Magnetic Fields / ROS Cancer Research Results

MF, Magnetic Fields: Click to Expand ⟱
Features: Therapy

Magnetic Fields — externally applied static or time-varying magnetic fields used to alter cellular signaling, redox state, ion handling, membrane behavior, metabolism, or neural activity without introducing a chemical agent. They are a physical therapeutic modality and include static magnetic fields (SMF), extremely-low-frequency magnetic fields (ELF-MF), pulsed electromagnetic fields (PEMF), and other non-rotating oscillating/time-varying magnetic fields. Common abbreviations include MF, SMF, ELF-MF, EMF, and PEMF. Biological effects are strongly dependent on field strength, frequency, waveform, gradient, duty cycle, exposure duration, and tissue or cell type. Rotating magnetic fields are excluded here because they are represented separately as pid 192; magnetic-nanoparticle-dependent magnetothermal or magnetomechanical effects are also better assigned primarily to the magnetic nanoparticle product.

Primary mechanisms (ranked):

  1. Redox modulation and ROS perturbation, including radical-pair and mitochondrial mechanisms; cancer cells may develop sustained oxidative stress whereas normal cells frequently show adaptive antioxidant responses.
  2. Ca²⁺ and ion-channel modulation, particularly TRPC, voltage-gated channels, intracellular Ca²⁺ handling, and ER–mitochondrial Ca²⁺ communication.
  3. Mitochondrial and bioenergetic modulation, including membrane potential, electron transport, ATP production, mitochondrial permeability, and metabolic reprogramming.
  4. Cell proliferation, cell-cycle, apoptosis, and senescence signaling through pathways including EGFR/PI3K/AKT/mTOR, MAPK/ERK, caspases, PARP, Bax and survivin.
  5. Membrane permeability and drug-uptake modulation, producing context-dependent chemosensitization to agents including doxorubicin, etoposide and methotrexate.
  6. Inflammatory and stress-response modulation including NF-κB, cytokine signaling, HSPs, ER stress and adaptive antioxidant pathways.
  7. Migration, invasion, angiogenesis and tumor-microenvironment modulation; effects are field-parameter and tumor-model dependent.

Bioavailability / PK relevance: Conventional pharmacokinetic concepts do not apply because the intervention is a physical field rather than an absorbed drug. Relevant exposure variables are magnetic flux density, field gradient, frequency, waveform, pulse width, repetition rate, duty cycle, spatial distribution, treatment duration and tissue depth. Magnetic fields can penetrate tissue without the concentration gradients characteristic of drugs, but induced electric fields and biological coupling vary markedly with geometry and frequency.

In-vitro vs systemic exposure relevance: Effects are not concentration-driven. Many experimental results cannot be generalized between devices because apparently small differences in waveform, frequency, flux density, orientation, gradient and exposure duration can change the biological response. Static fields ranging from millitesla to tesla and PEMF/ELF protocols ranging from weak fields to substantially stronger stimulation should therefore be treated as distinct exposure regimens rather than as a single dose-response continuum.

Clinical evidence status: Cancer treatment remains predominantly preclinical, with cell-culture and animal evidence plus limited supportive or adjunctive human use. Evidence supports parameter-dependent anticancer effects and chemosensitization, but non-rotating magnetic-field exposure alone is not an established standard anticancer therapy. PEMF has established clinical use in several musculoskeletal applications and has been studied as supportive therapy in oncology. Repetitive transcranial magnetic stimulation has substantially stronger human evidence in neurological and psychiatric applications, including investigational use in Alzheimer’s disease, but should not be interpreted as evidence that generic magnetic-field exposure is an established systemic cancer treatment.

Magnetic Fields can be Static, or pulsed. The most common therapy is a pulsed magnetic field in the uT or mT range.
The main pathways affected are:
Calcium Signaling: -influence the activity of voltage-gated calcium channels.
Oxidative Stress and Reactive Oxygen Species (ROS) Pathways
Heat Shock Proteins (HSPs) and Cellular Stress Responses
Cell Proliferation and Growth Signaling: MAPK/ERK pathway.
Gene Expression and Epigenetic Modifications: NF-κB
Angiogenesis Pathways: VEGF (improving VEGF for normal cells)
PEMF was found to have a 2-fold increase in drug uptake compared to traditional electrochemotherapy in rat melanoma models

