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⟱
4457- SeNPs,    Selenium nanoparticles: a review on synthesis and biomedical applications
- Review, Var, NA - NA, Diabetic, NA
*BioAv↑, *toxicity↓, *eff↑, chemoPv↑, *Inflam↓, antiOx↑, *selenoP↑, *ROS↓, *Dose↝, AntiCan↑, *Bacteria↓, eff↑, DNAdam↑, selectivity↑, *eff↑,
4189- Sesame,    Sesame oil mitigates memory impairment, oxidative stress, and neurodegeneration in a rat model of Alzheimer's disease. A pivotal role of NF-κB/p38MAPK/BDNF/PPAR-γ pathways
- in-vivo, AD, NA
*TNF-α↓, *IL1β↓, *ROS↓, *BDNF↑, *neuroP↑, *cognitive↑,
4190- Sesame,    Sesame Seeds: A Nutrient-Rich Superfood
- Review, NA, NA
*antiOx↑, *LDL↓, *Aβ↓, *TNF-α↓, *SOD↑, *SIRT1↑, *Catalase↑, *GSH↑, *MDA↓, *GSTs↑, *IL4↑, *GPx↑, *COX2↓, *PGE2↓, *NO↓, CDK2↑, COX2↑, MMP9↑, ICAM-1↓, *BDNF↑, *PPARγ↑, *AChE↓, *Inflam↓, *HO-1↑, *NF-kB↓, *ROS↓,
3194- SFN,    Sulforaphane impedes mitochondrial reprogramming and histone acetylation in polarizing M1 (LPS) macrophages
- in-vitro, Nor, NA
*OXPHOS↑, *M1↓, *IL1β↓, *IL6↓, *NOS2↓, *TNF-α↓, *ROS↓, *NO↓, *ACC↑,
3184- SFN,    The Integrative Role of Sulforaphane in Preventing Inflammation, Oxidative Stress and Fatigue: A Review of a Potential Protective Phytochemical
- Review, Nor, NA
*NRF2↑, *Inflam↓, *NF-kB↓, *ROS↓, *BioAv↝, *BioAv↝, *BioAv↝, *BioAv↝, *cardioP↑, *GPx↑, *SOD↑, *Catalase↑, *GPx↑, *HO-1↑, *NADPH↑, *NQO1↑, *LDH↓, *hepatoP↑, *ALAT↓, *AST↓, *IL6↓,
3183- SFN,    Sulforaphane potentiates the efficacy of chemoradiotherapy in glioblastoma by selectively targeting thioredoxin reductase 1
- in-vitro, GBM, NA
RadioS↑, TrxR1↓, ROS↑, ChemoSen↑, Prx↓,
3182- SFN,    Sulforaphane Modulates AQP8-Linked Redox Signalling in Leukemia Cells
- in-vitro, AML, NA
Prx↓, AQPs↓, NOX↓, tumCV↓, AntiCan↑, cardioP↑, neuroP↑, Inflam↓, chemoPv↑, angioG↓, TumMeta↓, selectivity↑, ROS↓,
3663- SFN,    Efficacy of Sulforaphane in Neurodegenerative Diseases
- Review, AD, NA - Review, Park, NA
*antiOx↑, *Inflam↓, *Half-Life↝, *NRF2↑, *NQO1↑, *HO-1↑, *TrxR↑, *ROS↓, *TNF-α↓, *IL1β↓, *IL6↓, *iNOS↓, *COX2↓, *Aβ↓, *GSH↑, *cognitive↑, *BACE↓, *HSP70/HSPA5↑, *neuroP↑, *ROS↓, *BBB↑, *MMP9↓,
3660- SFN,    Sulforaphane - role in aging and neurodegeneration
- Review, AD, NA
*antiOx↑, *Inflam↓, *NRF2↑, *NF-kB↓, *HDAC↓, *DNMTs↓, *neuroP↑, *AntiAge↑, *DNMT1↓, *DNMT3A↓, *memory↑, *HO-1↑, *ROS↓, *NO↓, *GSH↑, *NF-kB↓, *TNF-α↓, *IL10↑,
3659- SFN,    Epigenetic modification of Nrf2 by sulforaphane increases the antioxidative and anti-inflammatory capacity in a cellular model of Alzheimer's disease
- in-vitro, AD, NA
*NRF2↑, *ROS↓, *MDA↓, *SOD↑, *IL1β↓, *IL6↓, *NF-kB↓, *COX2↓, *iNOS↓, *Inflam↓,
3658- SFN,    Pre-Clinical Neuroprotective Evidences and Plausible Mechanisms of Sulforaphane in Alzheimer’s Disease
