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⟱
1899- MeJa,    Methyl jasmonate induces production of reactive oxygen species and alterations in mitochondrial dynamics that precede photosynthetic dysfunction and subsequent cell death
- in-vitro, NA, NA
ROS↑, MMP↓, eff↓, H2O2?,
1898- MeJa,    Methyl jasmonate and its potential in cancer therapy
- Review, Var, NA
ROS↑, selectivity↑, toxicity↝,
1776- MEL,    Therapeutic strategies of melatonin in cancer patients: a systematic review and meta-analysis
- Review, NA, NA
Remission↑, OS↑, neuroP↑, VEGF↓, KISS1↑, TumCP↓, ChemoSideEff↓, radioP↑, Dose∅, *ROS↓, DNArepair↑, ROS↑,
1782- MEL,    Melatonin in Cancer Treatment: Current Knowledge and Future Opportunities
- Review, Var, NA
AntiCan↑, Apoptosis↑, TumCP↓, TumCG↑, TumMeta↑, ChemoSideEff↓, radioP↑, ChemoSen↑, *ROS↓, *SOD↑, *GSH↑, *GPx↑, *Catalase↑, Dose∅, VEGF↓, eff↑, Hif1a↓, GLUT1↑, GLUT3↑, CAIX↑, P21↑, p27↑, PTEN↑, Warburg↓, PI3K↓, Akt↓, NF-kB↓, cycD1/CCND1↓, CDK4↓, CycB/CCNB1↓, CDK4↓, MAPK↑, IGF-1R↓, STAT3↓, MMP9↓, MMP2↓, MMP13↓, E-cadherin↑, Vim↓, RANKL↓, JNK↑, Bcl-2↓, P53↑, Casp3↑, Casp9↑, BAX↑, DNArepair↑, COX2↓, IL6↓, IL8↓, NO↓, T-Cell↑, NK cell↑, Treg lymp↓, FOXP3↓, CD4+↑, TNF-α↑, Th1 response↑, BioAv↝, RadioS↑, OS↑,
1780- MEL,    Utilizing Melatonin to Alleviate Side Effects of Chemotherapy: A Potentially Good Partner for Treating Cancer with Ageing
- Review, Var, NA
*antiOx↑, *toxicity↓, ChemoSen↑, *eff↑, *mitResp↑, *ATP↑, *ROS↓, *CardioT↓, *GSH↑, *NOS2↓, *lipid-P↓, eff↑, *HO-1↑, *NRF2↑, *NF-kB↑, TumCP↓, eff↑, neuroP↑,
1779- MEL,    Therapeutic Potential of Melatonin Counteracting Chemotherapy-Induced Toxicity in Breast Cancer Patients: A Systematic Review
- Review, BC, NA
QoL↑, OS↑, Dose∅, antiOx↑, ROS↑, SOD↑, Catalase↑, GPx↑, Risk↓, NK cell↑, IL1β↓, IL6↓, TNF-α↓, radioP↑, chemoP↑, TumVol↓, TumMeta↓, angioG↓, ChemoSen↑, eff↑,
1778- MEL,    Melatonin: a well-documented antioxidant with conditional pro-oxidant actions
- Review, Var, NA - Review, AD, NA
*ROS↓, *antiOx↓, ROS↑, selectivity↑, Dose↑, *mitResp↑, *ATP↑, *ROS↓, eff↑, ROS↑, Dose↑, *toxicity∅, ROS↑, eff↓, ROS↝, Dose↑, other↑,
1777- MEL,    Melatonin as an antioxidant: under promises but over delivers
- Review, NA, NA
*ROS↓, *Fenton↓, *antiOx↑, *toxicity∅, *GPx↑, *GSR↑, *GSH↑, *NO↓, *Iron↓, *Copper↓, *IL1β↓, *iNOS↓, *Casp3↓, *BBB↑, *RenoP↑, chemoP↑, *Ca+2↝, eff↑, *PKCδ?, ChemoSen↑, eff↑, Akt↓, DR5↑, selectivity↑, ROS↑, eff↑,
6419- MEL,    The potential influence of melatonin on mitochondrial quality control: a review