Pathways:
- most reports have ROS production increasing in cancer cells , while decreasing in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Raises AntiOxidant defense in Normal Cells: ROS↓">ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, VEGF↓(mostly regulated up in normal cells),
- cause Cell cycle arrest : TumCCA↑,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, GLUT1↓, LDH↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- Others: PI3K↓, AKT↓, STAT↓, Wnt↓, β-catenin↓, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, cytoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Magnetic Field Mechanisms in Cancer

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 ROS and redox homeostasis ↑ ROS (context-dependent); ↑ oxidative stress ↑ transient ROS followed by ↔ or ↓ ROS in adaptive protocols P, R, G Redox perturbation One of the most recurrent MF mechanisms. Direction is strongly field- and cell-dependent; sustained ROS elevation is reported in several cancer models and during chemotherapy sensitization.
2 Ca²⁺ and ion-channel signaling ↑ Ca²⁺ signaling or dysregulation; altered TRPC and voltage-sensitive channel activity ↑ transient signaling with homeostatic recovery (context-dependent) P, R Electrophysiological signal transduction Ca²⁺ is a major mechanistic bridge between membrane sensing, mitochondria, ROS, proliferation and apoptosis. Response depends strongly on waveform and frequency.
3 Mitochondrial function and membrane potential ↓ ΔΨm; altered respiration; ↑ mitochondrial stress ↔ or reversible modulation (context-dependent) P, R, G Bioenergetic destabilization Mitochondrial effects can arise downstream of ROS and Ca²⁺ signaling and contribute to apoptotic commitment.
4 Apoptosis and caspase signaling ↑ apoptosis; ↑ caspases; ↑ PARP cleavage; ↑ Bax; ↓ survivin ↔ or substantially weaker response in selective protocols R, G Programmed cell death Reported with several PEMF and time-varying field protocols and can be amplified when combined with chemotherapy.
5 EGFR PI3K AKT mTOR signaling ↓ EGFR/AKT/mTOR signaling (model-dependent) ↔ or mixed R, G Growth-signal suppression Particularly supported in static-field experiments; response varies with cell type, cell density and field intensity.
6 Cell cycle and proliferation ↓ proliferation; ↑ cell-cycle arrest or mitotic disruption ↔ or mixed G Growth suppression Effects are highly protocol-specific. Some exposures are neutral or can stimulate proliferation, so suppression should not be treated as universal.
7 DNA damage and DNA-damage response ↑ DNA damage; ↑ ATM/p53/p21 signaling (context-dependent) ↔ or mixed; protective responses reported with some protocols R, G Genotoxic stress and repair modulation Often secondary to ROS and particularly evident during combination treatment with chemotherapy or radiation. Magnetic fields alone are not consistently genotoxic, and some static-field protocols can reduce radiation-associated DNA damage.
8 Chemosensitization and drug uptake ↑ chemotherapy response; ↑ drug uptake or cytotoxicity ↔ or ↑ toxicity (drug-dependent) R, G Adjunctive anticancer effect Documented with doxorubicin, etoposide and other agents. Selectivity is not guaranteed; normal-cell toxicity must be evaluated for each field-drug combination.
9 Glutathione and antioxidant buffering ↓ GSH reserve or altered GSH/GSSG balance (context-dependent) ↑ GSH or antioxidant adaptation in some protocols R, G Redox buffering modulation GSH depletion is best interpreted as a consequence of oxidative load rather than a universal direct MF target.
10 NRF2 antioxidant response ↔ / mixed; inadequate adaptive response in some oxidative protocols ↑ NRF2 and antioxidant-response signaling in some protective protocols R, G Adaptive antioxidant defense NRF2 direction is not uniform enough to classify MF globally as either an NRF2 activator or inhibitor.
11 ER stress and unfolded protein response ↑ ER stress and UPR (model-dependent) ↑ adaptive stress response or ↔ R, G Proteostasis stress Can develop secondary to ROS, altered Ca²⁺ handling and mitochondrial dysfunction.
12 Mitochondrial permeability transition ↑ MPTP opening propensity ↔ or reversible opening R Mitochondrial death commitment Supported mechanistically for specific ELF-MF exposures through ROS-sensitive pathways; should not be generalized to all magnetic fields.
13 Glycolysis and cellular energetics ↓ glycolytic flux or altered ATP production (model-dependent) ↔ or metabolic adaptation R, G Metabolic reprogramming Some frequency-tuned exposures suppress glycolysis, but this is substantially less universal than ROS or Ca²⁺ modulation.
14 HIF-1α and angiogenic signaling ↓ HIF-1α / VEGF in selected models ↑ VEGF or tissue-repair signaling in some regenerative protocols G Angiogenesis modulation Potential cancer-versus-normal-tissue divergence is attractive but remains highly exposure- and model-specific.
15 NF-κB and inflammatory signaling ↓ NF-κB and inflammatory signaling in selected models ↓ inflammatory cytokines in many regenerative PEMF applications R, G Inflammation modulation Better established as an anti-inflammatory/regenerative PEMF effect than as a universal cancer-cell mechanism.
16 Migration invasion and angiogenesis ↓ migration; ↓ invasion; ↓ angiogenic signaling in selected models ↔ or pro-repair angiogenesis (context-dependent) G Metastatic phenotype modulation Direction varies substantially with field protocol and normal-versus-tumor context.
17 Radiosensitization ↑ radiation-induced ROS and DNA damage in selected protocols Mixed; radioprotection has also been reported with other protocols R, G Modification of radiation response Both radiosensitizing and radioprotective responses have been reported; field parameters and tissue context determine direction.
18 Clinical Translation Constraint Field-specific response; substantial tumor heterogeneity Potential tissue-specific physiological effects G Translation limitation No pharmacokinetic dose metric exists. Field strength, frequency, waveform, geometry, gradients, duration and induced electric fields must be specified. Most anticancer evidence remains preclinical and protocols are poorly standardized.