- Review, AD, NA
*NRF2↑, *antiOx↑, *neuroP↑, *Aβ↓, *BACE↓, *NQO1↑, *IL1β↓, *TNF-α↓, *IL6↓, *COX2↓, *iNOS↓, *NF-kB↓, *NLRP3↓, *Ca+2↓, *GSH↑, *MDA↓, *ROS↓, *SOD↑, *HO-1↑, *TrxR↑, *cognitive↑, *tau↓, *HSP70/HSPA5↑,
2555- SFN,    Chemopreventive functions of sulforaphane: A potent inducer of antioxidant enzymes and apoptosis
- Review, Var, NA
chemoPv↑, HDAC↓, TumCCA↑, Apoptosis↑, Mets↑, *NRF2↑, ROS⇅,
2552- SFN,  Chemo,    Chemopreventive activity of sulforaphane
- Review, Var, NA
chemoPv↑, TumCG↓, *ROS↓, *Inflam↓, *Dose↝, *NRF2↑, *HO-1↑, *NQO1↑, NF-kB↓, ROS↑,
2553- SFN,    Mechanistic review of sulforaphane as a chemoprotective agent in bladder cancer
- Review, Bladder, NA
antiOx↓, Inflam↓, ChemoSen↑, ROS⇅, *NRF2↑, *GSH↑, Catalase↑, HO-1↑, NAD↑, chemoP↑,
2444- SFN,    Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage
- in-vitro, Nor, MRC-5
*GlucoseCon↓, *ROS↓, *Trx↓, *HK2↓, *NRF2↑, *Catalase↑, *TXNIP↑, *PFKFB2↓, *G6PD↑,
2448- SFN,    Sulforaphane and bladder cancer: a potential novel antitumor compound
- Review, Bladder, NA
Apoptosis↑, TumCG↓, TumCI↓, TumMeta↓, glucoNG↓, ChemoSen↑, TumCCA↑, Casp3↑, Casp7↑, cl‑PARP↑, survivin↓, EGFR↓, HER2/EBBR2↓, ATP↓, Glycolysis↓, mt-OXPHOS↓, AKT1↓, HK2↓, Hif1a↓, ROS↑, NRF2↑, EMT↓, COX2↓, MMP2↓, MMP9↓, Zeb1↓, Snail↓, HDAC↓, HATs↓, MMP↓, Cyt‑c↓, Shh↓, Smo↓, Gli1↓, BioAv↝, BioAv↝, Dose↝,
1730- SFN,    Sulforaphane: An emergent anti-cancer stem cell agent
- Review, Var, NA
BioAv↓, BioAv↑, GSTA1↑, P450↓, TumCCA↑, HDAC↓, P21↑, p27↑, DNMT1↓, DNMT3A↓, cycD1/CCND1↑, DNAdam↑, BAX↑, Cyt‑c↑, Apoptosis↑, ROS↑, AIF↑, CDK1↑, Casp3↑, Casp8↑, Casp9↑, NRF2↑, NF-kB↓, TNF-α↓, IL1β↓, CSCs↓, CD133↓, CD44↓, ALDH↓, Nanog↓, OCT4↓, hTERT/TERT↓, MMP2↓, EMT↓, ALDH1A1↓, Wnt↓, NOTCH↓, ChemoSen↑, *Ki-67↓, *HDAC3↓, *HDAC↓,
1723- SFN,    Sulforaphane as a potential remedy against cancer: Comprehensive mechanistic review
- Review, Var, NA
*NRF2↑, ROS↑, MMP↓, Cyt‑c↑, cl‑PARP↑, Apoptosis↑, AMPK↑, GSH↓,
1722- SFN,    Sulforaphane as an anticancer molecule: mechanisms of action, synergistic effects, enhancement of drug safety, and delivery systems
- Review, Var, NA
TumCCA↑, CYP1A1↓, CYP3A4↓, Cyt‑c↑, Casp9↑, Apoptosis↑, ROS↑, MAPK↑, P53↑, BAX↑, ChemoSen↑, HDAC↓, GSH↓, HO-1↑,
1459- SFN,  AF,    Auranofin Enhances Sulforaphane-Mediated Apoptosis in Hepatocellular Carcinoma Hep3B Cells through Inactivation of the PI3K/Akt Signaling Pathway
- in-vitro, Liver, Hep3B - in-vitro, Liver, HepG2
eff↑, TumCCA↑, Apoptosis↑, MMP↓, BAX↑, cl‑PARP↑, Casp3↑, Casp8↑, Casp9↑, ROS↑, eff↓, PI3K↓, Akt↓, TrxR↓, BAX↑, Bcl-2∅,
1471- SFN,    ROS-mediated activation of AMPK plays a critical role in sulforaphane-induced apoptosis and mitotic arrest in AGS human gastric cancer cells
- in-vitro, GC, AGS