- Review, Nor, NA
*mt-ACC⇅, *PKM1↑, *PKM2↑, *Glycolysis↝, *PDKs↑, *FAO↑, *ETC↑, *OXPHOS↑, *ATP↑, Glycolysis↓, OXPHOS↑, *Ca+2↓, *ROS↓, *antiOx↑, *SOD2↑, *GPx↑, *Catalase↑, *MFN1↑, *MFN2↑, *OPA1↑, *YAP/TEAD↑, *Hippo↑, *SIRT1↑, *PGC-1α↑, *DRP1/DNM1L↓,
6418- MEL,  RES,    Melatonin improves mitochondrial function by preventing mitochondrial fission in cadmium-induced rat proximal tubular cell injury via SIRT1-PGC-1α pathway activation
- in-vivo, AD, NA
*neuroP↑, *DRP1/DNM1L↓, *FIS1↓, *ROS↓, *MMP↑, *SIRT1↑, *PGC-1α↑, *eff↑,
995- MEL,    Melatonin Treatment Triggers Metabolic and Intracellular pH Imbalance in Glioblastoma
- vitro+vivo, GBM, NA
LDHA↓, MCT4↓, lactateProd↓, i-pH↓, ROS↑, ATP↓, TumCD↑, TumCCA↑, PDH↓, Glycolysis↓, GlucoseCon↓, TumCG↓,
1063- MEL,    HDAC1 inhibition by melatonin leads to suppression of lung adenocarcinoma cells via induction of oxidative stress and activation of apoptotic pathways
- in-vitro, Lung, A549 - in-vitro, Lung, PC9
AntiCan↑, TumCMig↓, GSH↓, Casp3↑, Apoptosis↑, ROS↑, HDAC1↓, Ac-histone H3↑, PUMA↑, BAX↑, PCNA↓, Bcl-2↓,
1204- MET,    Metformin induces ferroptosis through the Nrf2/HO-1 signaling in lung cancer
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
MDA↑, ROS↑, Iron↑, GSH↓, T-SOD↓, Catalase↓, GPx4↓, xCT↓, NRF2↓, HO-1↓,
5785- MET,    Metformin improves healthspan and lifespan in mice
- in-vivo, Nor, NA
*AntiDiabetic↑, *AntiAge↑, *toxicity⇅, *CRM↑, *Strength↑, *LDL↓, *AMPK↑, *TAC↑, *ROS↓, *Inflam↓, Risk↓, *cardioP↑, *ALAT↓, *NRF2↑, *SOD2↑, *TrxR1↑, *NQO1↑, *NQO2↑,
5795- MET,    Metformin: A Review of Potential Mechanism and Therapeutic Utility Beyond Diabetes
- Review, AD, NA - Review, Park, NA - Review, Diabetic, NA
*AntiDiabetic↑, *AMPK↑, *glyC↓, *ROS↓, *cardioP↑, *neuroP↑, *Half-Life↝, *toxicity↝, *BioAv↑, *glucose↓, *AGEs↓, AntiCan↑, Risk↓, TumCP↓, Apoptosis↑, TumCCA↑, cycD1/CCND1↓, pRB↓, p27↓, mTOR↓, Casp↑, ROS↑, MMP↓, ChemoSen↑, *hepatoP↑, *CRM↑, *Insulin↓,
5800- MET,    Metformin as anticancer agent and adjuvant in cancer combination therapy: Current progress and future prospect
- Review, Var, NA
ChemoSen↑, RadioS↑, Imm↑, *AntiDiabetic↑, *AMPK↑, TumCP↓, hepatoP↑, ATP↓, AMP↑, glucoNG↓, ROS↑, compI↓, DNAdam↑, CSCs↓, NP/CIPN↓, chemoP↑, toxicity↓, Trx↓, eff↑, cycD1/CCND1↓, CDK4↓, CDK6↓, cycE/CCNE↓, CDK2↓,
2251- MF,  Rad,    BEMER Electromagnetic Field Therapy Reduces Cancer Cell Radioresistance by Enhanced ROS Formation and Induced DNA Damage
- in-vitro, Lung, A549 - in-vitro, HNSCC, UTSCC15 - in-vitro, CRC, DLD1 - in-vitro, PC, MIA PaCa-2
