ROS Cancer Research Results

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)

"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⟱
651- EGCG,    Epigallocatechin-3-Gallate Therapeutic Potential in Cancer: Mechanism of Action and Clinical Implications
ROS↑, p‑AMPK↑, mTOR↓, FAK↓, Smo↓, Gli1↓, HH↓, TumCMig↓, TumCI↓, NOTCH↓, JAK↓, STAT↓, Bcl-2↓, Bcl-xL↓, BAX↑, Casp9↑,
695- EGCG,  TFdiG,    The antioxidant and pro-oxidant activities of green tea polyphenols: a role in cancer prevention
- in-vitro, NA, HL-60
ROS↑, IronCh↑, Apoptosis↑,
694- EGCG,    Matcha green tea (MGT) inhibits the propagation of cancer stem cells (CSCs), by targeting mitochondrial metabolism, glycolysis and multiple cell signalling pathways
- in-vitro, BC, MCF-7
Glycolysis↓, GAPDH↓, ROS↑, OCR↓, ECAR↓, mTOR↓, OXPHOS↓,
692- EGCG,    EGCG: The antioxidant powerhouse in lung cancer management and chemotherapy enhancement
- Review, NA, NA
ROS↑, Apoptosis↑, DNAdam↑, CTR1↑, JWA↑, β-catenin/ZEB1↓, P53↑, Vim↓, VEGF↓, p‑Akt↓, Hif1a↓, COX2↓, ERK↓, NF-kB↓, Akt↓, Bcl-xL↓, miR-210↓,
676- EGCG,  Chemo,    The Potential of Epigallocatechin Gallate (EGCG) in Targeting Autophagy for Cancer Treatment: A Narrative Review
- Review, NA, NA
PI3k/Akt/mTOR↓, Apoptosis↑, ROS↑, TumAuto↑,
3225- EGCG,    Epigallocatechin‐3‐Gallate Ameliorates Diabetic Kidney Disease by Inhibiting the TXNIP/NLRP3/IL‐1β Signaling Pathway
- in-vitro, Nor, NA - in-vivo, Nor, NA
*RenoP↑, *NLRP3↓, *TXNIP↓, *ASC↓, *Casp1↓, *IL1β↓, *ROS↓, *TNF-α↓, *IL6↓, *IL18↓,
3223- EGCG,    The Effects of Green Tea Catechins in Hematological Malignancies
- Review, AML, NA
Prx↓, ROS↑,
3219- EGCG,    Nano-chemotherapeutic efficacy of (−) -epigallocatechin 3-gallate mediating apoptosis in A549 cells: Involvement of reactive oxygen species mediated Nrf2/Keap1signaling
- in-vitro, Lung, A549
ROS↑, RNS↓, MMP↓, NRF2↑, Keap1↓,
3218- EGCG,    Comparative efficacy of epigallocatechin-3-gallate against H2O2-induced ROS in cervical cancer biopsies and HeLa cell lines
- in-vitro, Cerv, HeLa
SOD↑, GPx↑, *antiOx↑, ROS↓,
3238- EGCG,    Green tea catechin, epigallocatechin-3-gallate (EGCG): mechanisms, perspectives and clinical applications
- Review, Var, NA
Telomerase↓, DNMTs↓, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, CDK6↓, HATs↓, HDAC↓, selectivity↑, uPA↓, NF-kB↓, TNF-α↓, *ROS↓, *antiOx↑, Hif1a↓, VEGF↓, MMP2↓, MMP9↓, FAK↓, TIMP2↑, Mcl-1↓, survivin↓, XIAP↓, PCNA↓, p16↑, P21↑, p27↑, pRB↑, P53↑, MDM2↑, ROS↑, Casp3↑, Casp8↑, Casp9↑, Cyt‑c↑, Diablo↑, BAX⇅, cl‑PPARα↓, PDGF↓, EGFR↓, FOXO↑, AP-1↓, JNK↓, COX2↓, angioG↓,
3215- EGCG,    Epigallocatechin gallate modulates ferroptosis through downregulation of tsRNA-13502 in non-small cell lung cancer
- in-vitro, NSCLC, A549 - in-vitro, NSCLC, H1299
TumCP↓, Ki-67↓, GPx4↓, ACSL4↑, Iron↑, MDA↑, ROS↑, Ferroptosis↑, eff↑, NRF2↑, HO-1↑,
3216- EGCG,    Epigallocatechin-3-gallate suppresses hemin-aggravated colon carcinogenesis through Nrf2-inhibited mitochondrial reactive oxygen species accumulation
- NA, Colon, Caco-2
NRF2↑, TumCP↓, mt-ROS↓, Keap1↓,
3201- EGCG,    Epigallocatechin Gallate (EGCG): Pharmacological Properties, Biological Activities and Therapeutic Potential
- Review, NA, NA
