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⟱
6460- TUR,  CUR,    Neuroprotective Effect of Turmeric Extract in Combination with Its Essential Oil and Enhanced Brain Bioavailability in an Animal Model
- in-vivo, AD, NA
*memory↑, *lipid-P↓, *GSH↑, *AChE↑, *Catalase↑, *BioAv↑, *P-gp↓, *BioAv↑, *SOD↑, *BBB↑, *ROS↓,
6458- TUR,    Curcumin, demethoxycurcumin, bisdemethoxycurcumin, tetrahydrocurcumin and turmerones differentially regulate anti-inflammatory and anti-proliferative responses through a ROS-independent mechanism
- in-vitro, lymphoma, U937
ROS∅, GSH∅,
5904- TV,    Pharmacological Properties and Molecular Mechanisms of Thymol: Prospects for Its Therapeutic Potential and Pharmaceutical Development
- Review, Var, NA - Review, Stroke, NA - Review, Diabetic, NA - Review, Obesity, NA - Review, AD, NA - Review, Arthritis, NA
*antiOx↑, *ROS↓, *Inflam↓, *Bacteria↓, AntiTum↑, IronCh↑, *HDL↑, *LDL↓, *BioAv↝, *Half-Life↝, *BioAv↑, *SOD↑, *GPx↑, *GSTs↑, *eff↑, radioP↑, *MDA↓, *other↑, *COX1↓, *COX2↓, *AntiAg↑, *RNS↓, *NO↓, *H2O2↓, *NOS2↓, *NADH↓, *Imm↑, Apoptosis↑, TumCP↓, angioG↓, TumCMig↓, Ca+2↑, TumCCA↑, DNAdam↑, BAX↑, Casp9↑, Casp8↑, Casp3↑, cl‑PARP↑, AIF↑, i-ROS↑, MMP↓, Cyt‑c↑, APAF1↑, Ca+2↑, MMP9↓, MMP2↓, PKCδ↓, ERK↓, H2O2↑, BAX↑, Bcl-2↓, DNAdam↑, lipid-P↑, ChemoSen↑, chemoP↑, *cardioP↑, *SOD↑, *Catalase↑, *GPx↑, *GSH↑, *BP↓, *AntiDiabetic↑, *Obesity↓, RenoP↑, *GastroP↑, hepatoP↑, *AChE↓, *cognitive↑, *BChE↓, *other↓, *BioAv↑,
3790- UA,    Therapeutic applications of ursolic acid: a comprehensive review and utilization of predictive tools
*Inflam↓, *antiOx↑, AntiCan↑, *neuroP↑, *hepatoP↑, *cardioP↑, *MMP↑, *ROS↓, *PGC-1α↑, *BDNF↑, *cognitive↑, Bcl-2↓, Cyt‑c↑, DR5↑, Casp9↑, Casp8↑, Casp3↑, TumCCA↑, *BioAv↓, *Dose↝, *Half-Life↓, *Half-Life↓,
3788- UA,  RosA,    Ursolic acid and rosmarinic acid ameliorate alterations in hippocampal neurogenesis and social memory induced by amyloid beta in mouse model of Alzheimer’s disease
- in-vivo, AD, NA
*neuroP↑, *Aβ↓, *p‑tau↓, *memory↑, *Inflam↓, *ROS↓,
2350- UA,    Ursolic acid-mediated changes in glycolytic pathway promote cytotoxic autophagy and apoptosis in phenotypically different breast cancer cells
- in-vitro, BC, MCF7 - in-vitro, BC, MDA-MB-231
Akt↓, Glycolysis↓, HK2↓, PKM2↓, ATP↓, lactateProd↓, AMPK↑, TumAuto↑, Apoptosis↑, ERK↓, MMP↓, NO↑, ROS↑, DNAdam↑,
119- UA,  CUR,  RES,    Combinatorial treatment with natural compounds in prostate cancer inhibits prostate tumor growth and leads to key modulations of cancer cell metabolism
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
ROS⇅, p‑STAT3↓, Src↓, AMPK↑, GlutMet↑, TCA↑, glut↓,
5017- UA,    Ursolic acid disturbs ROS homeostasis and regulates survival-associated gene expression to induce apoptosis in intestinal cancer cells
- in-vitro, Cerv, INT-407 - in-vitro, CRC, HCT116
AntiCan↑, TumCG↓, ROS↑, Apoptosis↑, TumCMig↓, CTNNB1↓, Twist↓, Bcl-2↓, survivin↓, NF-kB↓, Sp1/3/4↓, BAX↑, P21↑, P53↑, eff↓, TumCMig↓,
5020- UA,    Anticancer activity of ursolic acid on human ovarian cancer cells via ROS and MMP mediated apoptosis, cell cycle arrest and downregulation of PI3K/AKT pathway
- in-vitro, Ovarian, NA
tumCV↓, selectivity↑, BAX↑, Bcl-2↓, Apoptosis↑, ROS↑, TumCCA↑, Akt↓, PI3K↓,
5021- UA,    Anticancer effect of ursolic acid via mitochondria-dependent pathways
- Review, Var, NA