TumCP↓, Apoptosis↑, TumCCA↑, CycB/CCNB1↑, P21↑, p‑H3↑, p‑AMPK↑, eff↓, MMP↓, Cyt‑c↑, ROS↑, eff↓,
1470- SFN,  Rad,    Sulforaphane induces ROS mediated induction of NKG2D ligands in human cancer cell lines and enhances susceptibility to NK cell mediated lysis
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vitro, Lung, A549 - in-vitro, lymphoma, U937
eff↓, ROS↑, NKG2D↑,
1469- SFN,    Sulforaphane enhances the therapeutic potential of TRAIL in prostate cancer orthotopic model through regulation of apoptosis, metastasis, and angiogenesis
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vivo, Pca, NA
eff↑, ROS↑, MMP↓, Casp3↑, Casp9↑, DR4↑, DR5↑, BAX↑, Bak↑, BIM↑, NOXA↑, Bcl-2↓, Bcl-xL↓, Mcl-1↓, eff↓, TumCG↓, TumCP↓, eff↑, NF-kB↓, PI3K↓, Akt↓, MEK↓, ERK↓, angioG↓, FOXO3↑,
1468- SFN,    Cellular responses to dietary cancer chemopreventive agent D,L-sulforaphane in human prostate cancer cells are initiated by mitochondrial reactive oxygen species
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
ROS↑, DNAdam↑, MMP↓, Cyt‑c↑, TumCCA↑,
1467- SFN,    Sulforaphane generates reactive oxygen species leading to mitochondrial perturbation for apoptosis in human leukemia U937 cells
- in-vitro, AML, U937
Apoptosis↑, ROS↑, MMP↓, Casp3↑, Bcl-2↓, eff↓,
1466- SFN,    Sulforaphane inhibits thyroid cancer cell growth and invasiveness through the reactive oxygen species-dependent pathway
- vitro+vivo, Thyroid, FTC-133
TumCP↓, TumCCA↑, Apoptosis↑, TumCMig↓, TumCI↓, EMT↓, Slug↓, Twist↓, MMP2↓, MMP9↓, TumCG↓, p‑Akt↓, P21↑, ERK↑, p38↑, ROS↑, *toxicity∅, MMP↓, eff↓,
1465- SFN,    TRAIL attenuates sulforaphane-mediated Nrf2 and sustains ROS generation, leading to apoptosis of TRAIL-resistant human bladder cancer cells
- NA, Bladder, NA
eff↑, Apoptosis↑, Casp↑, MMP↓, BID↑, DR5↑, ROS↑, NRF2↑, eff↑, eff↓,
1464- SFN,    d,l-Sulforaphane Induces ROS-Dependent Apoptosis in Human Gliomablastoma Cells by Inactivating STAT3 Signaling Pathway
- in-vitro, GBM, NA
Apoptosis↑, Casp3↑, BAX↑, Bcl-2↓, ROS↑, p‑STAT3↓, JAK2↓, eff↓,
1463- SFN,    Sulforaphane induces reactive oxygen species-mediated mitotic arrest and subsequent apoptosis in human bladder cancer 5637 cells
- in-vitro, Bladder, 5637
tumCV↓, CycB/CCNB1↑, p‑CDK1↑, Apoptosis↑, Casp8↑, Casp9↑, Casp3↑, cl‑PARP↑, ROS↑, eff↓,
1460- SFN,    High levels of EGFR prevent sulforaphane-induced reactive oxygen species-mediated apoptosis in non-small-cell lung cancer cells
- in-vitro, Lung, NA
ROS↑, EGFR↓, eff↓, TumCCA↑, γH2AX↑, DNAdam↑, eff↓,
1472- SFN,    Sulforaphane Inhibits Autophagy and Induces Exosome-Mediated Paracrine Senescence via Regulating mTOR/TFE3
- in-vitro, ESCC, NA
TumCP↓, ROS↑, DNAdam↑,
1458- SFN,    Sulforaphane Impact on Reactive Oxygen Species (ROS) in Bladder Carcinoma
- Review, Bladder, NA