*AntiCan↑, *cardioP↑, *neuroP↑, *BioAv↝, *BioAv↓, *BioAv↓, *Dose↝, *Half-Life↝, *BioAv↑, *BBB↑, *hepatoP↓, *other↓, *Inflam↓, *NF-kB↓, *AP-1↓, *iNOS↓, *COX2↓, *ROS↓, *RNS↓, *IL8↓, *JAK↓, *PDGFR-BB↓, *IGF-1R↓, *MMP2↓, *P53↓, *NRF2↑, *TNF-α↓, *IL6↓, *E2Fs↑, *SOD1↑, *SOD2↑, Casp3↑, Cyt‑c↑, PARP↑, DNMTs↓, Telomerase↓, Hif1a↓, MMPs↓, BAX↑, Bak↑, Bcl-2↓, Bcl-xL↓, P53↑, PTEN↑, TumCP↓, MAPK↓, HGF/c-Met↓, TIMP1↑, HDAC↓, MMP9↓, uPA↓, GlutMet↓, ChemoSen↑, chemoP↑,
3203- EGCG,    (-)- Epigallocatechin-3-gallate induces GRP78 accumulation in the ER and shifts mesothelioma constitutive UPR into proapoptotic ER stress
- NA, MM, NA
ROS↑, Ca+2↝, GRP78/BiP↑, ATF4↑, XBP-1↑, CHOP↑, Casp3↑, Casp8↑, *GRP78/BiP↓, *UPR↓, UPR↑,
3205- EGCG,    The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human Diseas
- Review, Var, NA - Review, AD, NA
Beclin-1↑, ROS↑, Apoptosis↑, ER Stress↑, *Inflam↓, *cardioP↑, *antiOx↑, *LDL↓, *NF-kB↓, *MPO↓, *glucose↓, *ROS↓, ATG5↑, LC3B↑, MMP↑, lactateProd↓, VEGF↓, Zeb1↑, Wnt↑, IGF-1R↑, Fas↑, Bak↑, BAD↑, TP53↓, Myc↓, Casp8↓, LC3II↑, NOTCH3↓, eff↑, p‑Akt↓, PARP↑, *Cyt‑c↓, *BAX↓, *memory↑, *neuroP↑, *Ca+2?, GRP78/BiP↑, CHOP↑, ATF4↑, Casp3↑, Casp8↑, UPR↑,
3206- EGCG,    Insights on the involvement of (-)-epigallocatechin gallate in ER stress-mediated apoptosis in age-related macular degeneration
- Review, AMD, NA
*Ca+2↓, *ROS↓, *Apoptosis↓, *GRP78/BiP↓, *CHOP↓, *PERK↓, *IRE1↓, *p‑PARP↓, *Casp3↓, *Casp12↓, *ER Stress↓, *UPR↓,
3207- EGCG,    EGCG Enhances the Chemosensitivity of Colorectal Cancer to Irinotecan through GRP78-MediatedEndoplasmic Reticulum Stress
- in-vitro, CRC, RKO - in-vitro, CRC, HCT116
GRP78/BiP↑, MMP↓, ER Stress↑, ROS↓, UPR↑,
3210- EGCG,    Protective effect of epigallocatechin-3-gallate (EGCG) via Nrf2 pathway against oxalate-induced epithelial mesenchymal transition (EMT) of renal tubular cells
- in-vitro, Nor, NA
*ROS↓, *NRF2↑, *Catalase↑, *antiOx↑,
3211- EGCG,    Antioxidation Function of EGCG by Activating Nrf2/HO-1 Pathway in Mice with Coronary Heart Disease
- in-vivo, NA, NA
*cardioP↑, *VEGF↓, *MMP2↓, *SOD↑, *ROS↓, *HO-1↑, *NQO1↑, *NRF2↑,
3214- EGCG,    EGCG-induced selective death of cancer cells through autophagy-dependent regulation of the p62-mediated antioxidant survival pathway
- in-vitro, Nor, MRC-5 - in-vitro, Cerv, HeLa - in-vitro, Nor, HEK293 - in-vitro, BC, MDA-MB-231 - in-vitro, CRC, HCT116
mTOR↓, AMPK↑, selectivity↑, ROS↑, selectivity↑, HO-1↓, *NRF2↑, NRF2↓, *HO-1↑,
3591- EGCG,    Epigallocatechin-3-Gallate Provides Protection Against Alzheimer's Disease-Induced Learning and Memory Impairments in Rats
- in-vivo, AD, NA
*p‑tau↓, *BACE↓, *Aβ↓, *Ach↑, *AChE↓, *antiOx↑, *memory↑, *hepatoP↑, *ROS↓, *GPx↑, *SOD↑,
6049- EGCG,  SeNPs,    Epigallocatechin-3-gallate (EGCG)-stabilized selenium nanoparticles coated with Tet-1 peptide to reduce amyloid-β aggregation and cytotoxicity
- Study, AD, PC12
*Aβ↓, *Dose↝, *BioAv↑, *ROS↓,
1975- EGCG,    Molecular bases of thioredoxin and thioredoxin reductase-mediated prooxidant actions of (-)-epigallocatechin-3-gallate
- in-vitro, Cerv, HeLa
TrxR↓, Trx↓, ROS↑, Dose↑,
1974- EGCG,    Protective Effect of Epigallocatechin-3-Gallate in Hydrogen Peroxide-Induced Oxidative Damage in Chicken Lymphocytes
- in-vitro, Nor, NA
*ROS↓, *NO↓, *MMP↑, *i-Ca+2↓, *HO-1↑, *Catalase↑, *NRF2↑, *Trx1↑, *antiOx↑, *SOD↑, *Apoptosis↓,