Inflam↓, TNF-α↓, IL6↓, IL17↓, NF-kB↓, COX2↓, *AntiDiabetic↑, *hepatoP↑, ALAT↓, AST↓, TumCP↓, Apoptosis↑, TumCCA↑, TumAuto↑, tumCV↓, TumCMig↓, Glycolysis↓, ATP↓, lactateProd↓, HK2↓, PKA↓, COX2↓, mtDam↑, Casp3↑, Casp8↑, Casp9↑, Akt↓, ROS↑, MMP↓, P53↑,
5022- UA,    Ursolic Acid’s Alluring Journey: One Triterpenoid vs. Cancer Hallmarks
- Review, Var, NA
TumCP↓, Apoptosis↑, angioG↑, TumMeta↓, BioAv↓, Hif1a↓, Glycolysis↓, mitResp↓, Akt↓, MAPK↓, ERK↓, mTOR↓, P53↑, P21↑, E2Fs↑, STAT3↓, MMP↓, NLRP3↓, iNOS↓, CHK1↓, Chk2↓, BRCA1↓, E-cadherin↑, N-cadherin↓, Casp↑, p62↓, LC3II↑, Vim↓, ROS↑, CSCs↓, DNAdam↑, GutMicro↑, VEGF↓,
5023- UA,  CA,  RosA,    Therapeutic Effect of Rosemary and Its Active Constituent on Nervous System Disorders
- Review, Park, NA - Review, AD, NA
*memory↑, *cognitive↑, *ROS↓,
4869- Uro,    Urolithin A in Central Nervous System Disorders: Therapeutic Applications and Challenges
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*MitoP↑, *Inflam↓, *antiOx↑, *Risk↓, *Aβ↓, *p‑tau↓, *p62↓, *PARK2↑, *MMP↑, *ROS↓, *Strength↑, *CRP↓, *IL1β↓, *IL6↓, *TNF-α↓, *AMPK↑, *NF-kB↓, *MAPK↓, *p62↑, *NRF2↑, *SOD↑, *Catalase↑, *HO-1↑, *Ferroptosis↓, *lipid-P↓, *Cartilage↑, *PI3K↓, *Akt↓, *mTOR↓, *Apoptosis↓, *neuroP↑, *Bcl-2↓, *BAX↑, *Casp3↑, *ATP↑, *eff↑, *motorD↑, *NLRP3↓, *radioP↑, *BBB↑,
4859- Uro,  Rad,    Urolithin A Enhances Tight Junction Protein Expression in Endothelial Cells Cultured In Vitro via Pink1-Parkin-Mediated Mitophagy in Irradiated Astrocytes
- in-vitro, Nor, NA
*ROS↓, *VEGF↓,
4864- Uro,    Therapeutic Potential of Mitophagy-Inducing Microflora Metabolite, Urolithin A for Alzheimer's Disease
- Review, AD, NA
*neuroP↑, *Half-Life↝, *BBB↑, *toxicity↓, *Inflam↓, *Strength↑, *BACE↓, *Aβ↓, *MitoP↑, *SIRT1↑, *SIRT3↑, *AMPK↑, *PGC-1α↑, *mTOR↓, *PARK2↑, *Beclin-1↑, *ROS↓, *GutMicro↑, *Risk↓,
4860- Uro,    Urolithins–gut Microbial Metabolites with Potential Health Benefits
- Review, Nor, NA - Review, AD, NA - Review, Park, NA
*ROS↓, *Inflam↓, TumCG↓, *neuroP↑, *cardioP↑, *LDL↓, *BioAv↝, *BioAv↓, *BioAv↑, *SIRT1↑, *mTOR↑, *BDNF↑, *cognitive↑,
4857- Uro,    Evaluation and comparison of the anti-proliferative and anti-metastatic effects of urolithin A and urolithin B against esophageal cancer cells: an in vitro and in silico study
- in-vitro, ESCC, KYSE-30
tumCV↓, selectivity↑, TumCCA↑, ROS↑, Bcl-2↓, BAX↑, P21↑, MMP2↓, MMP9↓,
4874- Uro,  EGCG,    A Combination Therapy of Urolithin A+EGCG Has Stronger Protective Effects than Single Drug Urolithin A in a Humanized Amyloid Beta Knockin Mice for Late-Onset Alzheimer's Disease
- in-vivo, AD, NA
*motorD↑, *memory↑, *MitoP↑, *Aβ↓, *mitResp↑, *Nrf1↑, *PINK1↑, *PARK2↑, *ATG5↑, *Bcl-2↑, *H2O2↓, *ROS↓, *lipid-P↓, *mt-ATP↑,
4876- Uro,    Urolithin A in Health and Diseases: Prospects for Parkinson’s Disease Management
- Review, Park, NA - Review, AD, NA
*Inflam↓, *antiOx↓, *neuroP↑, *p‑tau↓, *Aβ↓, *eff↑, *BioAv↓, *BioAv↑, *GSH↑, *SOD↑, *lipid-P↓, *Catalase↑, *GSR↑, *GPx↑, *ROS↓, *NRF2↑, *GutMicro↑, *Risk↓, *BBB↓, *NLRP3↓, *MAOA↓,
4877- Uro,    Urolithin-A Derivative UAS03 Improves Cognitive Deficits and Memory by Activating Nrf2 Pathways to Alleviate Oxidative Stress and Neuroinflammation
- in-vivo, AD, NA
*cognitive↑, *memory↑, *neuroP↑, *NRF2↑, *ROS↓, *Inflam↓, *IL1β↓, *TNF-α↓, *COX2↓,
4880- Uro,    Urolithins: A Prospective Alternative against Brain Aging