RadioS↑, DNAdam↑, ROS↑, ChemoSen∅, Pyruv↓, ADP:ATP↓, ROS↑,
2249- MF,    Pulsed electromagnetic fields modulate energy metabolism during wound healing process: an in vitro model study
- in-vitro, Nor, L929
*TumCMig↑, *tumCV↑, *Glycolysis↑, *ROS↓, *mitResp↓, *other↝, *OXPHOS↓, *pH↑, *antiOx↑, *PFKM↑, *PFKL↑, *PKM2↑, *HK2↑, *GLUT1↑, *GPx1↑, *GPx4↑, *SOD1↑,
2241- MF,    Pulsed electromagnetic therapy in cancer treatment: Progress and outlook
- Review, Var, NA
other↝, p‑ERK↝, P53↝, Cyt‑c↝, OXPHOS↑, Apoptosis↑, ROS↑,
2247- MF,    Effects of Pulsed Electromagnetic Field Treatment on Skeletal Muscle Tissue Recovery in a Rat Model of Collagenase-Induced Tendinopathy: Results from a Proteome Analysis
- in-vivo, Nor, NA
*Glycolysis↓, *LDHB↑, *NAD↑, *ATP↑, *antiOx↑, *ROS↑, *YAP/TEAD↑, *PGC-1α↑, *TCA↑, *FAO↑, *OXPHOS↑,
2245- MF,    Quantum based effects of therapeutic nuclear magnetic resonance persistently reduce glycolysis
- in-vitro, Nor, NIH-3T3
Warburg↓, Hif1a↓, *Hif1a∅, Glycolysis↓, *lactateProd↓, *ADP:ATP↓, Pyruv↓, ADP:ATP↓, *PPP↓, *mt-ROS↑, *ROS↓, RPM↑, *ECAR↓,
2244- MF,    Little strokes fell big oaks: The use of weak magnetic fields and reactive oxygen species to fight cancer
- Review, Var, NA
RPM↑, Glycolysis∅, ROS↑, ChemoSen↑, RadioS↑, selectivity↑,
2236- MF,    Changes in Ca2+ release in human red blood cells under pulsed magnetic field
- in-vitro, Nor, NA
*Ca+2↓, *eff↓, *ROS↓,
2261- MF,    Tumor-specific inhibition with magnetic field
- in-vitro, Nor, GP-293 - in-vitro, Liver, HepG2 - in-vitro, Lung, A549
ROS↑, Ca+2↓, Apoptosis↑, *selectivity↑, TumCG↓, *i-Ca+2↓, i-Ca+2↑,
2260- MF,    Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
- in-vitro, GBM, U87MG - in-vitro, GBM, LN229 - in-vivo, NA, NA
TumCP↓, TumCG↓, OS↑, ROS↑, SOD2↑, eff↓, ECAR↓, OCR↑, selectivity↑, *toxicity∅, TumVol↓, PGC-1α↑, OXPHOS↑, Glycolysis↓, PKM2↓,
2253- MF,    Low-frequency pulsed electromagnetic field promotes functional recovery, reduces inflammation and oxidative stress, and enhances HSP70 expression following spinal cord injury
- in-vivo, Nor, NA
*Inflam↓, *TNF-α↓, *IL1β↓, *NF-kB↓, *iNOS↓, *ROS↓, Catalase↑, *SOD↑, *HSP70/HSPA5↑, *neuroP↑, *motorD↑, *antiOx↑,
4099- MF,    Extremely low frequency electromagnetic field reduces oxidative stress during the rehabilitation of post-acute stroke patients
- Trial, Stroke, NA
*ROS↓,
4105- MF,    Extremely low frequency electromagnetic fields stimulation modulates autoimmunity and immune responses: a possible immuno-modulatory therapeutic effect in neurodegenerative diseases