HDAC↓, eff↓, TumW↓, TumW↓, angioG↓, *toxicity↓, GutMicro↝, AntiCan↑, ROS↑, MMP↓, Cyt‑c↑, Bax:Bcl2↑, Casp3↑, Casp9↑, Casp8∅, cl‑PARP↑, TRAIL↑, DR5↑, eff↓, NRF2↑, ER Stress↑, COX2↓, EGFR↓, HER2/EBBR2↓, ChemoSen↑, NF-kB↓, TumCCA?, p‑Akt↓, p‑mTOR↓, p70S6↓, p19↑, P21↑, CD44↓, CSCs↓,
1457- SFN,    Sulforaphane Inhibits IL-1β-Induced IL-6 by Suppressing ROS Production, AP-1, and STAT3 in Colorectal Cancer HT-29 Cells
- in-vitro, CRC, HT-29
IL6↓, ROS↓, TumCP↓, TumCI↓, p38↓, AP-1↓,
1456- SFN,    Sulforaphane regulates cell proliferation and induces apoptotic cell death mediated by ROS-cell cycle arrest in pancreatic cancer cells
- in-vitro, PC, MIA PaCa-2 - in-vitro, PC, PANC1
tumCV↓, TumCP↓, cl‑PARP↑, cl‑Casp3↑, TumCCA↑, ROS↑, MMP↓, γH2AX↑, eff↓, *toxicity↓,
1455- SFN,    Sulforaphane Activates a lysosome-dependent transcriptional program to mitigate oxidative stress
- in-vitro, Cerv, HeLa - in-vitro, Nor, 1321N1
*ROS↓, *BioAv↑, LC3II↑, LAMP1?, TumAuto↑, TFEB↑, ROS↑, eff↓,
1452- SFN,    Sulforaphane Suppresses the Nicotine-Induced Expression of the Matrix Metalloproteinase-9 via Inhibiting ROS-Mediated AP-1 and NF-κB Signaling in Human Gastric Cancer Cells
- in-vitro, GC, AGS
MMP9↓, p38↓, ERK↓, AP-1↓, ROS↓, NF-kB↓, TumCI↓, MMP9↓, HDAC↓, Glycolysis↓, Hif1a↓, *memory↑, *cognitive↑,
1434- SFN,  GEM,    Sulforaphane Potentiates Gemcitabine-Mediated Anti-Cancer Effects against Intrahepatic Cholangiocarcinoma by Inhibiting HDAC Activity
- in-vitro, CCA, HuCCT1 - in-vitro, CCA, HuH28 - in-vivo, NA, NA
HDAC↓, ac‑H3↑, ChemoSen↑, tumCV↓, TumCP↓, TumCCA↑, Apoptosis↑, cl‑Casp3↑, TumCI↓, VEGF↓, VEGFR2↓, Hif1a↓, eNOS↓, EMT?, TumCG↓, Ki-67↓, TUNEL↑, P21↑, p‑Chk2↑, CDC25↓, BAX↑, *ROS↓, NQO1?,
1474- SFN,    Sulforaphane induces p53‑deficient SW480 cell apoptosis via the ROS‑MAPK signaling pathway
- in-vitro, Colon, SW480
TumCG↓, Apoptosis↑, MMP↓, Bax:Bcl2↑, Casp3↑, Casp7↑, Casp9↑, ROS↑, e-ERK↑, p38↑, P53∅, eff↓, ChemoSen↑,
1508- SFN,    Nrf2 targeting by sulforaphane: A potential therapy for cancer treatment
- Review, Var, NA
*BioAv↑, HDAC↓, TumCCA↓, eff↓, Wnt↓, β-catenin/ZEB1↓, Casp12?, Bcl-2↓, cl‑PARP↑, Bax:Bcl2↑, IAP1↓, Casp3↑, Casp9↑, Telomerase↓, hTERT/TERT↓, ROS?, DNMTs↓, angioG↓, VEGF↓, Hif1a↓, cMYB↓, MMP1↓, MMP2↓, MMP9↓, ERK↑, E-cadherin↑, CD44↓, MMP2↓, eff↑, IL2↑, IFN-γ↑, IL1β↓, IL6↓, TNF-α↓, NF-kB↓, ERK↓, NRF2↑, RadioS↑, ChemoSideEff↓,
1495- SFN,  doxoR,    Sulforaphane protection against the development of doxorubicin-induced chronic heart failure is associated with Nrf2 Upregulation
- in-vivo, Nor, NA
*CardioT↓, *NRF2↑, *eff↓, *ROS↓,
1494- SFN,  doxoR,    Sulforaphane potentiates anticancer effects of doxorubicin and attenuates its cardiotoxicity in a breast cancer model
- in-vivo, BC, NA - in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