- Review, AD, NA
*cognitive↑, *memory↑, *antiOx↑, *BBB↑, *ROS↓, *lipid-P↓, *Catalase↑, *SOD↑, *GSR↑, *GPx↑, *CREB↑, *BDNF↑, *neuroP↑, *Inflam↓, *MitoP↑, *Aβ↓, *tau↓, *NLRP3↓, *SIRT1↑, *SIRT3↑,
4856- Uro,    Study on the biological mechanism of urolithin a on nasopharyngeal carcinoma in vitro
- in-vitro, NPC, CNE1 - in-vitro, NPC, CNE2
Apoptosis↑, MMP↓, ROS↑, E-cadherin↑, BAX↑, cl‑Casp3↑, PARP↑, MMP2↓, MMP9↓, N-cadherin↓, Vim↓, Snail↓, eff↓, TumCP↓, TumCMig↓, TumCI↓, EMT↓,
4833- Uro,    Unveiling the potential of Urolithin A in Cancer Therapy: Mechanistic Insights to Future Perspectives of Nanomedicine
- Review, Var, NA - Review, AD, NA - Review, IBD, NA
BioAv↝, TumAuto↝, TumCG↓, TumMeta↓, ChemoSen↑, Imm↑, RadioS↑, BioAv↑, other↝, eff↓, *antiOx↓, *Inflam↓, AntiCan↓, AntiAge↑, chemoP↑, *neuroP↑, *ROS↓, *cognitive↑, *lipid-P↓, *cardioP↑, *TNF-α↓, *IL6↓, GutMicro↑, TumCCA↑, Apoptosis↑, angioG↓, NF-kB↓, PI3K↓, Akt↓, Casp↑, survivin↓, TumCP↓, cycD1/CCND1↓, cMyc↑, BAX↑, Bcl-2↓, COX2↓, P53↑, p38↑, *ROS↓, *SOD↑, *GPx↑, SIRT1↑, FOXO1↑, eff↑, ChemoSen↑,
4835- Uro,    Urolithin A, induces apoptosis and autophagy crosstalk in Oral Squamous Cell Carcinoma via mTOR /AKT/ERK1/2 pathway
- in-vitro, SCC, NA
TumCD↑, ER Stress↑, Akt↓, mtDam↓, p‑mTOR↓, *BioAv↝, ROS↑, TumCCA↑, Apoptosis↑, ERK↓,
4837- Uro,    Urolithins: The Gut Based Polyphenol Metabolites of Ellagitannins in Cancer Prevention, a Review
- Review, Var, NA
AntiCan↑, TumCCA↑, Apoptosis↑, TumAuto↑, *BioAv↝, *BioAv↑, RAS↓, ERK↓, AR↓, TumCP↓, PI3K↓, Akt↓, NF-kB↓, COX2↓, IL6↓, IL1β↓, Wnt↓, β-catenin/ZEB1↓, cMyc↓, P53↑, Casp3↑, PARP↑, ROS↓, toxicity↓,
4841- Uro,    Urolithin A induces cell cycle arrest and apoptosis by inhibiting Bcl-2, increasing p53-p21 proteins and reactive oxygen species production in colorectal cancer cells
- in-vitro, CRC, HT29 - in-vitro, CRC, SW480 - in-vitro, CRC, SW-620
TumCP↓, TumCCA↑, Apoptosis↑, P53↑, P21↑, Bcl-2↓, Cyt‑c↑, Casp↑, ROS↑, *ROS↓,
4854- Uro,    Urolithins: Emerging natural compound targeting castration-resistant prostate cancer (CRPC)
- Review, Pca, NA
AR↓, ROS↓, Apoptosis↑, selectivity↑, Dose↑, MDA↓, SOD↑, GPx↑, ROS↑, Casp3↑, Casp9↑,
4858- Uro,    The Metabolite Urolithin-A Ameliorates Oxidative Stress in Neuro-2a Cells, Becoming a Potential Neuroprotective Agent
- in-vitro, Nor, NA
*ROS?, *neuroP↑, *lipid-P↓, *Catalase↑, *SOD↑, *GPx↑, *GSR↑, *monoA↓, *tyrosinase↓,
4616- VitA,RetA,  VitC,  VitD3,  VitE,  Rad  Vitamins and Radioprotective Effect: A Review
- Review, NA, NA
*radioP↑, *ROS↓,
4314- VitB1/Thiamine,    Unraveling the molecular mechanisms of vitamin deficiency in Alzheimer's disease pathophysiology
- Review, AD, NA
*Risk↓, *GlucoseCon↑, *cognitive↑, *ATP↑, *ROS↓, *NADPH↑, *Aβ↓, *APP↓, *BACE↓,
4311- VitB1/Thiamine,    Benfotiamine treatment activates the Nrf2/ARE pathway and is neuroprotective in a transgenic mouse model of tauopathy
- in-vivo, AD, NA
*Aβ↓, *p‑tau↓, *ROS↓, *cognitive↑, *OS↑, *Mood↑, *neuroP↑, *Inflam↓, *NRF2↑, *PGC-1α↑, *AGEs↓, *4-HNE↓, *NQO1↑, *COX2↓, *TNF-α↓, *IL1β↓, *NF-kB↓, *GSK‐3β↓,
1888- VitB1/Thiamine,  DCA,    High Dose Vitamin B1 Reduces Proliferation in Cancer Cell Lines Analogous to Dichloroacetate
- in-vitro, PC, SK-N-BE - NA, PC, PANC1
p‑PDH↓, GlucoseCon↓, lactateProd↓, MMP↓, Casp3↑, eff↑, PDKs↓, selectivity↑, TumCG↓, Dose∅, MMP↓, ROS∅, toxicity↑, antiOx↑,
