Magnetic Fields 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):

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.
Ca²⁺ and ion-channel modulation, particularly TRPC, voltage-gated channels, intracellular Ca²⁺ handling, and ER–mitochondrial Ca²⁺ communication.
Mitochondrial and bioenergetic modulation, including membrane potential, electron transport, ATP production, mitochondrial permeability, and metabolic reprogramming.
Cell proliferation, cell-cycle, apoptosis, and senescence signaling through pathways including EGFR/PI3K/AKT/mTOR, MAPK/ERK, caspases, PARP, Bax and survivin.
Membrane permeability and drug-uptake modulation, producing context-dependent chemosensitization to agents including doxorubicin, etoposide and methotrexate.
Inflammatory and stress-response modulation including NF-κB, cytokine signaling, HSPs, ER stress and adaptive antioxidant pathways.
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↓, 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

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

 10 µM/ml + 1mT,2hr

 likely 50-60Hz and 1mT

in-vitro,

Bladder,

HTB-22

4uM/ml

 calculated IC50 value of AgNPs was 4.15 ± 0.20 μM/ml

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

50mT/30mins

3.29 0.4 mol/mL

6x improvement when LEMF added (50mT/15mins)

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

10 µM/ml+EMF(1mT)

4.15 μM/ml for AgNPs

P53↑, iNOS↑, NF-kB↑, Bcl-2↓, miR-125b↓, ROS↑, SOD↑,

2612-

Ba,

MF,

The effect of a static magnetic field and baicalin or baicalein interactions on amelanotic melanoma cell cultures (C32)

in-vitro,

Melanoma,

SOD1↑, SOD2↑, GPx1↑, Dose?, eff↝, SOD1↓, SOD2↓, GPx1↓,

2018-

CAP,

MF,

Capsaicin: Effects on the Pathogenesis of Hepatocellular Carcinoma

Review,

HCC,

TRPV1↑, eff↑, Akt↓, mTOR↓, p‑STAT3↑, MMP2↑, ER Stress↑, Ca+2↑, ROS↑, selectivity↑, MMP↓, Synergy↑,

654-

EGCG,

MNPs,

MF,

Characterization of mesenchymal stem cells with augmented internalization of magnetic nanoparticles: The implication of therapeutic potential

in-vitro,

Var,

human MSCs

*BioEnh↑,

657-

EGCG,

MNPs,

MF,

Interaction of poly-l-lysine coating and heparan sulfate proteoglycan on magnetic nanoparticle uptake by tumor cells

in-vitro,

GBM,

U87MG

10 µM EGCG

*BioEnh↑,

659-

EGCG,

MNPs,

MF,

Augmented cellular uptake of nanoparticles using tea catechins: effect of surface modification on nanoparticle-cell interaction

in-vivo,

Nor,

*BioEnh↑,

658-

EGCG,

MNPs,

MF,

Laminin Receptor-Mediated Nanoparticle Uptake by Tumor Cells: Interplay of Epigallocatechin Gallate and Magnetic Force at Nano-Bio Interface

in-vitro,

GBM,

LN229

*BioEnh↑,

401-

GoldNP,

MF,

In vitro evaluation of electroporated gold nanoparticles and extremely-low frequency electromagnetic field anticancer activity against Hep-2 laryngeal cancer cells

in-vitro,

Laryn,

HEp2

50mT/15mins

4.79 μg/mL IC50 for Au-NP

Casp3↑, P53↑, BAX↑, Bcl-2↓,

2235-

MF,

Increase of intracellular Ca2+ concentration in Listeria monocytogenes under pulsed magnetic field

in-vitro,

Inf,

~7mT, us duration, repeat every second

Ca+2↑, TumCD↑,

590-

MF,

VitC,

Sub-millitesla magnetic field effects on the recombination reaction of flavin and ascorbic acid radicals

in-vitro,

NA,

 <1 mT

RPM↑,

592-

MF,

VitC,

Alternative radical pairs for cryptochrome-based magnetoreception

RPM↑,

594-

MF,

VitC,

Static Magnetic Field Effect on the Fremy's Salt-Ascorbic Acid Chemical Reaction Studied by Continuous-Wave Electron Paramagnetic Resonance