CardioT↓, *GSH↑, *ROS↓, *NRF2↑, NRF2∅, HDAC↓, DNMTs↓, Casp3↑, ER-α36↓, Remission↑, eff↑, ROS↑, selectivity?,
1484- SFN,    Sulforaphane’s Multifaceted Potential: From Neuroprotection to Anticancer Action
- Review, Var, NA - Review, AD, NA
neuroP↑, AntiCan↑, NRF2↑, HDAC↓, eff↑, *ROS↓, neuroP↑, HDAC↓, *toxicity∅, BioAv↑, eff↓, cycD1/CCND1↓, CDK4↓, p‑RB1↓, Glycolysis↓, miR-30a-5p↑, TumCCA↑, TumCG↓, TumMeta↓, eff↑, ChemoSen↑, RadioS↑, CardioT↓, angioG↓, Hif1a↓, VEGF↓, *BioAv?, *Half-Life∅,
1483- SFN,    Targeting p62 by sulforaphane promotes autolysosomal degradation of SLC7A11, inducing ferroptosis for osteosarcoma treatment
- in-vitro, OS, 143B - in-vitro, Nor, HEK293 - in-vivo, OS, NA
AntiCan↑, *toxicity∅, Ferroptosis↑, ROS↑, lipid-P↑, GSH↓, p62↑, SLC12A5↓, eff↓, GPx4↓, i-Iron↑, eff↓, MDA↑, TumVol↓, TumW↓, Ki-67↓, LC3B↑, *Weight∅,
1482- SFN,    Sulforaphane induces apoptosis in T24 human urinary bladder cancer cells through a reactive oxygen species-mediated mitochondrial pathway: the involvement of endoplasmic reticulum stress and the Nrf2 signaling pathway
- in-vitro, Bladder, T24/HTB-9
tumCV↓, Apoptosis↑, Cyt‑c↑, Bax:Bcl2↑, Casp9↑, Casp3↑, Casp8∅, cl‑PARP↑, ROS↑, MMP↓, eff↓, ER Stress↑, p‑NRF2↑, HO-1↑,
1481- SFN,  docx,    Combination of Low-Dose Sulforaphane and Docetaxel on Mitochondrial Function and Metabolic Reprogramming in Prostate Cancer Cell Lines
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
ChemoSen↑, Casp3↑, ROS↑, Casp8↑, Cyt‑c↑, Glycolysis↓, GSH↓, GSH/GSSG↓, *toxicity↓,
1480- SFN,    Sulforaphane Induces Cell Death Through G2/M Phase Arrest and Triggers Apoptosis in HCT 116 Human Colon Cancer Cells
- in-vitro, CRC, HCT116
tumCV↓, TumCCA↑, Apoptosis↑, cycA1/CCNA1↑, CycB/CCNB1↑, CDC25↓, CDK1↓, ROS↑, eff↓, Cyt‑c↑, AIF↑, ER Stress↑,
1479- SFN,    Sulforaphane triggers Sirtuin 3-mediated ferroptosis in colorectal cancer cells via activating the adenosine 5'-monophosphate (AMP)-activated protein kinase/ mechanistic target of rapamycin signaling pathway
- in-vitro, CRC, HCT116
Ferroptosis↑, SIRT3↑, AMPK↑, mTOR↑, tumCV↓, ROS↑, MDA↑, Iron↑,
1478- SFN,  acet,    Anti-inflammatory and anti-oxidant effects of combination between sulforaphane and acetaminophen in LPS-stimulated RAW 264.7 macrophage cells
- in-vitro, Nor, NA
eff↑, NO↓, iNOS↓, COX2↓, IL1β↓, ROS↓,
1477- SFN,    Sulforaphane Induces Oxidative Stress and Death by p53-Independent Mechanism: Implication of Impaired Glutathione Recycling
- in-vitro, OS, MG63
tumCV↓, Apoptosis↑, Casp3↑, ROS↑, GSR↓, GPx↓,
1476- SFN,  PDT,    Enhancement of cytotoxic effect on human head and neck cancer cells by combination of photodynamic therapy and sulforaphane
- in-vitro, HNSCC, NA
eff↑, tumCV↓, ROS↑, eff↓, Casp↑,