4037- VitB12,  FA,    Mechanistic Link between Vitamin B12 and Alzheimer’s Disease
- Review, AD, NA
*antiOx↑, *ROS↓, *GSH↑, *Inflam↓, *IL6↓, *TNF-α↓, *other↑, *other↑, *other↑, *Aβ↓, *memory↑, *p‑tau↓, *APP↓, *BACE↓, *ATP↑, *neuroP↑,
4315- VitB2,    Unraveling the molecular mechanisms of vitamin deficiency in Alzheimer's disease pathophysiology
*GlucoseCon↑, *ATP↑, *homoC↓, *ROS↓, *Aβ↓, *Aβ↓, *Inflam↓,
4031- VitB3,    Nicotinamide Riboside-The Current State of Research and Therapeutic Uses
- Review, NA, NA
*cardioP↑, *neuroP↑, *NAD↑, *SIRT1↑, *NADPH↑, *ROS↓, *IL2↓, *IL5↓, *IL6↓, *TNF-α↓, *Inflam↓, *BioAv↝, *BioAv↑,
4317- VitB5,    Unraveling the molecular mechanisms of vitamin deficiency in Alzheimer's disease pathophysiology
- Review, AD, NA
*Ach↑, *ROS↓, *Inflam↓, *p‑tau↓, *Aβ↓, *Acetyl-CoA↑, *ATP↑, *ChAT↑, *memory↑,
1216- VitC,    Ascorbic acid induces ferroptosis via STAT3/GPX4 signaling in oropharyngeal cancer
- in-vitro, Laryn, FaDu - in-vitro, SCC, SCC-154
Iron↝, ROS↑, tumCV↓, Ki-67↓, TumCCA↑, Ferroptosis↑, GSH↓, ROS↑, MDA↑, STAT3↓, GPx4↓, p‑STAT3↓,
1819- VitC,  VitK3,    The association of vitamins C and K3 kills cancer cells mainly by autoschizis, a novel form of cell death. Basis for their potential use as coadjuvants in anticancer therapy
- Review, Var, NA
Dose?, TumCD↑, selectivity↑, H2O2↑, ROS↑, DNAdam↑,
606- VitC,    Understanding the Therapeutic Potential of Ascorbic Acid in the Battle to Overcome Cancer
- Review, NA, NA
ROS↑, H2O2↑, Fenton↑,
605- VitC,    Therapeutic Use of Vitamin C in Cancer: Physiological Considerations
- Review, NA, NA
ROS↑, ChemoSideEff↓,
599- VitC,    Generation of Hydrogen Peroxide in Cancer Cells: Advancing Therapeutic Approaches for Cancer Treatment
- Review, NA, NA
H2O2↑, DNAdam↑, ROS↑, Fenton↑, Apoptosis↑, necrosis↑,
598- VitC,    Ascorbic Acid in Cancer Treatment: Let the Phoenix Fly
- Review, NA, NA
H2O2↑, ROS↑, TET1↑, DNAdam↑, G6PD∅,
597- VitC,  dietSTF,  GlucDep,    The Result of Vitamin C Treatment of Patients with Cancer: Conditions Influencing the Effectiveness
other↝, H2O2↑, ROS↑,
596- VitC,    High-Dose Vitamin C in Advanced-Stage Cancer Patients
- Review, NA, NA
ChemoSideEff↓, ROS↑, H2O2↑, Fenton↑, Hif1a↝, Dose↑, BioAv↓, Dose↝, Half-Life↝, IL1β↓, IL2↓, IL8↓, TNF-α↓,
627- VitC,    High-Dose Vitamin C for Cancer Therapy
- Review, NA, NA
ROS↑, PARP↑, GAPDH↓, DNAdam↑, ATP↓,
635- VitC,  VitK3,    The combination of ascorbate and menadione causes cancer cell death by oxidative stress and replicative stress
- in-vitro, NA, NA
RNR↓, GSH↓, Trx1↓, GPx↓, lipid-P↑, AIF↑, ROS↑,
633- VitC,    Diverse antitumor effects of ascorbic acid on cancer cells and the tumor microenvironment
- Analysis, NA, NA
Fenton↑, ROS↑, EMT↓, DNAdam↑, PARP↑, NAD↓, ATP↓, Apoptosis↑,
632- VitC,    High-Dose Vitamin C: Preclinical Evidence for Tailoring Treatment in Cancer Patients
- Review, NA, NA
SVCT-2∅, ROS↑, Hif1a↓, PARP∅, TET2↑,
631- VitC,    Vitamin C preferentially kills cancer stem cells in hepatocellular carcinoma via SVCT-2
- vitro+vivo, Liver, NA
SVCT-2∅, ROS↑, DNAdam↑, ATP↓, TumCCA↑, Apoptosis↑, OS↑, CD133↓, EpCAM↓, OV6↓, γH2AX↑,
629- VitC,  Cu,  Fe,    The antioxidant ascorbic acid mobilizes nuclear copper leading to a prooxidant breakage of cellular DNA: implications for chemotherapeutic action against cancer
- in-vitro, NA, NA
ROS↑, DNAdam↑, NAD↓,