1976- EGCG,    Epigallocatechin-3-gallate exhibits anti-tumor effect by perturbing redox homeostasis, modulating the release of pro-inflammatory mediators and decreasing the invasiveness of glioblastoma cells
- in-vitro, GBM, U87MG
ROS↑, MMP↓, Casp3↑, Cyt‑c↑, Trx1↓, Ceru↓, IL6↓, IL8↓, MCP1↓, RANTES?, uPA↝, ROS↑,
1303- EGCG,    (-)-Epigallocatechin-3-gallate induces apoptosis in human endometrial adenocarcinoma cells via ROS generation and p38 MAP kinase activation
- in-vitro, EC, NA
TumCP↓, ER-α36↓, cycD1/CCND1↓, ERK↑, Jun↓, BAX↑, Bcl-2↓, cl‑Casp3↑, ROS↑, p38↑,
1516- EGCG,    Epigallocatechin Gallate (EGCG): Pharmacological Properties, Biological Activities and Therapeutic Potential
- Review, NA, NA
*Dose∅, Half-Life∅, BioAv∅, BBB↑, toxicity∅, eff↓, Apoptosis↑, Casp3↑, Cyt‑c↑, cl‑PARP↑, DNMTs↓, Telomerase↓, angioG↓, Hif1a↓, NF-kB↓, MMPs↓, BAX↑, Bak↑, Bcl-2↓, Bcl-xL↓, P53↑, PTEN↑, IGF-1↓, H3↓, HDAC1↓, *LDH↓, *ROS↓,
2309- EGCG,  Chemo,    Targeting Glycolysis with Epigallocatechin-3-Gallate Enhances the Efficacy of Chemotherapeutics in Pancreatic Cancer Cells and Xenografts
- in-vitro, PC, MIA PaCa-2 - in-vitro, Nor, HPNE - in-vitro, PC, PANC1 - in-vivo, NA, NA
TumCG↓, eff↑, ROS↑, ECAR↓, ChemoSen↑, selectivity↑, Glycolysis↓, PFK↓, PKA↓, HK2∅, LDHA∅, PFKP↓, PKM2↓, H2O2↑, TumW↓,
2310- EGCG,    Epigallocatechin-3-gallate downregulates PDHA1 interfering the metabolic pathways in human herpesvirus 8 harboring primary effusion lymphoma cells
- in-vitro, lymphoma, PEL
GLUT3↑, PDHA1↓, GDH↓, ROS↑, Glycolysis↓, OXPHOS↓,
2563- EGCG,    Cardioprotective effect of epigallocatechin gallate in myocardial ischemia/reperfusion injury and myocardial infarction: a meta-analysis in preclinical animal studies
- Review, NA, NA
cardioP↑, ROS↑, AntiAg↑, eff↑, COX1↓,
2422- EMD,    Anti-Cancer Effects of Emodin on HepG2 Cells as Revealed by 1H NMR Based Metabolic Profiling
- in-vitro, HCC, HepG2
HK2↓, PKM2↓, LDHA↓, Glycolysis↓, TumCCA↑, ROS↓, glut↓, Hif1a↓,
988- EMD,    Emodin Induced Necroptosis and Inhibited Glycolysis in the Renal Cancer Cells by Enhancing ROS
- in-vitro, RCC, NA
Necroptosis↑, p‑RIP1↑, MLKL↑, ROS↑, Glycolysis↓, GLUT1↓, PI3K↓, Akt↓,
1245- EMD,    Emodin Exhibits Strong Cytotoxic Effect in Cervical Cancer Cells by Activating Intrinsic Pathway of Apoptosis
- in-vitro, Cerv, HeLa
TumCG↓, TumCP↓, Apoptosis↑, ROS↑, Casp3↑, Casp9↑, MMP↓, DNAdam↑, GSH↓,
1332- EMD,    Induction of Apoptosis in HepaRG Cell Line by Aloe-Emodin through Generation of Reactive Oxygen Species and the Mitochondrial Pathway
- in-vivo, Nor, HepaRG
*tumCV↓, *ROS↑, *MMP↓, *Fas↑, *P53↑, *P21↑, *Bax:Bcl2↑, *Casp3↑, *Casp8↑, *Casp9↑, *cl‑PARP↑, *TumCCA↑, *P21↑, *cycE/CCNE↑, *cycA1/CCNA1↓, *CDK2↓,
1327- EMD,    Emodin induces apoptosis in human lung adenocarcinoma cells through a reactive oxygen species-dependent mitochondrial signaling pathway
- in-vitro, Lung, A549
Cyt‑c↑, Casp2↑, Casp3↑, Casp9↑, ERK↓, Akt↓, ROS↑, MMP↓, Bcl-2↓, BAX↑,
1322- EMD,    The versatile emodin: A natural easily acquired anthraquinone possesses promising anticancer properties against a variety of cancers
- Review, Var, NA
Apoptosis↑, TumCP↓, ROS↑, TumAuto↑, EMT↓, TGF-β↓, DNAdam↑, ER Stress↑, TumCCA↑, ATP↓, NF-kB↓, CYP1A1↑, STAC2↓, JAK↓, PI3K↓, Akt↓, MAPK↓, FASN↓, HER2/EBBR2↓, ChemoSen↑, eff↑, ChemoSen↑, angioG↓, VEGF↓, MMP2↓, eNOS↓, FOXD3↑, MMP9↓, TIMP1↑,
