Magnetic Fields / ROS Cancer Research Results

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

Non-Static Magnetic Fields (AC / Pulsed / Oscillating MF)
Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Reactive oxygen species (ROS) ↑ ROS (P→R); often sustained (G) ↑ ROS (P); ↔/↓ net ROS (R→G) P, R, G Upstream redox perturbation MF perturbs electron/radical dynamics: normal cells often adapt (ROS setpoint ↓), cancer cells less so
2 NRF2 antioxidant response ↔ / insufficient NRF2 induction (R→G) ↑ NRF2 activation (R→G) R, G Adaptive redox defense Explains mixed ROS direction in normal cells (initial ↑ then adaptive ↓)
3 Glutathione (GSH) homeostasis ↓ GSH (R→G) ↔ or transient ↓ (R) with recovery (G) R, G Redox buffering capacity GSH depletion reflects sustained oxidative load; recovery indicates successful adaptation
4 Superoxide dismutase (SOD) / antioxidant enzymes ↔ or inadequate enzyme upshift (G) ↑ SOD/GPx/CAT capacity (G) G Longer-term antioxidant remodeling Often the “endpoint” readout that correlates with ROS-normalization in normal tissue
5 Mitochondrial ETC / respiration ↓ ETC efficiency; ↑ electron leak (P→R) ↔ mild, reversible ETC perturbation (P→R) P, R Bioenergetic destabilization ETC perturbation is a mechanistic bridge between MF exposure and ROS/ΔΨm changes
6 Mitochondrial membrane potential (ΔΨm / MMP) ↓ ΔΨm (R); may progress (G) ↔ preserved or reversible dip (R) R, G Mitochondrial dysfunction thresholding ΔΨm loss typically follows ROS/ETC disruption rather than preceding it
7 Ca²⁺ signaling (VGCC / ER–mitochondria Ca²⁺ flux) ↑ dysregulated Ca²⁺ influx/transfer (P→R); overload may persist (G) ↑ transient Ca²⁺ signaling (P); homeostasis restored (R→G) P, R, G Stress signal amplification Ca²⁺ dysregulation links ROS/ETC perturbation to ER stress and mitochondrial dysfunction (amplifies ΔΨm loss and UPR commitment)
8 Mitochondrial permeability transition pore (MPTP) ↑ MPTP opening propensity (R); sustained opening possible (G) ↔ transient or closed (R→G) P, R, G Commitment point for mitochondrial failure MPTP opening integrates ROS, Ca²⁺ overload, and ΔΨm loss; acts as a threshold event converting reversible stress into irreversible mitochondrial dysfunction
9 ER stress / UPR ↑ ER stress (R); CHOP-commitment possible (G) ↑ adaptive UPR (R); resolves (G) R, G Proteostasis stress Often downstream of ROS + Ca²⁺ handling perturbations
10 DNA damage (oxidative) ↑ damage markers (R→G) ↔ or repaired (G) R, G Checkpoint pressure Generally secondary to ROS; interpret as stress consequence not “direct genotoxicity”
11 LDH / glycolytic flux ↓ glycolytic performance (R→G) ↔ flexible substrate switching (R→G) R, G Metabolic vulnerability Redox imbalance can destabilize high-rate glycolysis in cancer-biased contexts
12 Thioredoxin system (Trx / TrxR) ↓ functional reserve / overload (R→G) ↔ preserved capacity (G) R, G Parallel antioxidant system stress Useful when GSH-only does not explain redox phenotype 
Time-Scale Flag: TSF = P / R / G
  P: 0–30 min (physical / electron / radical effects)
  R: 30 min–3 hr (redox signaling & stress response)
  G: >3 hr (gene-regulatory adaptation)
MPTP: opening represents a mitochondrial commitment event integrating ROS and Ca²⁺ stress; sustained opening indicates irreversible bioenergetic failure.
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⟱
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, MCF-7 - in-vitro, Bladder, HTB-22
Apoptosis↑, P53↑, iNOS↑, NF-kB↑, Bcl-2↓, ROS↑, SOD↑, TumCCA↑, eff↑, 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↑, 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, MCF-7
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↓, 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↓, ATP↑, MMP↑, ROS↑, OXPHOS↑, mitResp↑,
582- MF,  immuno,  VitC,    Magnetic field boosted ferroptosis-like cell death and responsive MRI using hybrid vesicles for cancer immunotherapy
- in-vitro, Pca, TRAMP-C1 - in-vivo, NA, NA