Analysis,

NA,

RPM↑,

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,

 0.27 T at a transition time of 102 μs with pulse intervals of 1 Hz.

human red blood cells

*Ca+2↓, *eff↓, *ROS↓,

2237-

MF,

The Effect of Pulsed Electromagnetic Field Stimulation of Live Cells on Intracellular Ca2+ Dynamics Changes Notably Involving Ion Channels

in-vitro,

AML,

KG-1

40 mins

 10 Hz [DC: 30%, intensity:26.2 mT], 30 Hz [DC: 30%, intensity:20.3 mT], and 50 Hz [DC: 30%, 15 mT].

in-vitro,

Nor,

HUVECs

Ca+2↑, selectivity↑, *Inflam↓, *TNF-α↓, *NF-kB↓, *Ca+2↓,

2238-

MF,

Electromagnetic fields act via activation of voltage-gated calcium channels to produce beneficial or adverse effects

Review,

Var,

*BMD↑, *VGCC↑, *Ca+2↑, *NO↑, *eff↓,

2239-

MF,

Time-varying magnetic fields increase cytosolic free Ca2+ in HL-60 cells

in-vitro,

AML,

HL-60

Ca+2↑, eff↝,

2240-

MF,

Pulsed electromagnetic field induces Ca2+-dependent osteoblastogenesis in C3H10T1/2 mesenchymal cells through the Wnt-Ca2+/Wnt-β-catenin signaling pathway

in-vitro,

Nor,

C3H10T1/2

30 Hz, 1 mT, 2 h/day

PEMF output waveform consisted of a 400 kV/m pulsed burst (pulse width 0.2 m s; pulse wait 0.02 m s; burst width 5 m s; burst wait 60 m s; pulse rise 0.3 m s; pulse fall 2.0 m s) repeated at 30 Hz.

*Ca+2↑, *Diff↑, *BMD↑, *Wnt↑, *β-catenin/ZEB1↑, *eff↝,

530-

MF,

Low frequency sinusoidal electromagnetic fields promote the osteogenic differentiation of rat bone marrow mesenchymal stem cells by modulating miR-34b-5p/STAC2

in-vivo,

Nor,

15 Hz, 0.4 -1 mT

rat bone marrow mesenchymal stem cells

*miR-34b-5p↓, *ALP↑, *RUNX2↑, *BMP2↑, *OCN↑, *OPN↑, *β-catenin/ZEB1↑, *STAC2↑, *Diff↑, *BMD↑,

520-

MF,

Exposure to a 50-Hz magnetic field induced mitochondrial permeability transition through the ROS/GSK-3β signaling pathway

in-vitro,

Nor,

50 Hz, 0.4 mT, 60mins

Human amniotic epithelial cells

*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,

*RPM↑, *ROS↝,

522-

MF,

Low Magnetic Field Exposure Alters Prostate Cancer Cell Properties

in-vitro,

Pca,

PC3

20nT, 4hr

MMP2↑, MMP9↑, miR-21↑, miR-155↑, miR-210↑, miR-200c↓, miR-126↓,

524-

MF,

Inhibition of Angiogenesis Mediated by Extremely Low-Frequency Magnetic Fields (ELF-MFs)

vitro+vivo,

PC,

MS-1

2mT, 50Hz

mouse cell line injected in mice

vitro+vivo,

PC,

HUVECs

other↓, TumCP↓, TumCMig↓, VEGFR2/KDR/Flk1↓, TumVol↓, HSP70/HSPA5↓, HSP90↓, TumCCA↑, angioG↓,

525-

MF,

Pulsed electromagnetic fields regulate metabolic reprogramming and mitochondrial fission in endothelial cells for angiogenesis

in-vitro,

Nor,

HUVECs

4mT,  80 Hz

*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

Thomas-EMF is a low-intensity, frequency-modulated (25-6 Hz) EMF pattern.