Showing Research Papers: 1801 to 1850 of 2174
Prev Page 37 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 ⓘ

antiOx↓, 1,   antiOx↑, 1,   Catalase↑, 1,   CYP1A1↓, 1,   Ferroptosis↑, 2,   GPx↓, 1,   GPx4↓, 1,   GSH↓, 4,   GSH/GSSG↓, 1,   GSR↓, 1,   GSTA1↑, 1,   HO-1↑, 3,   Iron↑, 1,   i-Iron↑, 1,   lipid-P↑, 1,   MDA↑, 2,   Mets↑, 1,   NQO1?, 1,   NRF2↑, 6,   NRF2∅, 1,   p‑NRF2↑, 1,   mt-OXPHOS↓, 1,   Prx↓, 2,   ROS?, 1,   ROS↓, 4,   ROS↑, 30,   ROS⇅, 2,   SIRT3↑, 1,   TrxR↓, 1,   TrxR1↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 2,   ATP↓, 1,   CDC25↓, 2,   MEK↓, 1,   MMP↓, 13,  

Core Metabolism/Glycolysis ⓘ

AKT1↓, 1,   AMPK↑, 2,   p‑AMPK↑, 1,   CYP3A4↓, 1,   glucoNG↓, 1,   Glycolysis↓, 4,   HK2↓, 1,   NAD↑, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 2,   Apoptosis↑, 17,   Bak↑, 1,   BAX↑, 7,   Bax:Bcl2↑, 4,   Bcl-2↓, 4,   Bcl-2∅, 1,   Bcl-xL↓, 1,   BID↑, 1,   BIM↑, 1,   Casp↑, 2,   Casp12?, 1,   Casp3↑, 14,   cl‑Casp3↑, 2,   Casp7↑, 2,   Casp8↑, 4,   Casp8∅, 2,   Casp9↑, 9,   p‑Chk2↑, 1,   Cyt‑c↓, 1,   Cyt‑c↑, 9,   DR4↑, 1,   DR5↑, 3,   Ferroptosis↑, 2,   hTERT/TERT↓, 2,   IAP1↓, 1,   iNOS↓, 1,   MAPK↑, 1,   Mcl-1↓, 1,   NOXA↑, 1,   p27↑, 1,   p38↓, 2,   p38↑, 2,   survivin↓, 1,   Telomerase↓, 1,   TRAIL↑, 1,   TUNEL↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 2,   p70S6↓, 1,  

Transcription & Epigenetics ⓘ

p‑H3↑, 1,   ac‑H3↑, 1,   HATs↓, 1,   miR-30a-5p↑, 1,   tumCV↓, 9,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 3,  

Autophagy & Lysosomes ⓘ

LC3B↑, 1,   LC3II↑, 1,   p62↑, 1,   TFEB↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 5,   DNMT1↓, 1,   DNMT3A↓, 1,   DNMTs↓, 2,   P53↑, 1,   P53∅, 1,   cl‑PARP↑, 8,   γH2AX↑, 2,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK1↑, 1,   p‑CDK1↑, 1,   CDK2↑, 1,   CDK4↓, 1,   cycA1/CCNA1↑, 1,   CycB/CCNB1↑, 3,   cycD1/CCND1↓, 1,   cycD1/CCND1↑, 1,   p19↑, 1,   P21↑, 5,   p‑RB1↓, 1,   TumCCA?, 1,   TumCCA↓, 1,   TumCCA↑, 13,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   ALDH1A1↓, 1,   CD133↓, 1,   CD44↓, 3,   cMYB↓, 1,   CSCs↓, 2,   EMT?, 1,   EMT↓, 3,   ERK↓, 3,   ERK↑, 2,   e-ERK↑, 1,   FOXO3↑, 1,   Gli1↓, 1,   HDAC↓, 11,   mTOR↑, 1,   p‑mTOR↓, 1,   Nanog↓, 1,   NOTCH↓, 1,   OCT4↓, 1,   PI3K↓, 2,   Shh↓, 1,   Smo↓, 1,   p‑STAT3↓, 1,   TumCG↓, 7,   Wnt↓, 2,  