P: 0–30 min     R: 30 min–3 hr     G: >3 hr

MPTP: opening represents a mitochondrial commitment event integrating ROS and Ca²⁺ stress; sustained opening indicates irreversible bioenergetic failure.




Alzheimer’s disease relevance: Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive magnetic neuromodulation modality with randomized human evidence for modest improvement in global cognition in mild cognitive impairment and Alzheimer’s disease. The strongest recent evidence supports excitatory stimulation of cortical cognitive-network regions, particularly the dorsolateral prefrontal cortex. The mechanism is principally neural-network and synaptic modulation rather than the systemic ROS-based mechanism often discussed for low-intensity PEMF. Meta-analyses generally report cognitive benefit, but protocol heterogeneity, small trials and uncertain durability remain important limitations. rTMS should therefore be classified as investigational or adjunctive for AD rather than an established disease-modifying treatment.

Clinical evidence status: Multiple RCTs and meta-analyses support a modest short-term cognitive signal. Longer-term benefit remains less certain, optimal frequency/intensity/site protocols are not standardized, and evidence does not establish prevention or reversal of Alzheimer pathology.

Magnetic Stimulation in Alzheimer’s Disease

Rank Pathway / Axis Modulation TSF Primary Effect Notes / Interpretation
1 Cortical network excitability ↑ P, R Neuromodulation High-frequency rTMS and excitatory stimulation of cortical network hubs can increase cortical responsiveness.
2 Synaptic plasticity ↑ R, G Plasticity enhancement Repeated stimulation can produce LTP-like network effects and is a leading explanation for persistence beyond the stimulation session.
3 Cognitive-network connectivity ↑ G Network normalization DLPFC and related cortical networks are the most consistently studied targets.
4 Global cognition ↑ G Clinical cognitive improvement Recent meta-analyses show modest improvement in MMSE, MoCA or ADAS-Cog outcomes, although heterogeneity remains substantial.
5 Neuroinflammation and neurotrophic signaling ↓ inflammation; ↑ neurotrophic signaling (context-dependent) G Secondary neurobiological effects Supported mainly by mechanistic and preclinical studies; less directly established than cortical-network effects in human AD.
6 Clinical Translation Constraint ↔ G Protocol heterogeneity Optimal stimulation site, frequency, intensity, pulse count, session number and maintenance schedule remain unresolved; long-term disease modification has not been demonstrated.