- Review, AD, NA
*Inflam↓, *neuroP↑, *NO↑, *ROS↓, *NO↓, *MCP1↑, *HSP70/HSPA5↑, *antiOx↑, *NRF2↑, *NF-kB↓,
4147- MF,    PEMFs Restore Mitochondrial and CREB/BDNF Signaling in Oxidatively Stressed PC12 Cells Targeting Neurodegeneration
- in-vitro, AD, PC12
*ROS↓, *Catalase↑, *MMP↑, *Casp3↓, *p‑ERK↓, *cAMP↑, *p‑CREB↑, *BDNF↑, *neuroP↑,
4093- MF,    Low-intensity electromagnetic fields induce human cryptochrome to modulate intracellular reactive oxygen species
- in-vivo, NA, NA
*ROS↑, *eff↑,
4092- MF,    Mechanisms and therapeutic effectiveness of pulsed electromagnetic field therapy in oncology
- Review, Var, NA
Apoptosis↑, selectivity↑, ROS↑, Catalase↓, TumVol↓, angioG↓,
4116- MF,    Low‑frequency pulsed electromagnetic field promotes functional recovery, reduces inflammation and oxidative stress, and enhances HSP70 expression following spinal cord injury
- in-vivo, NA, NA
*Inflam↓, *TNF-α↓, *IL1β↓, *iNOS↓, *ROS↓, *Catalase↑, *SOD↑, HSP70/HSPA5↑,
4110- MF,    Pulsed Electromagnetic Fields: A Novel Attractive Therapeutic Opportunity for Neuroprotection After Acute Cerebral Ischemia
- Review, Stroke, NA
*ROS↓, *Inflam↓, *other↝, *neuroP↑, *Apoptosis↓, *Hif1a↝,
4112- MF,    Novel protective effects of pulsed electromagnetic field ischemia/reperfusion injury rats
- in-vivo, Stroke, NA
*cardioP↑, *Bcl-2↑, *BAX↓, *ROS↓,
4104- MF,    Effects of exposure to extremely low-frequency electromagnetic fields on spatial and passive avoidance learning and memory, anxiety-like behavior and oxidative stress in male rats
- in-vivo, NA, NA
*memory↑, *ROS↑,
4118- MF,    Effects of transcranial magnetic stimulation on neurobiological changes in Alzheimer's disease
- Review, AD, NA
*cognitive↑, *BDNF↑, *neuroP↑, *memory↑, *ROS↓, *antiOx↑, *Aβ↓, *eff↑,
4103- MF,    Comparing the Effects of Long-term Exposure to Extremely Low-frequency Electromagnetic Fields With Different Values on Learning, Memory, Anxiety, and β-amyloid Deposition in Adult Rats
- in-vivo, NA, NA
*Dose↝, *memory↑, *ROS↑, *MDA↑,
3728- MF,    Long-term exposure to ELF-MF ameliorates cognitive deficits and attenuates tau hyperphosphorylation in 3xTg AD mice
- in-vivo, AD, NA
*cognitive↑, *neuroP↑, *Apoptosis↓, *ROS↓, *p‑tau↓, *GSK‐3β↓, *CDK5↓,
3457- MF,    Cellular stress response to extremely low‐frequency electromagnetic fields (ELF‐EMF): An explanation for controversial effects of ELF‐EMF on apoptosis
- Review, Var, NA
Apoptosis↑, H2O2↑, ROS↑, eff↑, eff↑, Ca+2↑, MAPK↑, *Catalase↑, *SOD1↑, *GPx1↑, *GPx4↑, *NRF2↑, TumAuto↑, ER Stress↑, HSPs↑, SIRT3↑, ChemoSen↑, UPR↑, other↑, PI3K↓, JNK↑, p38↑, eff↓, *toxicity?,