Showing Research Papers: 2301 to 2350 of 2408
Prev Page 47 of 49 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2408

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Fenton↑, 4,   Ferroptosis↑, 1,   GPx↓, 1,   GPx↑, 1,   GPx4↓, 1,   GSH↓, 2,   GSH∅, 1,   H2O2↑, 7,   Iron↝, 1,   lipid-P↑, 2,   MDA↓, 1,   MDA↑, 1,   ROS↓, 2,   ROS↑, 25,   ROS⇅, 1,   ROS∅, 2,   i-ROS↑, 1,   SOD↑, 1,   Trx1↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↑, 2,   ATP↓, 5,   mitResp↓, 1,   MMP↓, 7,   mtDam↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   AMPK↑, 2,   cMyc↓, 1,   cMyc↑, 1,   G6PD∅, 1,   GAPDH↓, 1,   GlucoseCon↓, 1,   glut↓, 1,   GlutMet↑, 1,   Glycolysis↓, 3,   HK2↓, 2,   lactateProd↓, 3,   NAD↓, 2,   p‑PDH↓, 1,   PDKs↓, 1,   PKM2↓, 1,   RNR↓, 1,   SIRT1↑, 1,   TCA↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 7,   APAF1↑, 1,   Apoptosis↑, 15,   BAX↑, 7,   Bcl-2↓, 7,   Casp↑, 3,   Casp3↑, 6,   cl‑Casp3↑, 1,   Casp8↑, 3,   Casp9↑, 4,   Chk2↓, 1,   Cyt‑c↑, 3,   DR5↑, 1,   Ferroptosis↑, 1,   iNOS↓, 1,   MAPK↓, 1,   necrosis↑, 1,   p38↑, 1,   survivin↓, 2,   TumCD↑, 2,  