P: 0–30 min     R: 30 min–3 hr     G: >3 hr
ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






ROS">Copper (ionic / nano)
+++↓[Fe][F]ROS-dominant






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






ROS">Alpha-lipoic acid (ALA)
±↑[D][M]NRF2-dominant






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






ROS">Quercetin
±↑/↓[D][Fe]NRF2-dominant






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
356- AgNPs,  MF,    Anticancer and antibacterial potentials induced post short-term exposure to electromagnetic field and silver nanoparticles and related pathological and genetic alterations: in vitro study
- in-vitro, BC, MCF7 - in-vitro, Bladder, HTB-22
Apoptosis↑, P53↑, iNOS↑, NF-kB↑, Bcl-2↓, ROS↑, SOD↑, TumCCA↑, Synergy↑, Catalase↑, other↑,
400- AgNPs,  MF,    Polyvinyl Alcohol Capped Silver Nanostructures for Fortified Apoptotic Potential Against Human Laryngeal Carcinoma Cells Hep-2 Using Extremely-Low Frequency Electromagnetic Field
- in-vitro, Laryn, HEp2
TumCP↓, Casp3↑, P53↑, Beclin-1/ATG6↑, TumAuto↑, GSR↑, ROS↑, MDA↑, ROS↑, SIRT1↑, Ca+2↑, Endon↑, DNAdam↑, Apoptosis↑, NF-kB↓,
402- AgNPs,  MF,    Anticancer and antibacterial potentials induced post short-term exposure to electromagnetic field and silver nanoparticles and related pathological and genetic alterations: in vitro study
- in-vitro, BC, MCF7
P53↑, iNOS↑, NF-kB↑, Bcl-2↓, miR-125b↓, ROS↑, SOD↑,
2018- CAP,  MF,    Capsaicin: Effects on the Pathogenesis of Hepatocellular Carcinoma
- Review, HCC, NA
TRPV1↑, eff↑, Akt↓, mTOR↓, p‑STAT3↑, MMP2↑, ER Stress↑, Ca+2↑, ROS↑, selectivity↑, MMP↓, Synergy↑,
587- MF,  VitC,    Effect of stationary magnetic field strengths of 150 and 200 mT on reactive oxygen species production in soybean
ROS↑, SOD↓, other↓,
2236- MF,    Changes in Ca2+ release in human red blood cells under pulsed magnetic field
- in-vitro, Nor, NA
*Ca+2↓, *eff↓, *ROS↓,
520- MF,    Exposure to a 50-Hz magnetic field induced mitochondrial permeability transition through the ROS/GSK-3β signaling pathway
- in-vitro, Nor, NA
*MPT↑, *Cyt‑c↑, *ROS↑, *p‑GSK‐3β↑, *eff↓, *MMP∅, *BAX↓, *Bcl-2∅,
521- MF,    Magnetic field effects in biology from the perspective of the radical pair mechanism
- Analysis, NA, NA
*RPM↑, *ROS↝,
525- MF,    Pulsed electromagnetic fields regulate metabolic reprogramming and mitochondrial fission in endothelial cells for angiogenesis
- in-vitro, Nor, HUVECs
*angioG↑, *GPx1↑, *GPx4↑, *SOD↑, *PFKM↑, *PFKL↑, *PKM2↑, *PFKP↑, *HK2↑, *GLUT1↑, *GLUT4↑, *ROS↓, *MMP↝, *Glycolysis↑, *OXPHOS↓,
526- MF,    Inhibition of Cancer Cell Growth by Exposure to a Specific Time-Varying Electromagnetic Field Involves T-Type Calcium Channels
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF7 - in-vitro, Pca, HeLa - vitro+vivo, Melanoma, B16-BL6 - in-vitro, Nor, HEK293
TumCG↓, Ca+2↑, selectivity↑, *Ca+2∅, ROS↑, HSP70/HSPA5↑, AntiCan↑,
527- MF,    Effects of Fifty-Hertz Electromagnetic Fields on Granulocytic Differentiation of ATRA-Treated Acute Promyelocytic Leukemia NB4 Cells
- in-vitro, AML, APL NB4
ROS↑, other↑, p‑ERK↑, TumCP↓,
529- MF,    Low-frequency magnetic field therapy for glioblastoma: Current advances, mechanisms, challenges and future perspectives
- Review, GBM, NA
Ca+2↑, ROS↑, ChemoSen↑, QoL↑, OS↑,
532- MF,    A 50 Hz magnetic field influences the viability of breast cancer cells 96 h after exposure
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF7 - in-vitro, Nor, MCF10
TumCP↓, MMP↓, ROS↑, eff↝, selectivity↑,
533- MF,    Effects of extremely low-frequency magnetic fields on human MDA-MB-231 breast cancer cells: proteomic characterization
- in-vitro, BC, MDA-MB-231 - in-vitro, Nor, MCF10
TumCD↑, necrosis↑, mt-ROS↑, other↑, *STAT3↓, STAT3↑,
537- MF,  immuno,    Integrating electromagnetic cancer stress with immunotherapy: a therapeutic paradigm
- Review, Var, NA
Apoptosis↑, ROS↑, TumAuto↑, Ca+2↑, ATP↓, eff↑, eff↑,
538- MF,    The extremely low frequency electromagnetic stimulation selective for cancer cells elicits growth arrest through a metabolic shift
- in-vitro, BC, MDA-MB-231 - in-vitro, Melanoma, MSTO-211H
TumCG↓, Ca+2↑, COX2/PTGS2↓, ATP↑, MMP↑, ROS↑, OXPHOS↑, mitResp↑,
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↑,
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/KDR/Flk1↓, P-gp/ABCB1↓,
3465- MF,    Magnetic fields and angiogenesis
- Review, Var, NA
angioG↓, *angioG↑, selectivity↑, Ca+2↝, ROS↝,
3466- MF,    The effect of magnetic fields on tumor occurrence and progression: Recent advances