Fenton↑, Ferroptosis↑, ROS↑, TumCG↓, Iron↑, GPx4↓,
587- MF,  VitC,    Effect of stationary magnetic field strengths of 150 and 200 mT on reactive oxygen species production in soybean
ROS↑, SOD↓, other↓,
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↑,
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∅,
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, MCF-7 - 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↓,
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, MCF-7 - 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↑,
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↑, eff↑, eff↑, Ca+2↑, MAPK↑, *Catalase↑, *SOD1↑, *GPx1↑, *GPx4↑, *NRF2↑, TumAuto↑, ER Stress↑, HSPs↑, SIRT3↑, ChemoSen↑, UPR↑, other↑, PI3K↓, JNK↑, p38↑, eff↓, *toxicity?,
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↓,
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↑,
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↓,
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↑,
2241- MF,    Pulsed electromagnetic therapy in cancer treatment: Progress and outlook
- Review, Var, NA
other↝, p‑ERK↝, P53↝, Cyt‑c↝, OXPHOS↑, Apoptosis↑, 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↓,
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↑,
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, MCF-7 - 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↓,
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↑,
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, MCF-7
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↑,
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↑,
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↑,
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↑,
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↑,
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↓,
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↑,
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↓, Apoptosis↑, selectivity↑, Ca+2↑, Catalase↑,
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, MCF-7
selectivity↑, Apoptosis↑, TumCI↓, tumCV↓, TumVol↓, eff↓, eff↑, ROS↑, Ca+2↑, TumCMig↓,
3486- MF,    Pulsed electromagnetic field potentiates etoposide-induced MCF-7 cell death
- in-vitro, NA, NA
ChemoSen↑, tumCV↓, cl‑PARP↑, Casp7↑, Casp9↑, survivin↓, BAX↑, DNAdam↑, ROS↑, eff↓,
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↓,
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↑,
2259- MFrot,  MF,    Method and apparatus for oncomagnetic treatment
- in-vitro, GBM, NA
MMP↓, Bcl-2↓, BAX↑, Bak↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, ROS↑, lactateProd↑, Apoptosis↑, MPT↑, *selectivity↑, eff↑, MMP↓, selectivity↑, TCA?, H2O2↑, eff↑, *antiOx↑, H2O2↑, eff↓, GSH/GSSG↓, *toxicity∅, OS↑,
2258- MFrot,  MF,    EXTH-68. ONCOMAGNETIC TREATMENT SELECTIVELY KILLS GLIOMA CANCER CELLS BY INDUCING OXIDATIVE STRESS AND DNA DAMAGE
- in-vitro, GBM, GBM - in-vitro, Nor, SVGp12
TumVol↓, OS↑, γH2AX↑, DNAdam↑, selectivity↑, ROS↑, TumCD↑, eff↑, eff↓,
199- MFrot,  MF,    Modulation of Cellular Response to Different Parameters of the Rotating Magnetic Field (RMF)—An In Vitro Wound Healing Study
- in-vivo, Wounds, L929 - NA, NA, HaCaT
*ROS↑, *Ca+2↓, *other↝, *other↝, *other↝, *other↝, *other↝, *other?,
198- MFrot,  MF,    Biological effects of rotating magnetic field: A review from 1969 to 2021
- Review, Var, NA
AntiCan↑, breath↑, Pain↓, Appetite↑, Strength↑, BowelM↑, TumMeta↓, TumCCA↑, ETC↓, MMP↓, TumCD↑, selectivity↑, ROS↑, Casp3↑, TumCG↓, TumCCA↑, ChrMod↑, TumMeta↓, Imm↑, DCells↑, Akt↓, OS⇅, toxicity↓, QoL↑, hepatoP↑, Pain↓, Weight↑, Strength↑, Sleep↑, IL6↓, CD4+↑, CD8+↑, Ca+2↑, radioP↑, chemoP↑, *BMD↑, *AntiAge↑, *AMPK↑, *P21↓, *P53↓, *mTOR↓, *OS↑, *β-Endo↑, *5HT↓,
186- MFrot,  MF,    Selective induction of rapid cytotoxic effect in glioblastoma cells by oscillating magnetic fields
- in-vitro, GBM, GBM - in-vitro, Lung, NA
mt-ROS↑, Casp3↑, selectivity↑, TumCD↑, ETC↓, H2O2↑, eff↓, GSH↑, MMP↓,