Migration ⓘ

AP-1↓, 2,   E-cadherin↑, 1,   ER-α36↓, 1,   Ki-67↓, 2,   LAMP1?, 1,   MMP1↓, 1,   MMP2↓, 5,   MMP9↓, 5,   MMP9↑, 1,   Slug↓, 1,   Snail↓, 1,   TumCI↓, 5,   TumCMig↓, 1,   TumCP↓, 7,   TumMeta↓, 3,   Twist↓, 1,   Zeb1↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 5,   EGFR↓, 3,   eNOS↓, 1,   Hif1a↓, 5,   NO↓, 1,   VEGF↓, 3,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

AQPs↓, 1,   SLC12A5↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 3,   COX2↑, 1,   ICAM-1↓, 1,   IFN-γ↑, 1,   IL1β↓, 3,   IL2↑, 1,   IL6↓, 2,   Inflam↓, 2,   JAK2↓, 1,   NF-kB↓, 6,   TNF-α↓, 2,  

Cellular Microenvironment ⓘ

NOX↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   BioAv↝, 2,   ChemoSen↑, 10,   Dose↝, 1,   eff↓, 24,   eff↑, 12,   P450↓, 1,   RadioS↑, 3,   selectivity?, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

EGFR↓, 3,   GutMicro↝, 1,   HER2/EBBR2↓, 2,   hTERT/TERT↓, 2,   IL6↓, 2,   Ki-67↓, 2,  

Functional Outcomes ⓘ

AntiCan↑, 5,   cardioP↑, 1,   CardioT↓, 2,   chemoP↑, 1,   chemoPv↑, 4,   ChemoSideEff↓, 1,   neuroP↑, 3,   NKG2D↑, 1,   Remission↑, 1,   TumVol↓, 1,   TumW↓, 3,  
Total Targets: 209

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 4,   Catalase↑, 3,   GPx↑, 3,   GSH↑, 6,   GSTs↑, 1,   HO-1↑, 6,   MDA↓, 3,   NQO1↑, 4,   NRF2↑, 12,   OXPHOS↑, 1,   ROS↓, 17,   selenoP↑, 1,   SOD↑, 4,   Trx↓, 1,   TrxR↑, 2,  

Core Metabolism/Glycolysis ⓘ

ACC↑, 1,   ALAT↓, 1,   G6PD↑, 1,   GlucoseCon↓, 1,   HK2↓, 1,   LDH↓, 1,   LDL↓, 1,   NADPH↑, 1,   PFKFB2↓, 1,   PPARγ↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

iNOS↓, 3,  

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 2,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,   DNMT3A↓, 1,   DNMTs↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 2,   HDAC3↓, 1,  

Migration ⓘ

Ca+2↓, 1,   Ki-67↓, 1,   MMP9↓, 1,   TXNIP↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 3,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 4,   IL10↑, 1,   IL1β↓, 5,   IL4↑, 1,   IL6↓, 5,   Inflam↓, 7,   M1↓, 1,   NF-kB↓, 6,   PGE2↓, 1,   TNF-α↓, 6,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   BDNF↑, 2,   tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 3,   BACE↓, 2,   NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv?, 1,   BioAv↑, 3,   BioAv↝, 4,   Dose↝, 2,   eff↓, 1,   eff↑, 2,   Half-Life↝, 1,   Half-Life∅, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   IL6↓, 5,   Ki-67↓, 1,   LDH↓, 1,   NOS2↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   cardioP↑, 1,   CardioT↓, 1,   cognitive↑, 4,   hepatoP↑, 1,   memory↑, 2,   neuroP↑, 4,   toxicity↓, 4,   toxicity∅, 3,   Weight∅, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 80

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 immunotherapy
7 Berbamine
7 brusatol
7 Carnosine
7 Celastrol
7 diet Methionine-Restricted Diet
7 Disulfiram
7 HydroxyTyrosol
6 2-DeoxyGlucose
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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