Kinase & Signal Transduction(tgid=6) ⓘ

Sp1/3/4↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 2,   OV6↓, 1,   tumCV↓, 4,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

LC3II↑, 1,   p62↓, 1,   TumAuto↑, 3,   TumAuto↝, 1,  

DNA Damage & Repair(tgid=10) ⓘ

BRCA1↓, 1,   CHK1↓, 1,   DNAdam↑, 11,   P53↑, 6,   PARP↑, 4,   PARP∅, 1,   cl‑PARP↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   E2Fs↑, 1,   P21↑, 4,   TumCCA↑, 11,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CD133↓, 1,   CSCs↓, 1,   CTNNB1↓, 1,   EMT↓, 2,   EpCAM↓, 1,   ERK↓, 5,   FOXO1↑, 1,   mTOR↓, 1,   p‑mTOR↓, 1,   PI3K↓, 3,   RAS↓, 1,   Src↓, 1,   STAT3↓, 2,   p‑STAT3↓, 2,   TumCG↓, 4,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 2,   E-cadherin↑, 2,   Ki-67↓, 1,   MMP2↓, 3,   MMP9↓, 3,   N-cadherin↓, 2,   PKA↓, 1,   PKCδ↓, 1,   Snail↓, 1,   TET1↑, 1,   TumCI↓, 1,   TumCMig↓, 5,   TumCP↓, 7,   TumMeta↓, 2,   Twist↓, 1,   Vim↓, 2,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 2,   angioG↑, 1,   Hif1a↓, 2,   Hif1a↝, 1,   NO↑, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

SVCT-2∅, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 4,   IL17↓, 1,   IL1β↓, 2,   IL2↓, 1,   IL6↓, 2,   IL8↓, 1,   Imm↑, 1,   Inflam↓, 1,   NF-kB↓, 4,   TNF-α↓, 2,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2,   BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 3,   Dose?, 1,   Dose↑, 2,   Dose↝, 1,   Dose∅, 1,   eff↓, 3,   eff↑, 2,   Half-Life↝, 1,   RadioS↑, 1,   selectivity↑, 5,   TET2↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AR↓, 2,   AST↓, 1,   BRCA1↓, 1,   GutMicro↑, 2,   IL6↓, 2,   Ki-67↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,   AntiCan↓, 1,   AntiCan↑, 3,   AntiTum↑, 1,   chemoP↑, 2,   ChemoSideEff↓, 2,   hepatoP↑, 1,   OS↑, 1,   radioP↑, 1,   RenoP↑, 1,   toxicity↓, 1,   toxicity↑, 1,  
Total Targets: 172