3480- MF,    Cellular and Molecular Effects of Magnetic Fields
- Review, NA, NA
ROS↑, *Ca+2↑, *Inflam↓, *Akt↓, *mTOR↓, selectivity↑, *memory↑, *MMPs↑, *VEGF↑, *FGF↑, *PDGF↑, *TNF-α↑, *HGF/c-Met↑, *IL1↑,
3477- MF,    Electromagnetic fields regulate calcium-mediated cell fate of stem cells: osteogenesis, chondrogenesis and apoptosis
- Review, NA, NA
*Ca+2↑, *VEGF↑, *angioG↑, Ca+2↑, ROS↑, Necroptosis↑, TumCCA↑, Apoptosis↑, *ATP↑, *FAK↑, *Wnt↑, *β-catenin/ZEB1↑, *ROS↑, p38↑, MAPK↑, β-catenin/ZEB1↓, CSCs↓, TumCP↓, ROS↑, RadioS↑, Ca+2↑, eff↓, NO↑,
3500- MF,    Moderate Static Magnet Fields Suppress Ovarian Cancer Metastasis via ROS-Mediated Oxidative Stress
- in-vitro, Ovarian, SKOV3
ROS↑, CSCs↓, CD44↓, SOX2↓, cMyc↓, TumMeta↓, TumCI↓, TumCMig↓, CD133↓, Nanog↓,
3470- MF,    Pulsed electromagnetic fields inhibit IL-37 to alleviate CD8+ T cell dysfunction and suppress cervical cancer progression
- in-vitro, Cerv, HeLa
TNF-α↑, IL6↑, ROS↑, Apoptosis↑, TumCP↓, TumCMig↓, TumCI↓,
3469- MF,    Pulsed Electromagnetic Fields (PEMF)—Physiological Response and Its Potential in Trauma Treatment
- Review, NA, NA
*eff↑, *eff↝, *other↑, Ca+2↑, ROS↑, HSP70/HSPA5↑, *NOTCH↑, *HEY1↑, *p38↑, *MAPK↑,
3468- MF,    An integrative review of pulsed electromagnetic field therapy (PEMF) and wound healing
- Review, NA, NA
*other↑, *necrosis↓, *IL6↑, *TGF-β↑, *iNOS↑, *MMP2↑, *MCP1↑, *HO-1↑, *Inflam↓, *IL1β↓, *IL6↓, *TNF-α↓, *BioAv↑, eff⇅, DNAdam↑, Apoptosis↑, ROS↑, TumCP↓, *ROS↓, *FGF↑,
3466- MF,    The effect of magnetic fields on tumor occurrence and progression: Recent advances
- Review, Var, NA
angioG↓, ROS↝, EGFR↝, TumCG↓,
3465- MF,    Magnetic fields and angiogenesis
- Review, Var, NA
angioG↓, *angioG↑, selectivity↑, Ca+2↝, ROS↝,
3464- MF,    Progressive Study on the Non-thermal Effects of Magnetic Field Therapy in Oncology
- Review, Var, NA
AntiTum↑, TumCG↓, TumCCA↑, Apoptosis↑, TumAuto↑, Diff↑, angioG↓, TumMeta↓, EPR↑, ChemoSen↑, ROS↑, DNAdam↑, P53↑, Akt↓, MAPK↑, Casp9↑, VEGFR2↓, P-gp↓,
3462- MF,    The Effect of a Static Magnetic Field on microRNA in Relation to the Regulation of the Nrf2 Signaling Pathway in a Fibroblast Cell Line That Had Been Treated with Fluoride Ions
- in-vitro, Nor, NA
*NRF2↑, *Keap1↓, *SOD↑, *GPx↑, *ROS↓, *MDA↓, *SOD1↑, *SOD2↑, *GSR↑,
3485- MF,    Cytoprotective effects of low-frequency pulsed electromagnetic field against oxidative stress in glioblastoma cells
- in-vitro, GBM, U87MG
*antiOx↑, *ROS↓, *cytoP↑,