Thomas-EMF used in our experiments is a complex time-modulated pattern (25–6 HZ)

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

2mT, 50Hz

ROS↑, other↑, p‑ERK↑, TumCP↓,

528-

MF,

Caff,

Pulsed electromagnetic fields affect the intracellular calcium concentrations in human astrocytoma cells

in-vitro,

GBM,

U373MG

3mT, 50Hz

Ca+2↑, TumCP∅, TumCD∅, eff↑,

529-

MF,

Low-frequency magnetic field therapy for glioblastoma: Current advances, mechanisms, challenges and future perspectives

Review,

GBM,

Ca+2↑, ROS↑, ChemoSen↑, QoL↑, OS↑,

2242-

MF,

Electromagnetic stimulation increases mitochondrial function in osteogenic cells and promotes bone fracture repair

in-vitro,

Nor,

2.5G, 5G, 10G, 15G, and 20G

*MMP↑, *Diff↑, *OXPHOS↑, *BMD↑, ATP∅,

531-

MF,

6-mT 0-120-Hz magnetic fields differentially affect cellular ATP levels

in-vitro,

Cerv,

HeLa

6mT, 0,50,120Hz

in-vitro,

CRC,

HCT116

in-vitro,

BC,

MCF7

in-vitro,

Lung,

A549

in-vitro,

Nor,

RPE-1

in-vitro,

Nor,

GP-293

ATP⇅,

532-

MF,

A 50 Hz magnetic field influences the viability of breast cancer cells 96 h after exposure

in-vitro,

BC,

MDA-MB-231

0.1 mT and 1.0 mT, 50Hz, 96h

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

1mT, 50Hz for 4 h

in-vitro,

Nor,

MCF10

TumCD↑, necrosis↑, mt-ROS↑, other↑, *STAT3↓, STAT3↑,

534-

MF,

Effect of extremely low frequency electromagnetic field parameters on the proliferation of human breast cancer

in-vitro,

BC,

MCF7

0.5,1mT 8-39Hz

square wave

in-vitro,

BC,

MDA-MB-231

in-vivo,

Nor,

MCF10

Ca+2↑, Apoptosis↑, eff↝, eff↑, selectivity↑, eff↝, eff↝,

535-

MF,

Electromagnetic Fields Trigger Cell Death in Glioblastoma Cells through Increasing miR-126-5p and Intracellular Ca2+ Levels

in-vitro,

Pca,

PC3

2.4GHz

in-vitro,

GBM,

A172

in-vitro,

Pca,

HeLa

Apoptosis↑, miR-129-5p↑, Ca+2↑, eff↝,

536-

MF,

Comparison of pulsed and continuous electromagnetic field generated by WPT system on human dermal and neural cells

in-vitro,

Nor,

SH-SY5Y

87–207 kHz, 1.01–1.05 kW, 1.3–1.7 mT

in-vitro,

GBM,

T98G

in-vitro,

Nor,

HDFa

other∅,

537-

MF,

immuno,

Integrating electromagnetic cancer stress with immunotherapy: a therapeutic paradigm

Review,

Var,

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↑,

585-

MF,

VitC,

Impact of pulsed magnetic field treatment on enzymatic inactivation and quality of cloudy apple juice

other↓,

3471-

MF,

The prevention effect of pulsed electromagnetic fields treatment on senile osteoporosis in vivo via improving the inflammatory bone microenvironment

in-vivo,

Nor,

PEMF with 40 min/day, five days per week

24 Sprague Dawley (SD) rats

*BMD↑, *NLRP3↓, *proCasp1↓, *cl‑Casp1↓, *IL1β↓, *GSDMD↓,

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,

Normal Human Dermal Fibroblasts

*NRF2↑, *Keap1↓, *SOD↑, *GPx↑, *ROS↓, *MDA↓, *SOD1↑, *SOD2↑, *GSR↑,

3463-

MF,

Pulsed Electromagnetic Fields Alleviates Hepatic Oxidative Stress and Lipids Accumulation in db/db mice

in-vivo,

NA,

2 h of pulsed electromagnetic fields (15.38 Hz, 2 mT)

db/db mice

*hepatoP↑, *MDA↓, *GSSG↓, *GSH↑, *GPx↑, *antiOx↑, *SREBP1/SREBF1↓,

3464-

MF,

Progressive Study on the Non-thermal Effects of Magnetic Field Therapy in Oncology

Review,

Var,

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,

angioG↓, *angioG↑, selectivity↑, Ca+2↝, ROS↝,

3466-

MF,

The effect of magnetic fields on tumor occurrence and progression: Recent advances