Showing Research Papers: 1 to 50 of 58
Page 1 of 2 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 58

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   Catalase↑, 2,   Fenton↑, 1,   Ferroptosis↑, 1,   GPx4↓, 1,   GSH↑, 1,   GSH/GSSG↓, 1,   GSR↑, 1,   H2O2↑, 4,   Iron↑, 1,   MDA↑, 1,   OXPHOS↑, 3,   Prx6↑, 1,   ROS↑, 42,   mt-ROS↑, 2,   RPM↑, 2,   SIRT3↑, 1,   SOD↓, 1,   SOD↑, 2,   SOD2↑, 1,  

Mitochondria & Bioenergetics ⓘ

ADP:ATP↓, 2,   ATP↓, 2,   ATP↑, 1,   ETC↓, 2,   mitResp↑, 1,   MMP↓, 7,   MMP↑, 1,   MPT↑, 1,   OCR↑, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   DHCR24↑, 1,   ECAR↓, 1,   Glycolysis↓, 3,   Glycolysis∅, 1,   lactateProd↑, 1,   PKM2↓, 1,   Pyruv↓, 2,   SIRT1↑, 1,   TCA?, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 4,   p‑Akt↓, 1,   Apoptosis↑, 17,   Bak↑, 1,   BAX↑, 3,   Bcl-2↓, 4,   Casp3↑, 4,   cl‑Casp3↑, 1,   Casp7↑, 1,   Casp9↑, 3,   Cyt‑c↑, 1,   Cyt‑c↝, 1,   Endon↑, 1,   Ferroptosis↑, 1,   iNOS↑, 2,   JNK↑, 1,   MAPK↑, 3,   Necroptosis↑, 1,   necrosis↑, 1,   p38↑, 2,   survivin↓, 1,   TRPV1↑, 1,   TumCD↑, 4,  

Transcription & Epigenetics ⓘ

BowelM↑, 1,   ChrMod↑, 1,   other↓, 1,   other↑, 5,   other↝, 1,   tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

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

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   TumAuto↑, 5,  

DNA Damage & Repair ⓘ

DNAdam↑, 7,   P53↑, 4,   P53↝, 1,   cl‑PARP↑, 2,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CycB/CCNB1↓, 1,   TumCCA↑, 7,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   CD44↓, 1,   CSCs↓, 2,   Diff↑, 1,   p‑ERK↑, 1,   p‑ERK↝, 1,   GSK‐3β↑, 1,   miR-125b↓, 1,   mTOR↓, 1,   Nanog↓, 1,   PI3K↓, 2,   SOX2↓, 1,   STAT3↑, 1,   p‑STAT3↑, 1,   TumCG↓, 8,  

Migration ⓘ

Ca+2↓, 1,   Ca+2↑, 16,   i-Ca+2↑, 1,   MMP2↑, 1,   TumCI↓, 3,   TumCMig↓, 3,   TumCP↓, 8,   TumMeta↓, 4,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   EPR↑, 1,   Hif1a↓, 1,   NO↑, 1,   VEGF↓, 1,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