1323- EMD,    Anticancer action of naturally occurring emodin for the controlling of cervical cancer
- Review, Cerv, NA
TumCCA↑, DNAdam↑, mTOR↓, Casp3↑, Casp8↑, Casp9↑, TGF-β↑, SMAD3↓, p‑SMAD4↓, ROS↑, MMP↓, CXCR4↓, HER2/EBBR2↓, ER Stress↓, TumAuto↑, NOTCH1↓,
1324- EMD,    Is Emodin with Anticancer Effects Completely Innocent? Two Sides of the Coin
- Review, Var, NA
*toxicity↑, *BioAv↓, Akt↓, ERK↓, ROS↑, MMP↓, Bcl-2↓, BAX↑, TumCCA↑,
1321- EMD,    Antitumor effects of emodin on LS1034 human colon cancer cells in vitro and in vivo: roles of apoptotic cell death and LS1034 tumor xenografts model
- in-vitro, CRC, LS1034 - in-vivo, NA, NA
tumCV↓, TumCCA↑, ROS↑, Ca+2↑, MMP↓, Apoptosis↑, Cyt‑c↑, Casp9↑, Bax:Bcl2↑,
1318- EMD,    Aloe-emodin Induces Apoptosis in Human Liver HL-7702 Cells through Fas Death Pathway and the Mitochondrial Pathway by Generating Reactive Oxygen Species
- in-vitro, Nor, HL7702
*TumCCA↑, *ROS↑, *MMP↓, *Fas↑, *P53↑, *P21↓, *Bax:Bcl2↑, *cl‑Casp3↑, *cl‑Casp8↑, *cl‑Casp9↑, *cl‑PARP↑,
1326- EMD,    Emodin induces a reactive oxygen species-dependent and ATM-p53-Bax mediated cytotoxicity in lung cancer cells
- in-vitro, Lung, A549
Apoptosis↑, ROS↑, P53↑, BAX↑, ATM↑,
1328- EMD,    Emodin induces apoptosis of human tongue squamous cancer SCC-4 cells through reactive oxygen species and mitochondria-dependent pathways
- in-vitro, Tong, SCC4
TumCCA↑, P21↑, Chk2↑, CycB/CCNB1↓, cDC2↓, Apoptosis↑, Cyt‑c↑, Casp9↑, Casp3↑, ROS↑, MMP↓, Bax:Bcl2↑, ER Stress↑,
1331- EMD,    Aloe-emodin induces apoptosis of human nasopharyngeal carcinoma cells via caspase-8-mediated activation of the mitochondrial death pathway
- in-vitro, NPC, NA
TumCCA↑, CycB/CCNB1↑, DNAdam↑, Casp3↑, cl‑PARP↑, MMP↓, Ca+2↑, ROS↑,
5525- EP,    Cell responses without receptors and ligands, using nanosecond pulsed electric fields (nsPEFs)
- Review, Var, NA
CellMemb↑, Ca+2↑, ER Stress↑, ROS↑, MMP↓, VGCC↓, VGSC↓, Dose↝,
5526- EP,    Nanosecond Pulsed Electric Field Modulates Electron Transport and Mitochondrial Structure and Function
- Review, Var, NA
CellMemb↑, ROS↑, ETC↝, OCR↓, MMP↓,
5529- EP,    Effects of nsPEFs on Electron Transport and Mitochondrial Structures and Functions
- Review, Var, NA
ETC↓, OCR↓, CellMemb↑, mt-ROS↑, MMP↓,
5494- EP,    An Overview of Subnanosecond Pulsed Electric Field Biological Effects: Toward Contactless Technologies for Cancer Treatment
- Review, Var, NA
other↝, ROS↑, Temp∅, CellMemb↑, Ca+2↑, Apoptosis↑, TumCD↑, MMP↓, necrosis↑, TumVol↓, Remission↑,
5495- EP,    Irreversible electroporation in focal therapy for prostate cancer: current status and future directions
- Review, Pca, NA
Ca+2↑, ATP↓, mtDam↑, ROS↑, CellMemb↑,
5519- EP,    Nanosecond Pulsed Electric Fields (nsPEFs) for Precision Intracellular Oncotherapy: Recent Advances and Emerging Directions
- Review, Var, NA
MMP↓, Ca+2↑, eff↑, ER Stress↑, selectivity↑, CSCs↓, CD44↓, CD133↓, ROS↑, Imm↑, DNAdam↑, MOMP↑, Cyt‑c↑, Casp9↑, Casp3↑, Casp9↑, TumCD↑, Fas↑, UPR↑, Dose↝, Dose↝, Dose↓, Dose↑, HMGB1↓, eff↑, EPR↑, ChemoSen↑, ETC↝, *AntiAge↑, *Hif1a↑, *SIRT1↑,
5521- EP,    Nanosecond Pulsed Electric Fields (nsPEFs) Modulate Electron Transport in the Plasma Membrane and the Mitochondria
- in-vitro, BC, 4T1 - in-vitro, Nor, H9c2
ETC↓, ROS↑, *mt-ROS↑,