- Review, Var, NA
angioG↓, ROS↝, EGFR↝, TumCG↓,
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/CCL2↑, *HO-1↑, *Inflam↓, *IL1β↓, *IL6↓, *TNF-α↓, *BioAv↑, eff⇅, DNAdam↑, Apoptosis↑, ROS↑, TumCP↓, *ROS↓, *FGF↑,
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↑,
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↓,
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↑,
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↑,
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↑,
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↑,
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↓,
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↑,
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↑,
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↑,
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↓,
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↑,
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↑, RadioS↑, eff↑, Ca+2↑, MAPK↑, *Catalase↑, *SOD1↑, *GPx1↑, *GPx4↑, *NRF2↑, TumAuto↑, ER Stress↑, HSPs↑, SIRT3↑, ChemoSen↑, UPR↑, other↑, PI3K↓, JNK↑, p38↑, eff↓, *toxicity?,
500- MF,    Anti-Oxidative and Immune Regulatory Responses of THP-1 and PBMC to Pulsed EMF Are Field-Strength Dependent
- in-vitro, AML, THP1
ROS↑, Prx6↑, DHCR24↑, IL10↑,
496- MF,    Low-Frequency Magnetic Fields (LF-MFs) Inhibit Proliferation by Triggering Apoptosis and Altering Cell Cycle Distribution in Breast Cancer Cells
- in-vitro, BC, MCF7 - in-vitro, BC, ZR-75-1 - in-vitro, BC, T47D - in-vitro, BC, MDA-MB-231
ROS↑, PI3K↓, Akt↓, GSK‐3β↑, Apoptosis↑, cl‑PARP↑, cl‑Casp3↑, BAX↑, Bcl-2↓, CycB/CCNB1↓, TumCCA↑, p‑Akt↓, TumCP↓, selectivity↑, eff↓,
491- MF,    Pre-exposure of neuroblastoma cell line to pulsed electromagnetic field prevents H2 O2 -induced ROS production by increasing MnSOD activity
- in-vitro, neuroblastoma, SH-SY5Y
*Dose∅, *ROS↓,
490- MF,    Extremely Low Frequency Magnetic Field (ELF-MF) Exposure Sensitizes SH-SY5Y Cells to the Pro-Parkinson's Disease Toxin MPP(.)
- in-vitro, Park, SH-SY5Y
ROS↑,
194- MF,    Electromagnetic Field as a Treatment for Cerebral Ischemic Stroke
- Review, Stroke, NA
*BAD↓, *BAX↓, *Casp3↓, *Bcl-xL↑, *p‑Akt↑, *MMP9↓, *p‑ERK↑, *HIF-1↓, *ROS↓, *VEGF↑, *Ca+2↓, *SOD↑, *IL2↑, *p38↑, *HSP70/HSPA5↑, *Apoptosis↓, *ROS↓, *NO↓,
507- MF,    Effects of extremely low frequency electromagnetic fields on the tumor cell inhibition and the possible mechanism
- in-vitro, Liver, HepG2 - in-vitro, Lung, A549 - in-vitro, Nor, GP-293
MMP↓, TumCG↓, ROS↑, *Ca+2↓, Ca+2↑, selectivity↑, i-pH↑,
509- MF,    Is extremely low frequency pulsed electromagnetic fields applicable to gliomas? A literature review of the underlying mechanisms and application of extremely low frequency pulsed electromagnetic fields
- Review, NA, NA
Ca+2↑, TumAuto↑, Apoptosis↑, angioG↓, ROS↑,
508- MF,  doxoR,    Synergistic cytotoxic effects of an extremely low-frequency electromagnetic field with doxorubicin on MCF-7 cell line
- in-vitro, BC, MCF7
ROS↑, Apoptosis↑, TumCCA↑,
503- MF,    Effects of acute and chronic low frequency electromagnetic field exposure on PC12 cells during neuronal differentiation
- in-vitro, NA, PC12
ROS↑, Ca+2↑,
5241- MF,    A review on the use of magnetic fields and ultrasound for non-invasive cancer treatment
- Review, Var, NA
other↑, BloodF↑, Glycolysis↓, ATP↓, VEGF↓, ROS↑, P-gp/ABCB1↓, Apoptosis↑, selectivity↑, Ca+2↑, Catalase↑,
4571- MF,    Magnetic Fields and Reactive Oxygen Species
- Review, NA, NA
*ROS⇅, *ETC↓, Dose↝, Dose↝,
4568- MF,    Extremely low-frequency pulses of faint magnetic field induce mitophagy to rejuvenate mitochondria
- Study, NA, NA
*ETC↓, *OCR↑, *MMP↑, *ROS⇅, *MMP⇅,
4356- MF,    Pulsed electromagnetic fields synergize with graphene to enhance dental pulp stem cell-derived neurogenesis by selectively targeting TRPC1 channels
- in-vitro, Nor, NA
*Diff↑, *TRPC1↑, *ROS↑,
4355- MF,    Ambient and supplemental magnetic fields promote myogenesis via a TRPC1-mitochondrial axis: evidence of a magnetic mitohormetic mechanism
- in-vitro, Nor, C2C12
*mt-OCR↑, *mt-ROS↑, *ECAR↑, *Dose↝, *Ca+2↑, *ATP↑, *other↑, *eff↓, *eff↝,
4354- MF,  doxoR,    Modulated TRPC1 Expression Predicts Sensitivity of Breast Cancer to Doxorubicin and Magnetic Field Therapy: Segue Towards a Precision Medicine Approach
- in-vivo, BC, MDA-MB-231 - in-vivo, BC, MCF7
selectivity↑, Apoptosis↑, TumCI↓, tumCV↓, TumVol↓, eff↓, ChemoSen↑, ROS↑, Ca+2↑, TumCMig↓,