P-gp↓, 2,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   COX2↓, 1,   DCells↑, 1,   IL10↑, 1,   IL6↓, 1,   IL6↑, 1,   Imm↑, 1,   NF-kB↓, 1,   NF-kB↑, 2,   TNF-α↑, 1,  

Cellular Microenvironment ⓘ

i-pH↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 5,   ChemoSen∅, 1,   eff↓, 9,   eff↑, 11,   eff⇅, 1,   eff↝, 1,   RadioS↑, 3,   selectivity↑, 15,  

Clinical Biomarkers ⓘ

BloodF↑, 1,   IL6↓, 1,   IL6↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   AntiTum↑, 1,   Appetite↑, 1,   breath↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   OS↑, 4,   OS⇅, 1,   Pain↓, 2,   QoL↑, 2,   radioP↑, 1,   Sleep↑, 1,   Strength↑, 2,   toxicity↓, 1,   TumVol↓, 4,   Weight↑, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 153

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   Catalase↑, 1,   GPx1↑, 1,   GPx4↑, 1,   HO-1↑, 1,   MDA↑, 1,   NRF2↑, 1,   OXPHOS↑, 1,   ROS↓, 2,   ROS↑, 8,   mt-ROS↑, 2,   SOD1↑, 1,  

Mitochondria & Bioenergetics ⓘ

ADP:ATP↓, 1,   ATP↑, 3,   MMP∅, 1,   MPT↑, 1,   mt-OCR↑, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   ECAR↓, 1,   ECAR↑, 1,   FAO↑, 1,   Glycolysis↓, 1,   lactateProd↓, 1,   LDHB↑, 1,   NAD↑, 1,   PPP↓, 1,   TCA↑, 1,  

Cell Death ⓘ

Akt↓, 1,   BAX↓, 1,   Bcl-2∅, 1,   Cyt‑c↑, 1,   HEY1↑, 1,   HGF/c-Met↑, 1,   iNOS↑, 1,   MAPK↑, 1,   necrosis↓, 1,   p38↑, 1,   YAP/TEAD↑, 1,  

Transcription & Epigenetics ⓘ

other?, 1,   other↑, 3,   other↝, 5,  

DNA Damage & Repair ⓘ

P53↓, 1,  

Cell Cycle & Senescence ⓘ

P21↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,   FGF↑, 2,   p‑GSK‐3β↑, 1,   mTOR↓, 2,   NOTCH↑, 1,   STAT3↓, 1,   Wnt↑, 1,  

Migration ⓘ

Ca+2↓, 2,   Ca+2↑, 3,   Ca+2∅, 1,   i-Ca+2↓, 1,   FAK↑, 1,   MMP2↑, 1,   MMPs↑, 1,   PDGF↑, 1,   TGF-β↑, 1,   TRPC1↑, 1,   β-catenin/ZEB1↑, 1,   β-Endo↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↑, 1,   Hif1a∅, 1,   VEGF↑, 2,  

Immune & Inflammatory Signaling ⓘ

IL1↑, 1,   IL1β↓, 1,   IL6↓, 1,   IL6↑, 1,   Inflam↓, 2,   MCP1↑, 1,   TNF-α↓, 1,   TNF-α↑, 1,  

Synaptic & Neurotransmission ⓘ

5HT↓, 1,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

BMD↑, 1,   IL6↓, 1,   IL6↑, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   memory↑, 3,   OS↑, 1,   toxicity?, 1,   toxicity∅, 2,  
Total Targets: 89

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
58 Magnetic Fields
13 Magnetic Field Rotating
3 Silver-NanoParticles
3 immunotherapy
2 Vitamin C (Ascorbic Acid)
2 doxorubicin
1 Capsaicin
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#:2
  wNotes=0  sortOrder:rid,rpid

 

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