Review,

Var,

angioG↓, ROS↝, EGFR↝, TumCG↓,

3467-

MF,

Pulsed Magnetic Field Induces Angiogenesis and Improves Cardiac Function of Surgically Induced Infarcted Myocardium in Sprague-Dawley Rats

in-vivo,

Nor,

10 Hz 4 mT PMF and 15 Hz 6 mT PMF

rats

*angioG↑, *cardioP↑,

3468-

MF,

An integrative review of pulsed electromagnetic field therapy (PEMF) and wound healing

Review,

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,

*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↓,

Showing Research Papers: 1 to 50 of 279
Page 1 of 6 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 279

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,
Total Targets: 343

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 9, Catalase↑, 8, GPx↑, 4, GPx∅, 1, GPx1↑, 5, GPx3↑, 1, GPx4↑, 5, GSH↑, 1, GSH∅, 1, GSR↑, 3, GSSG↓, 1, HO-1↑, 1, Iron↑, 1, Keap1↓, 1, MDA↓, 5, MDA↑, 1, NRF2↑, 3, ROMO1↑, 1, ROS↓, 29, ROS↑, 8, ROS⇅, 2, ROS↝, 1, ROS∅, 1, mt-ROS↑, 2, RPM↑, 1, SOD↑, 9, SOD1↑, 5, SOD2↓, 1, SOD2↑, 6, TAC↑, 1, Trx↓, 1,

Mitochondria & Bioenergetics(tgid=3) ⓘ

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

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 2, ATP↑, 3, cAMP↑, 2, ECAR↓, 1, ECAR↑, 1, FABP4↓, 1, FAO↓, 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, PONs↓, 1, PPP↓, 1, SREBP1/SREBF1↓, 1, TCA↑, 1,

Cell Death(tgid=5) ⓘ

Apoptosis↓, 6, BAD↓, 1, BAX↓, 3, Bcl-2↑, 1, Bcl-2∅, 1, Bcl-xL↑, 1, Casp1↓, 1, cl‑Casp1↓, 1, proCasp1↓, 1, Casp3↓, 2, Cyt‑c↑, 2, GSDMD?, 1, GSDMD↓, 1, HEY1↑, 1, iNOS↓, 3, iNOS↑, 1, necrosis↓, 1, p38↑, 2, p‑p38↓, 1, YAP/TEAD↑, 1,

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 2, Akt↑, 2, p‑Akt↓, 1, p‑Akt↑, 1, p‑CREB↑, 1, ERK↓, 1, ERK↑, 2, p‑ERK↓, 1, p‑ERK↑, 2, HGF/c-Met↑, 1, p‑IKKα↓, 2, p‑IκB↓, 1, p‑JNK↓, 1, p‑JNK↑, 3, MAPK↓, 1, MAPK↑, 2, mTOR↓, 4, mTOR↑, 2, mTOR↝, 1, p‑P70S6K↑, 1, PDGFR-BB↑, 1, PI3K↓, 1, PI3K↑, 1, PKA↑, 1, PKCδ↓, 1, PTEN↑, 1, RKIP↑, 1, STAT3↓, 2, p‑STAT3↓, 1,

Transcription & Epigenetics(tgid=7) ⓘ

miR-34b-5p↓, 1, other?, 3, other↓, 2, other↑, 15, other↝, 10, RUNX2↑, 1, RUNX2∅, 1, SOX9↑, 2, tumCV↑, 1,

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1, HSP70/HSPA5↑, 5, HSPs↑, 1,

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,

Cell Cycle & Senescence(tgid=11) ⓘ

CDK5↓, 1, E2Fs↑, 1, P21↓, 1,

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

ALDH↑, 1, BMP2↑, 2, BMPs↓, 1, BMPs↑, 1, cFos↑, 1, Diff↓, 1, Diff↑, 9, Diff↝, 1, FGF↑, 5, IGF-1↑, 1, MSCs↑, 1, NOTCH↑, 1, NOTCH1↑, 1, TumCG↑, 1, TumCG∅, 1, Wnt↑, 3,