Showing Research Papers: 1 to 50 of 95
Page 1 of 2 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 95

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

NA↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 1,   Catalase↑, 3,   Fenton↑, 1,   GPx4↓, 1,   GSH↓, 2,   GSH↑, 1,   GSH/GSSG↓, 2,   GSR↑, 1,   H2O2↑, 6,   mt-H2O2↑, 1,   Iron↓, 1,   Iron↑, 2,   i-Iron↓, 1,   lipid-P↑, 2,   MDA↑, 2,   Prx6↑, 1,   ROS↓, 2,   ROS↑, 55,   ROS⇅, 1,   ROS↝, 3,   mt-ROS↑, 2,   RPM↑, 3,   SOD↓, 2,   SOD↑, 2,   SOD2↑, 1,   Thiols↓, 1,   xCT/SLC7A11↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ADP:ATP↓, 2,   compII↓, 1,   ETC↓, 5,   mitResp↓, 1,   mitResp↑, 1,   mtDam↑, 2,   OCR↓, 1,   OCR↑, 1,   OXPHOS↑, 3,   PGC-1α↑, 1,   SDH↓, 2,   SIRT3↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ATP↓, 2,   ATP↑, 1,   DHCR24↑, 1,   ECAR↓, 1,   Glycolysis↓, 3,   Glycolysis∅, 1,   GSK‐3β↑, 1,   lactateProd↑, 1,   PKM2↓, 1,   Pyruv↓, 2,   SIRT1↑, 1,   TCA?, 1,   Warburg↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 25,   Bak↑, 1,   BAX↑, 3,   Bax:Bcl2↑, 1,   Bcl-2↓, 4,   Casp↑, 1,   Casp3↑, 7,   cl‑Casp3↑, 2,   Casp7↑, 2,   Casp8↑, 1,   Casp9↑, 3,   Cyt‑c↑, 2,   Cyt‑c↝, 1,   Endon↑, 1,   Ferroptosis↑, 2,   iNOS↑, 2,   Necroptosis↑, 1,   necrosis↑, 1,   p38↑, 2,   survivin↓, 1,   TumCD↑, 5,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 5,   p‑Akt↓, 2,   BCAP↓, 1,   EGFR↝, 1,   p‑ERK↑, 1,   p‑ERK↝, 1,   JNK↑, 1,   MAPK↑, 3,   mTOR↓, 2,   PI3K↓, 2,   STAT3↑, 1,   p‑STAT3↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