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

4-HNE↓, 1,   antiOx↓, 2,   antiOx↑, 5,   Catalase↑, 6,   Ferroptosis↓, 1,   GPx↑, 6,   GSH↑, 4,   GSR↑, 3,   GSTs↑, 1,   H2O2↓, 2,   HDL↑, 1,   HO-1↑, 1,   lipid-P↓, 7,   MDA↓, 1,   NADH↓, 1,   NQO1↑, 1,   Nrf1↑, 1,   NRF2↑, 4,   PARK2↑, 3,   RNS↓, 1,   ROS?, 1,   ROS↓, 23,   SIRT3↑, 2,   SOD↑, 8,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 5,   mt-ATP↑, 1,   mitResp↑, 1,   MMP↑, 2,   PGC-1α↑, 3,   PINK1↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

Acetyl-CoA↑, 1,   AMPK↑, 2,   CREB↑, 1,   GlucoseCon↑, 2,   homoC↓, 1,   LDL↓, 2,   NAD↑, 1,   NADPH↑, 2,   SIRT1↑, 4,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↓, 1,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-2↑, 1,   Casp3↑, 1,   Ferroptosis↓, 1,   MAPK↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 1,   other↓, 1,   other↑, 4,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   MitoP↑, 4,   p62↓, 1,   p62↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

GSK‐3β↓, 1,   mTOR↓, 2,   mTOR↑, 1,   PI3K↓, 1,   tyrosinase↓, 1,  

Migration(tgid=13) ⓘ

AntiAg↑, 1,   APP↓, 2,   Cartilage↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↓, 1,   BBB↑, 4,   GastroP↑, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 1,   COX2↓, 3,   CRP↓, 1,   IL1β↓, 3,   IL2↓, 1,   IL5↓, 1,   IL6↓, 4,   Imm↑, 1,   Inflam↓, 15,   NF-kB↓, 2,   TNF-α↓, 6,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   AChE↑, 1,   BChE↓, 1,   BDNF↑, 3,   ChAT↑, 1,   MAOA↓, 1,   monoA↓, 1,   tau↓, 1,   p‑tau↓, 6,  

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1,   Aβ↓, 12,   BACE↓, 3,   NLRP3↓, 3,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 3,   BioAv↑, 8,   BioAv↝, 5,   Dose↝, 1,   eff↑, 3,   Half-Life↓, 2,   Half-Life↝, 2,  

Clinical Biomarkers(tgid=22) ⓘ

BP↓, 1,   CRP↓, 1,   GutMicro↑, 2,   IL6↓, 4,   NOS2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiDiabetic↑, 2,   cardioP↑, 5,   cognitive↑, 9,   hepatoP↑, 2,   memory↑, 8,   Mood↑, 1,   motorD↑, 2,   neuroP↑, 13,   Obesity↓, 1,   OS↑, 1,   radioP↑, 2,   Risk↓, 4,   Strength↑, 2,   toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 120