Showing Research Papers: 901 to 950 of 2174
Prev Page 19 of 44 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2174

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ceru↓, 1,   CYP1A1↑, 1,   Ferroptosis↑, 1,   GPx↑, 1,   GPx4↓, 1,   GSH↓, 1,   H2O2↑, 1,   HO-1↓, 1,   HO-1↑, 1,   Iron↑, 1,   Keap1↓, 2,   MDA↑, 1,   NRF2↓, 1,   NRF2↑, 3,   OXPHOS↓, 2,   Prx↓, 1,   RNS↓, 1,   ROS↓, 3,   ROS↑, 35,   mt-ROS↓, 1,   mt-ROS↑, 1,   SOD↑, 1,   Trx↓, 1,   Trx1↓, 1,   TrxR↓, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 2,   ETC↓, 2,   ETC↝, 2,   MMP↓, 15,   MMP↑, 1,   mtDam↑, 1,   OCR↓, 3,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACSL4↑, 1,   AMPK↑, 1,   p‑AMPK↑, 1,   ECAR↓, 2,   FASN↓, 1,   GAPDH↓, 1,   GDH↓, 1,   glut↓, 1,   GlutMet↓, 1,   Glycolysis↓, 5,   HK2↓, 1,   HK2∅, 1,   lactateProd↓, 1,   LDHA↓, 1,   LDHA∅, 1,   PDHA1↓, 1,   PFK↓, 1,   PFKP↓, 1,   PI3k/Akt/mTOR↓, 1,   PKM2↓, 2,   cl‑PPARα↓, 1,  