Showing Research Papers: 1451 to 1500 of 2398
Prev Page 30 of 48 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2398

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↓, 2,   Catalase↑, 2,   compI↓, 1,   GPx↑, 1,   GPx4↓, 1,   GSH↓, 2,   H2O2?, 1,   H2O2↑, 1,   HO-1↓, 1,   Iron↑, 1,   MDA↑, 1,   NRF2↓, 1,   OXPHOS↑, 3,   ROS↑, 29,   ROS↝, 3,   RPM↑, 2,   SIRT3↑, 1,   SOD↑, 1,   SOD2↑, 1,   T-SOD↓, 1,   Trx↓, 1,   xCT↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ADP:ATP↓, 2,   ATP↓, 2,   MMP↓, 2,   OCR↑, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

Ac-histone H3↑, 1,   AMP↑, 1,   CAIX↑, 1,   cMyc↓, 1,   ECAR↓, 1,   glucoNG↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 4,   Glycolysis∅, 1,   lactateProd↓, 1,   LDHA↓, 1,   MCT4↓, 1,   PDH↓, 1,   PKM2↓, 1,   Pyruv↓, 2,   Warburg↓, 2,  

Cell Death(tgid=5) ⓘ

Akt↓, 3,   Apoptosis↑, 11,   BAX↑, 2,   Bcl-2↓, 2,   Casp↑, 1,   Casp3↑, 2,   Casp9↑, 2,   Cyt‑c↝, 1,   DR5↑, 1,   JNK↑, 2,   MAPK↑, 4,   Necroptosis↑, 1,   p27↓, 1,   p27↑, 1,   p38↑, 2,   PUMA↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

KISS1↑, 1,   other↑, 2,   other↝, 1,   pRB↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,   HSP70/HSPA5↑, 2,   HSPs↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 2,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 4,   DNArepair↑, 2,   P53↑, 2,   P53↝, 1,   PCNA↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   CDK4↓, 3,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 3,   cycE/CCNE↓, 1,   P21↑, 1,   TumCCA↑, 4,  

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

CD133↓, 1,   CD44↓, 1,   CSCs↓, 3,   Diff↑, 1,   p‑ERK↝, 1,   HDAC1↓, 1,   IGF-1R↓, 1,   mTOR↓, 1,   Nanog↓, 1,   PI3K↓, 2,   PTEN↑, 1,   SOX2↓, 1,   STAT3↓, 1,   TumCG↓, 5,   TumCG↑, 1,  

Migration(tgid=13) ⓘ

Ca+2↓, 1,   Ca+2↑, 4,   Ca+2↝, 1,   i-Ca+2↑, 1,   E-cadherin↑, 1,   MMP13↓, 1,   MMP2↓, 1,   MMP9↓, 1,   Treg lymp↓, 1,   TumCI↓, 2,   TumCMig↓, 3,   TumCP↓, 9,   TumMeta↓, 3,   TumMeta↑, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 5,   EGFR↝, 1,   EPR↑, 1,   Hif1a↓, 2,   NO↓, 1,   NO↑, 1,   VEGF↓, 2,   VEGFR2↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↑, 1,   GLUT3↑, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   COX2↓, 1,   FOXP3↓, 1,   IL1β↓, 1,   IL6↓, 2,   IL6↑, 1,   IL8↓, 1,   Imm↑, 1,   NF-kB↓, 1,   NK cell↑, 2,   T-Cell↑, 1,   Th1 response↑, 1,   TNF-α↓, 1,   TNF-α↑, 2,  

Cellular Microenvironment(tgid=17) ⓘ

i-pH↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 1,   RANKL↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,   ChemoSen↑, 9,   ChemoSen∅, 1,   Dose↑, 3,   Dose∅, 3,   eff↓, 5,   eff↑, 11,   eff⇅, 1,   RadioS↑, 5,   selectivity↑, 8,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↝, 1,   IL6↓, 2,   IL6↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 3,   AntiTum↑, 1,   chemoP↑, 3,   ChemoSideEff↓, 2,   hepatoP↑, 1,   neuroP↑, 2,   NP/CIPN↓, 1,   OS↑, 4,   QoL↑, 1,   radioP↑, 3,   Remission↑, 1,   Risk↓, 3,   toxicity↓, 1,   toxicity↝, 1,   TumVol↓, 3,  
Total Targets: 169