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
122 Silver-NanoParticles
99 Curcumin
94 Quercetin
88 Magnetic Fields
74 Thymoquinone
56 Resveratrol
55 Shikonin
54 Vitamin C (Ascorbic Acid)
50 Berberine
50 Sulforaphane (mainly Broccoli)
49 Radiotherapy/Radiation
47 Lycopene
45 EGCG (Epigallocatechin Gallate)
43 Baicalein
42 Alpha-Lipoic-Acid
40 Selenite (Sodium)
40 Ashwagandha(Withaferin A)
40 Piperlongumine
39 Selenium NanoParticles
38 Artemisinin
37 Betulinic acid
36 Hydrogen Gas
34 Rosmarinic acid
33 Capsaicin
32 Silymarin (Milk Thistle) silibinin
29 Propolis -bee glue
29 Fisetin
28 Copper and Cu NanoParticles
28 Apigenin (mainly Parsley)
27 Chemotherapy
27 Honokiol
26 Allicin (mainly Garlic)
26 Emodin
25 doxorubicin
25 Phenethyl isothiocyanate
24 Luteolin
24 Magnetic Field Rotating
23 Chrysin
22 Cisplatin
22 Vitamin K2
21 Chlorogenic acid
21 Gambogic Acid
20 Coenzyme Q10
20 chitosan
20 Juglone
18 Boron
17 salinomycin
17 Parthenolide
16 Urolithin
15 Ellagic acid
15 Eugenol
14 Photodynamic Therapy
14 Auranofin
14 Boswellia (frankincense)
14 Carnosic acid
14 Carvacrol
14 Selenium
14 Crocetin
14 Phenylbutyrate
13 Dichloroacetate
13 Dandelion Root
13 Pterostilbene
12 Melatonin
12 Caffeic acid
12 VitK3,menadione
11 5-fluorouracil
11 Astaxanthin
11 Cinnamon
11 Graviola
11 Piperine
10 Beta-Caryophyllene
10 α-Bisabolol / Chamomile oil
10 Ursolic acid
10 diet FMD Fasting Mimicking Diet
10 Ferulic acid
10 Plumbagin
10 Nimbolide
9 SonoDynamic Therapy UltraSound
9 Andrographis
9 D-limonene
9 Bacopa monnieri
9 borneol
9 Centella asiatica / Gotu kola → asiaticoside
9 Diclofenac
8 Hydroxycinnamic-acid
8 Disulfiram
8 Electrical Pulses
8 Sulfasalazine
8 Hyperthermia
8 Methylene blue
8 Moringa oleifera
8 Propyl gallate
7 3-bromopyruvate
7 EMF
7 Gold NanoParticles
7 Gemcitabine (Gemzar)
7 Metformin
7 immunotherapy
7 Berbamine
7 brusatol
7 Carnosine
7 Celastrol
7 diet Methionine-Restricted Diet
7 eicosapentaenoic acid
7 HydroxyTyrosol
6 2-DeoxyGlucose
6 Anethole/trans-Anethole
6 Docetaxel
6 Biochanin A
6 Butyrate
6 Chlorophyllin
6 Citric Acid
6 Carvone
6 Aflavin-3,3′-digallate
6 Fenbendazole
5 1,8-Cineole
5 Brucea javanica
5 Bromelain
5 erastin
5 Thymol-Thymus vulgaris
5 Chocolate
5 Cichoric acid / Chicoric acid
5 Spermidine
5 Huperzine A/Huperzia serrata
5 Date Fruit Extract
5 Docosahexaenoic Acid
5 Evodiamine
5 Garcinol
5 HydroxyCitric Acid
5 Magnolol
5 nicotinamide adenine dinucleotide
5 Rutin
4 chemodynamic therapy
4 Zinc
4 Vitamin E
4 Cucurbitacin
4 diet Short Term Fasting
4 Geraniol
4 γ-linolenic acid (Borage Oil)
4 Linalool
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 Dihydrocaffeic Acid
3 Oxygen, Hyperbaric
3 Shilajit/Fulvic Acid
3 Ginkgo biloba
3 Orlistat
3 MCToil
3 Methylsulfonylmethane
3 Mushroom Lion’s Mane
3 Oleuropein
3 α-Santalol/Sandalwood oil
3 Shankhpushpi
3 Terpinen-4-ol / Tea Tree Oil
3 Turmerones
3 Vitamin B1/Thiamine
2 5-Hydroxytryptophan
2 Astragalus
2 DTS(dibenzyl trisulphide) from Anamu
2 Fennel Oil/Foeniculum vulgare
2 Aromatherapy
2 Ascorbyl Palmitate
2 Atorvastatin
2 Aloe anthraquinones
2 beta-glucans
2 Baicalin
2 xanthohumol
2 Cannabidiol
2 beta-carotene(VitA)
2 Bufalin/Huachansu
2 Bruteridin(bergamot juice)
2 Caffeic Acid Phenethyl Ester (CAPE)
2 Cat’s Claw
2 Carica papaya leaf extract
2 Calorie Restriction Mimetics
2 Galantamine
2 CUSP9
2 Folic Acid, Vit B9
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 epirubicin
1 Lapatinib
1 Ras-selective lethal 3
1 Celecoxib
1 methotrexate
1 Aspirin
1 Rivastigmine
1 methylseleninic acid
1 Cyclopamine
1 Cysteamine
1 Dichloroacetophenone(2,2-)
1 Deguelin
1 diet Fermented Foods
1 diet Ketogenic
1 diet Plant based
1 Lemongrass Extract/Citral
1 Echinacea
1 Cannabichromene
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 No Product/Mechanism Only
1 Oleocanthal
1 sericin
1 Kaempferol
1 benzo(a)pyrene
1 Hyperoside
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 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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