Cell Death ⓘ

Akt↓, 5,   p‑Akt↓, 2,   Apoptosis↑, 11,   BAD↑, 1,   Bak↑, 3,   BAX↑, 7,   BAX⇅, 1,   Bax:Bcl2↑, 2,   Bcl-2↓, 6,   Bcl-xL↓, 4,   Casp2↑, 1,   Casp3↑, 12,   cl‑Casp3↑, 1,   Casp8↓, 1,   Casp8↑, 4,   Casp9↑, 9,   Chk2↑, 1,   Cyt‑c↑, 8,   Diablo↑, 1,   Fas↑, 2,   Ferroptosis↑, 1,   HGF/c-Met↓, 1,   JNK↓, 1,   JWA↑, 1,   MAPK↓, 2,   Mcl-1↓, 1,   MDM2↑, 1,   MLKL↑, 1,   MOMP↑, 1,   Myc↓, 1,   Necroptosis↑, 1,   necrosis↑, 1,   p27↑, 1,   p38↑, 1,   p‑RIP1↑, 1,   survivin↓, 1,   Telomerase↓, 3,   TumCD↑, 2,  

Kinase & Signal Transduction ⓘ

FOXD3↑, 1,   HER2/EBBR2↓, 2,  

Transcription & Epigenetics ⓘ

H3↓, 1,   HATs↓, 1,   other↝, 1,   pRB↑, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 2,   ER Stress↓, 1,   ER Stress↑, 6,   GRP78/BiP↑, 3,   UPR↑, 4,   XBP-1↑, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3B↑, 1,   LC3II↑, 1,   TumAuto↑, 3,  

DNA Damage & Repair ⓘ

ATM↑, 1,   DNAdam↑, 6,   DNMTs↓, 3,   p16↑, 1,   P53↑, 5,   PARP↑, 2,   cl‑PARP↑, 2,   PCNA↓, 1,   TP53↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   CycB/CCNB1↓, 1,   CycB/CCNB1↑, 1,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 1,   P21↑, 2,   TumCCA↑, 7,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   CD44↓, 1,   cDC2↓, 1,   CSCs↓, 1,   EMT↓, 1,   ERK↓, 3,   ERK↑, 1,   FOXO↑, 1,   Gli1↓, 1,   HDAC↓, 2,   HDAC1↓, 1,   HH↓, 1,   IGF-1↓, 1,   IGF-1R↑, 1,   Jun↓, 1,   mTOR↓, 4,   NOTCH↓, 1,   NOTCH1↓, 1,   NOTCH3↓, 1,   PI3K↓, 2,   PTEN↑, 2,   Smo↓, 1,   STAT↓, 1,   TumCG↓, 2,   VGCC↓, 1,   VGSC↓, 1,   Wnt↑, 1,  

Migration ⓘ

AntiAg↑, 1,   AP-1↓, 1,   Ca+2↑, 6,   Ca+2↝, 1,   ER-α36↓, 1,   FAK↓, 2,   Ki-67↓, 1,   MMP2↓, 2,   MMP9↓, 3,   MMPs↓, 2,   PDGF↓, 1,   PKA↓, 1,   SMAD3↓, 1,   p‑SMAD4↓, 1,   STAC2↓, 1,   TGF-β↓, 1,   TGF-β↑, 1,   TIMP1↑, 2,   TIMP2↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 6,   uPA↓, 2,   uPA↝, 1,   Vim↓, 1,   Zeb1↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   ATF4↑, 2,   EGFR↓, 1,   eNOS↓, 1,   EPR↑, 1,   Hif1a↓, 5,   miR-210↓, 1,   VEGF↓, 4,  

Barriers & Transport ⓘ

BBB↑, 1,   CellMemb↑, 5,   CTR1↑, 1,   GLUT1↓, 1,   GLUT3↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 2,   CXCR4↓, 1,   HMGB1↓, 1,   IL6↓, 1,   IL8↓, 1,   Imm↑, 1,   JAK↓, 2,   MCP1↓, 1,   NF-kB↓, 4,   RANTES?, 1,   TNF-α↓, 1,  

Cellular Microenvironment ⓘ

Temp∅, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv∅, 1,   ChemoSen↑, 5,   Dose↓, 1,   Dose↑, 2,   Dose↝, 3,   eff↓, 1,   eff↑, 7,   Half-Life∅, 1,   selectivity↑, 5,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   HER2/EBBR2↓, 2,   IL6↓, 1,   Ki-67↓, 1,   Myc↓, 1,   TP53↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   chemoP↑, 1,   Remission↑, 1,   toxicity∅, 1,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 230