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1,   antiOx↑, 9,   Catalase↑, 5,   Copper↓, 1,   Fenton↓, 1,   GPx↑, 4,   GPx1↑, 2,   GPx4↑, 2,   GSH↑, 3,   GSR↑, 2,   HO-1↑, 2,   Iron↓, 1,   Keap1↓, 1,   lipid-P↓, 1,   MDA↓, 1,   MDA↑, 1,   MFN1↑, 1,   MFN2↑, 1,   NQO1↑, 1,   NRF2↑, 5,   OPA1↑, 1,   OXPHOS↓, 1,   OXPHOS↑, 2,   ROS↓, 25,   ROS↑, 5,   mt-ROS↑, 1,   SOD↑, 4,   SOD1↑, 3,   SOD2↑, 3,   TAC↑, 1,   TrxR1↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ADP:ATP↓, 1,   ATP↑, 5,   DRP1/DNM1L↓, 2,   ETC↑, 1,   FIS1↓, 1,   Insulin↓, 1,   mitResp↓, 1,   mitResp↑, 2,   MMP↑, 2,   PGC-1α↑, 3,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

mt-ACC⇅, 1,   ALAT↓, 1,   AMPK↑, 3,   cAMP↑, 1,   p‑CREB↑, 1,   CRM↑, 2,   ECAR↓, 1,   FAO↑, 2,   glucose↓, 1,   glyC↓, 1,   Glycolysis↓, 1,   Glycolysis↑, 1,   Glycolysis↝, 1,   HK2↑, 1,   lactateProd↓, 1,   LDHB↑, 1,   LDL↓, 1,   NAD↑, 1,   PDKs↑, 1,   PFKL↑, 1,   PFKM↑, 1,   PKM1↑, 1,   PKM2↑, 2,   PPP↓, 1,   SIRT1↑, 2,   TCA↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↓, 2,   BAX↓, 1,   Bcl-2↑, 1,   Casp3↓, 2,   HEY1↑, 1,   HGF/c-Met↑, 1,   Hippo↑, 1,   iNOS↓, 3,   iNOS↑, 1,   MAPK↑, 1,   necrosis↓, 1,   p38↑, 1,   YAP/TEAD↑, 2,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 2,   other↝, 2,   tumCV↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

HSP70/HSPA5↑, 2,   NQO2↑, 1,  

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

p‑ERK↓, 1,   FGF↑, 2,   GSK‐3β↓, 1,   mTOR↓, 1,   NOTCH↑, 1,   Wnt↑, 1,  

Migration(tgid=13) ⓘ

Ca+2↓, 2,   Ca+2↑, 2,   Ca+2↝, 1,   i-Ca+2↓, 1,   CDK5↓, 1,   FAK↑, 1,   MMP2↑, 1,   MMPs↑, 1,   PDGF↑, 1,   PKCδ?, 1,   TGF-β↑, 1,   TumCMig↑, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

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

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   GLUT1↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1↑, 1,   IL1β↓, 4,   IL6↓, 1,   IL6↑, 1,   Inflam↓, 7,   MCP1↑, 2,   NF-kB↓, 2,   NF-kB↑, 1,   TNF-α↓, 3,   TNF-α↑, 1,  

Cellular Microenvironment(tgid=17) ⓘ

pH↑, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

BDNF↑, 2,   p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1,   Aβ↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   IL6↓, 1,   IL6↑, 1,   NOS2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,   AntiDiabetic↑, 3,   cardioP↑, 3,   CardioT↓, 1,   cognitive↑, 2,   cytoP↑, 1,   hepatoP↑, 1,   memory↑, 4,   motorD↑, 1,   neuroP↑, 8,   RenoP↑, 1,   Strength↑, 1,   toxicity?, 1,   toxicity↓, 1,   toxicity⇅, 1,   toxicity↝, 1,   toxicity∅, 3,  
Total Targets: 156

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)
25 doxorubicin
25 Emodin
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 Gemcitabine (Gemzar)
7 EMF
7 Gold NanoParticles
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
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 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 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 entinostat
1 Camptothecin
1 Resiquimod
1 Anzaroot, Astragalus fasciculifolius Bioss
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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