ChrMod↑, 2,   cMyc↓, 2,   miR-125b↓, 1,   miR-486↑, 1,   other↓, 1,   other↑, 6,   other↝, 1,   SOX2↓, 2,   tumCV↓, 5,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 3,   HSP70/HSPA5↑, 3,   HSPs↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1/ATG6↑, 2,   LC3II↑, 1,   lysoMP↑, 1,   p62↑, 1,   TumAuto↑, 6,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 9,   P53↑, 6,   P53↝, 1,   cl‑PARP↑, 2,   Telomerase↓, 2,   TOP2↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CycB/CCNB1↓, 2,   mitA↑, 1,   TumCCA↑, 10,  

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

CD133↓, 2,   CSCs↓, 2,   Diff↑, 1,   Nanog↓, 2,   TumCG↓, 13,   TumCP↓, 15,  

Migration(tgid=13) ⓘ

Ca+2↓, 1,   Ca+2↑, 19,   Ca+2↝, 2,   i-Ca+2↑, 1,   EMT↓, 1,   MMP2↓, 1,   MMP2↑, 1,   MMP9↓, 1,   TumCI↓, 4,   TumCMig↓, 6,   TumMeta↓, 4,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 6,   Hif1a↓, 1,   NO↑, 1,   VEGF↓, 1,   VEGFR2/KDR/Flk1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

CellMemb↑, 1,   EPR↑, 1,   MMP?, 1,   MMP↓, 9,   MMP↑, 1,   MPT↑, 2,   TRPV1↑, 1,   TRPV1↝, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 2,   CD44↓, 2,   CD8+↑, 2,   COX2/PTGS2↓, 1,   CXCL12↓, 1,   CXCL9↓, 1,   DCells↑, 2,   FOXP3↓, 1,   IFN-γ↓, 1,   IL1↑, 1,   IL10↑, 2,   IL6↓, 1,   IL6↑, 1,   Imm↑, 1,   Imm↝, 1,   NF-kB↓, 1,   NF-kB↑, 2,   PD-L1↑, 1,   T-Cell↑, 1,   TNF-α↑, 2,  

Cellular Microenvironment(tgid=17) ⓘ

pH↓, 1,   i-pH↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 12,   ChemoSen∅, 1,   Dose↝, 11,   eff↓, 13,   eff↑, 9,   eff⇅, 1,   eff↝, 5,   MDR1↓, 1,   P-gp/ABCB1↓, 3,   RadioS↑, 6,   selectivity↑, 21,   Synergy↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

BloodF↑, 1,   BMD↑, 1,   EGFR↝, 1,   IL6↓, 1,   IL6↑, 1,   PD-L1↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   AntiTum↑, 1,   Appetite↑, 1,   BowelM↑, 1,   breath↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   OS↑, 7,   OS⇅, 1,   Pain↓, 2,   QoL↑, 3,   radioP↑, 2,   Sleep↑, 1,   Strength↑, 2,   toxicity↓, 1,   TumVol↓, 6,   Weight↑, 1,  
Total Targets: 204