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 6,   Catalase↑, 2,   GPx↑, 1,   HO-1↑, 3,   MPO↓, 1,   NQO1↑, 1,   NRF2↑, 5,   RNS↓, 1,   ROS↓, 11,   ROS↑, 2,   mt-ROS↑, 1,   SOD↑, 3,   SOD1↑, 1,   SOD2↑, 1,   Trx1↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,   MMP↑, 1,  

Core Metabolism/Glycolysis ⓘ

glucose↓, 1,   LDH↓, 1,   LDL↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Apoptosis↓, 2,   BAX↓, 1,   Bax:Bcl2↑, 2,   Casp1↓, 1,   Casp12↓, 1,   Casp3↓, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   Casp8↑, 1,   cl‑Casp8↑, 1,   Casp9↑, 1,   cl‑Casp9↑, 1,   Cyt‑c↓, 1,   Fas↑, 2,   iNOS↓, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,   other↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↓, 1,   ER Stress↓, 1,   GRP78/BiP↓, 2,   IRE1↓, 1,   PERK↓, 1,   UPR↓, 2,  

DNA Damage & Repair ⓘ

P53↓, 1,   P53↑, 2,   p‑PARP↓, 1,   cl‑PARP↑, 2,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   cycA1/CCNA1↓, 1,   cycE/CCNE↑, 1,   E2Fs↑, 1,   P21↓, 1,   P21↑, 2,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1R↓, 1,  

Migration ⓘ

AP-1↓, 1,   Ca+2?, 1,   Ca+2↓, 1,   i-Ca+2↓, 1,   MMP2↓, 2,   TXNIP↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↑, 1,   NO↓, 1,   PDGFR-BB↓, 1,   VEGF↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

ASC↓, 1,   COX2↓, 1,   IL18↓, 1,   IL1β↓, 1,   IL6↓, 2,   IL8↓, 1,   Inflam↓, 2,   JAK↓, 1,   NF-kB↓, 2,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   p‑tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 2,   BACE↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 3,   BioAv↑, 2,   BioAv↝, 1,   Dose↝, 2,   Dose∅, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

IL6↓, 2,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   AntiCan↑, 1,   cardioP↑, 3,   hepatoP↓, 1,   hepatoP↑, 1,   memory↑, 2,   neuroP↑, 2,   RenoP↑, 1,   toxicity↑, 1,  
Total Targets: 100

