; invasion ↓ ↔ or pathway modulation (context-dependent) G Reduced invasive phenotype Not universal across tumor types and frequently secondary to broader kinase, ER, or epigenetic effects.
12 HIF-1α VEGF angiogenesis axis HIF-1α ↓; VEGF ↓; MMP2 and MMP9 ↓; angiogenesis ↓ Angiogenic signaling ↔ or ↓ (model-dependent) G Anti-angiogenic and anti-invasive activity Predominantly demonstrated in preclinical tumor and endothelial models.
13 Mitochondrial ROS modulation ROS ↓ at lower exposure or ROS ↑ at cytotoxic exposure (dose-dependent) (model-dependent) Oxidative stress ↓ commonly; ROS ↑ possible (high concentration only) P, R, G Context-dependent antioxidant or pro-oxidant activity ROS neutralization should not be assigned as a fixed direction. Pro-oxidant mitochondrial stress can participate in apoptosis, while lower exposure commonly activates antioxidant and anti-inflammatory responses.
14 NRF2 antioxidant response NRF2 signaling ↑ or ↓ (context-dependent) NRF2 and antioxidant enzymes ↑ commonly R, G Secondary redox adaptation NRF2 activation may protect normal tissue but could also support tumor stress tolerance in some settings; it is not a consistent primary anticancer mechanism.
15 Chemosensitization Drug response ↑; NF-κB, AKT, STAT3, EMT, and resistance signaling ↓ (model-dependent) Treatment injury ↓ or ↔ (model-dependent) R, G Potential enhancement of cytotoxic therapy Reported with several chemotherapy agents in preclinical models, but sequence, dose, hormonal context, antioxidant effects, and pharmacokinetic interactions can alter the result. Clinical benefit is unproven.
16 Radiosensitization Radiation response ↑; survival signaling ↓; DNA-damage persistence ↑ (model-dependent) Radiation injury ↓ or ↑ (model-dependent) R, G Potential radiation-response modification Predominantly preclinical. Genistein has also shown normal-tissue radioprotective effects in some models, making timing and dose critical.
17 Clinical Translation Constraint Free intracellular exposure often below concentrations used for direct cytotoxicity Hormonal and off-target effects remain possible at lower exposure G Limited translation of laboratory cytotoxicity Extensive glucuronide and sulfate conjugation, variable absorption, ER-dependent bidirectional effects, topoisomerase-related genotoxicity, heterogeneous formulations, small biomarker trials, and absence of demonstrated survival benefit limit oncology use.

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⟱
7108- GEN,    Genistein: A Review on its Anti-Inflammatory Properties
- Review, Nor, NA
*cardioP↑, *Inflam↓, *NF-kB↓, *PGE2↓, *iNOS↓, *ROS↓, *COX2↓, *toxicity↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↓, 1,  

Cell Death(tgid=5) ⓘ

iNOS↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   PGE2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   toxicity↑, 1,  
Total Targets: 8

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
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#:85  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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