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 7,   Catalase↑, 6,   GPx↑, 2,   GPx1↑, 4,   GPx4↑, 4,   GSR↑, 2,   HO-1↑, 1,   Iron↑, 1,   Keap1↓, 1,   MDA↓, 2,   MDA↑, 1,   NRF2↑, 3,   ROMO1↑, 1,   ROS↓, 29,   ROS↑, 8,   ROS⇅, 2,   ROS↝, 1,   ROS∅, 1,   mt-ROS↑, 2,   RPM↑, 1,   SOD↑, 7,   SOD1↑, 4,   SOD2↑, 4,   TAC↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ADP:ATP↓, 1,   ETC↓, 2,   mitResp↓, 1,   OCR↑, 1,   mt-OCR↑, 1,   OXPHOS↓, 2,   OXPHOS↑, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 2,   ATP↑, 3,   cAMP↑, 1,   ECAR↓, 1,   ECAR↑, 1,   FAO↑, 1,   Glycolysis↓, 1,   Glycolysis↑, 2,   GSK‐3β↓, 1,   p‑GSK‐3β↑, 1,   HK2↑, 2,   lactateProd↓, 1,   LDHB↑, 1,   NAD↑, 1,   PFKL↑, 2,   PFKM↑, 2,   PFKP↑, 1,   PKM2↑, 2,   PPP↓, 1,   TCA↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 3,   BAD↓, 1,   BAX↓, 3,   Bcl-2↑, 1,   Bcl-2∅, 1,   Bcl-xL↑, 1,   Casp3↓, 2,   Cyt‑c↑, 1,   HEY1↑, 1,   iNOS↓, 3,   iNOS↑, 1,   necrosis↓, 1,   p38↑, 2,   p‑p38↓, 1,   YAP/TEAD↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 1,   p‑Akt↓, 1,   p‑Akt↑, 1,   p‑CREB↑, 1,   ERK↓, 1,   p‑ERK↓, 1,   p‑ERK↑, 1,   HGF/c-Met↑, 1,   p‑IKKα↓, 1,   p‑IκB↓, 1,   p‑JNK↓, 1,   MAPK↓, 1,   MAPK↑, 1,   mTOR↓, 3,   PDGFR-BB↑, 1,   STAT3↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other?, 1,   other↑, 3,   other↝, 7,   tumCV↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,   HSP70/HSPA5↑, 3,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK5↓, 1,   P21↓, 1,  

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

cFos↑, 1,   Diff↑, 1,   FGF↑, 3,   IGF-1↑, 1,   NOTCH↑, 1,   Wnt↑, 1,  

Migration(tgid=13) ⓘ

ARG1/2↑, 1,   Ca+2↓, 5,   Ca+2↑, 4,   Ca+2∅, 1,   i-Ca+2↓, 1,   FAK↑, 1,   MMP-10↓, 1,   MMP1↓, 1,   MMP2↑, 1,   MMP9↓, 2,   MMPs↑, 1,   PDGF↑, 1,   TGF-β↑, 2,   TGF-β1↑, 1,   TIMP1↑, 1,   TIMP2↑, 1,   TumCMig↑, 1,   β-catenin/ZEB1↑, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 4,   HIF-1↓, 1,   Hif1a↝, 1,   Hif1a∅, 1,   NO↓, 3,   NO↑, 1,   VEGF↑, 3,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↑, 2,   GLUT4↑, 1,   MMP↑, 2,   MMP⇅, 1,   MMP↝, 1,   MMP∅, 1,   MPT↑, 1,   TRPC1↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

GM-CSF↑, 1,   IL1↓, 1,   IL1↑, 1,   IL10↑, 1,   IL1β↓, 3,   IL1β↑, 1,   IL2↑, 1,   IL4↑, 1,   IL6↓, 2,   IL6↑, 1,   Inflam↓, 9,   IP-10/CXCL-10↑, 1,   MCP1/CCL2↑, 2,   mPGES-1↓, 1,   MyD88↓, 1,   NF-kB↓, 3,   p‑p65↓, 1,   TLR4↓, 1,   TNF-α↓, 4,   TNF-α↑, 1,   TREM-1↓, 1,  

Cellular Microenvironment(tgid=17) ⓘ

pH↑, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 1,   5HT↑, 1,   Ach↑, 1,   AChE↓, 1,   BDNF↑, 4,   NGF↑, 1,   β-Endo↑, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ?, 1,   Aβ↓, 4,   p‑tau↓, 1,   β-Amyloid↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   Dose↝, 2,   Dose∅, 1,   eff↓, 3,   eff↑, 3,   eff↝, 2,   selectivity↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

BMD↑, 1,   IL6↓, 2,   IL6↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 2,   cardioP↑, 1,   chemoP↑, 1,   cognitive↑, 7,   cytoP↑, 1,   memory↑, 8,   motorD↑, 3,   neuroP↑, 9,   OS↑, 2,   Stroke↓, 1,   toxicity?, 1,   toxicity∅, 6,  
Total Targets: 186

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
95 Magnetic Fields
21 Magnetic Field Rotating
3 Silver-NanoParticles
3 doxorubicin
2 immunotherapy
1 Capsaicin
1 Vitamin C (Ascorbic Acid)
1 Radiotherapy/Radiation
1 Chemotherapy
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#:172  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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