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
121 Silver-NanoParticles
92 Quercetin
88 Magnetic Fields
80 Curcumin
74 Thymoquinone
55 Shikonin
54 Vitamin C (Ascorbic Acid)
52 Resveratrol
49 Berberine
49 Sulforaphane (mainly Broccoli)
47 Lycopene
44 Radiotherapy/Radiation
43 Baicalein
42 Alpha-Lipoic-Acid
40 Selenite (Sodium)
40 Ashwagandha(Withaferin A)
40 Piperlongumine
39 Selenium NanoParticles
38 Artemisinin
38 EGCG (Epigallocatechin Gallate)
37 Betulinic acid
36 Hydrogen Gas
34 Rosmarinic acid
33 Capsaicin
32 Silymarin (Milk Thistle) silibinin
29 Propolis -bee glue
29 Fisetin
28 Apigenin (mainly Parsley)
27 Honokiol
26 Allicin (mainly Garlic)
25 Chemotherapy
25 Phenethyl isothiocyanate
24 Luteolin
24 Magnetic Field Rotating
23 Copper and Cu NanoParticles
23 Chrysin
22 Vitamin K2
21 doxorubicin
21 Gambogic Acid
20 Cisplatin
20 chitosan
20 Chlorogenic acid
20 Juglone
18 Boron
17 salinomycin
17 Parthenolide
16 Urolithin
15 Coenzyme Q10
14 Photodynamic Therapy
14 Auranofin
14 Boswellia (frankincense)
14 Carnosic acid
14 Carvacrol
14 Phenylbutyrate
13 Selenium
13 Ellagic acid
13 Emodin
13 Pterostilbene
12 Caffeic acid
12 VitK3,menadione
11 5-fluorouracil
11 Astaxanthin
11 Dichloroacetate
11 Graviola
11 Piperine
10 Melatonin
10 Ursolic acid
10 diet FMD Fasting Mimicking Diet
10 Ferulic acid
10 Plumbagin
9 SonoDynamic Therapy UltraSound
9 Andrographis
9 Bacopa monnieri
9 borneol
8 Hydroxycinnamic-acid
8 Electrical Pulses
8 Sulfasalazine
8 Hyperthermia
8 Methylene blue
8 Moringa oleifera
8 Propyl gallate
7 3-bromopyruvate
7 Gold NanoParticles
7 Gemcitabine (Gemzar)
7 Metformin
7 Berbamine
7 brusatol
7 Carnosine
7 Celastrol
7 diet Methionine-Restricted Diet
7 Disulfiram
7 HydroxyTyrosol
6 2-DeoxyGlucose
6 immunotherapy
6 Biochanin A
6 Butyrate
6 Chlorophyllin
6 Citric Acid
6 Aflavin-3,3′-digallate
6 Nimbolide
5 Docetaxel
5 Brucea javanica
5 Bromelain
5 erastin
5 Thymol-Thymus vulgaris
5 Chocolate
5 Cinnamon
5 Spermidine
5 Crocetin
5 Huperzine A/Huperzia serrata
5 Garcinol
5 HydroxyCitric Acid
5 Magnolol
5 nicotinamide adenine dinucleotide
5 Rutin
4 chemodynamic therapy
4 EMF
4 Zinc
4 Vitamin E
4 diet Short Term Fasting
4 γ-linolenic acid (Borage Oil)
4 Magnesium
4 Naringin
4 Taurine
3 5-Aminolevulinic acid
3 Anthocyanins
3 Glucose
3 temozolomide
3 Black phosphorus
3 Paclitaxel
3 Catechins
3 Choline
3 Date Fruit Extract
3 Oxygen, Hyperbaric
3 Shilajit/Fulvic Acid
3 Ginkgo biloba
3 Orlistat
3 MCToil
3 Methylsulfonylmethane
3 Mushroom Lion’s Mane
3 Oleuropein
3 Shankhpushpi
3 Vitamin B1/Thiamine
2 5-Hydroxytryptophan
2 Astragalus
2 Aromatherapy
2 Ascorbyl Palmitate
2 Atorvastatin
2 Aloe anthraquinones
2 beta-glucans
2 Baicalin
2 beta-carotene(VitA)
2 Bufalin/Huachansu
2 Bruteridin(bergamot juice)
2 Caffeic Acid Phenethyl Ester (CAPE)
2 Cat’s Claw
2 Calorie Restriction Mimetics
2 Galantamine
2 Folic Acid, Vit B9
2 Fenbendazole
2 Galloflavin
2 Potassium
2 Methyl Jasmonate
2 Methylglyoxal
2 Myricetin
2 Vitamin B3,Niacin
2 Niclosamide (Niclocide)
2 Pachymic acid
2 Sanguinarine
2 Psoralidin
2 Radio Frequency
2 Sesame seeds and Oil
2 Iron
2 Salvia miltiorrhiza
2 Vitamin D3
1 cetuximab
1 Anzaroot, Astragalus fasciculifolius Bioss
1 entinostat
1 Camptothecin
1 Resiquimod
1 Ajoene (compound of Garlic)
1 Acetyl-l-carnitine
1 alpha Linolenic acid
1 Anti-oxidants
1 Sorafenib (brand name Nexavar)
1 tamoxifen
1 almonertinib
1 D-limonene
1 epirubicin
1 Lapatinib
1 Ras-selective lethal 3
1 Cannabidiol
1 Celecoxib
1 Aspirin -acetylsalicylic acid
1 methylseleninic acid
1 Rivastigmine
1 Docosahexaenoic Acid
1 diet Ketogenic
1 diet Plant based
1 Exercise
1 Fucoidan
1 Gallic acid
1 verapamil
1 hydroxychloroquine
1 Ginseng
1 hydrogen sulfide
1 Rapamycin
1 Ivermectin
1 lambertianic acid
1 Myrrh
1 N-Acetyl-Cysteine
1 Oleocanthal
1 sericin
1 benzo(a)pyrene
1 Hyperoside
1 Kaempferol
1 Perilla
1 Salvia officinalis
1 Oxaliplatin
1 Scoulerine
1 polyethylene glycol
1 acetaminophen
1 Formononetin
1 Silicic Acid
1 Squalene
1 Osimertinib
1 Adagrasib
1 Glutathione
1 statins
1 Safflower yellow
1 triptolide
1 Vitamin A, Retinoic Acid
1 Vitamin B12
1 Vitamin B2,Riboflavin
1 Vitamin B5,Pantothenic Acid
1 glucose deprivation
1 Transarterial Chemoembolization
1 probiotics
1 xanthohumol
1 Zinc Oxide
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#:%  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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