Migration(tgid=13) ⓘ

ARG1/2↑, 1, Ca+2↓, 6, Ca+2↑, 11, Ca+2↝, 2, Ca+2∅, 1, i-Ca+2↓, 1, Cartilage↑, 2, COL1∅, 1, COL2A1↑, 2, F-actin↑, 1, FAK↑, 2, ITGB1↑, 1, MMP-10↓, 1, MMP1↓, 1, MMP2↑, 2, MMP9↓, 3, MMP9↑, 2, MMPs↑, 1, Netrins↑, 1, OPN↑, 1, PDGF↑, 1, SMAD4↑, 1, SMAD5↑, 1, STAC2↑, 1, TGF-β↑, 4, TGF-β1↑, 1, TIMP1↑, 2, TIMP2↑, 1, TumCMig↑, 1, β-catenin/ZEB1↑, 4,

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 7, angioG↝, 1, EGR4↑, 1, HIF-1↓, 1, Hif1a↑, 2, Hif1a↝, 1, Hif1a∅, 2, HIF2a↑, 1, NO↓, 4, NO↑, 5, NPY↑, 1, VEGF↓, 1, VEGF↑, 11, VEGFR2/KDR/Flk1↑, 1,

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1, CellMemb↑, 1, GLUT1↑, 2, GLUT4↑, 1, MMP↑, 3, MMP⇅, 1, MMP↝, 1, MMP∅, 1, MPT↑, 1, TRPC1↑, 1, VGCC↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1, COX2/PTGS2↓, 2, CXCc↓, 1, GM-CSF↑, 1, IFN-γ↓, 1, IL1↓, 2, IL1↑, 1, IL10↑, 5, IL17↓, 1, IL1β↓, 6, IL1β↑, 1, IL2↑, 1, IL4↑, 1, IL6↓, 6, IL6↑, 1, IL8↓, 2, Inflam↓, 30, Inflam∅, 1, IP-10/CXCL-10↑, 1, MCP1/CCL2↓, 1, MCP1/CCL2↑, 2, MIP‑1α/CCL3↓, 1, mPGES-1↓, 1, MyD88↓, 1, NF-kB↓, 6, NLRP3↓, 2, p‑p65↓, 1, PGE2↓, 3, PGE2↑, 1, PSA↓, 1, TLR4↓, 1, TNF-α↓, 8, TNF-α↑, 1, Treg lymp↓, 1, TREM-1↓, 1,

Cellular Microenvironment(tgid=17) ⓘ

pH↑, 1,

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 2, 5HT↑, 2, Ach↑, 1, AChE↓, 1, BDNF↑, 11, NGF↑, 1, PSD95↑, 1, β-Endo↑, 2,

Protein Aggregation(tgid=19) ⓘ

APP∅, 1, Aβ?, 1, Aβ↓, 9, Aβ∅, 2, BACE/β-secretase↓, 1, p‑tau↓, 2, β-Amyloid↓, 1,

Hormonal & Nuclear Receptors(tgid=20) ⓘ

PPARγ↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1, BioAv↑, 1, BioEnh↑, 4, Dose↝, 33, Dose∅, 1, eff↓, 6, eff↑, 19, eff↝, 5, selectivity↑, 2, Synergy↑, 1,

Clinical Biomarkers(tgid=22) ⓘ

ALP↑, 2, ALP∅, 1, BloodF↑, 4, BMD↑, 12, IL6↓, 6, IL6↑, 1, LDH↓, 1, NSE↑, 1, OCN↑, 1, OCN∅, 1, PSA↓, 1, PV↓, 3, UFR↑, 2, UR↓, 1,

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 2, cardioP↑, 3, chemoP↑, 1, cognitive↑, 21, cognitive∅, 1, cytoP↑, 1, hepatoP↑, 1, memory↑, 19, memory∅, 2, Mood⇅, 1, motorD↑, 10, neuroP↑, 19, OS↑, 2, Pain↓, 8, QoL↑, 5, Strength↑, 1, Stroke↓, 1, toxicity?, 1, toxicity↓, 6, toxicity∅, 9, Weight∅, 1,

Infection & Microbiome(tgid=24) ⓘ

GutMicro↑, 1,
Total Targets: 298

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#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

Magnetic Fields Cancer Research Results

Magnetic Field Mechanisms in Cancer

Magnetic Stimulation in Alzheimer’s Disease

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Metal & Cofactor Biology(tgid=2) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Cellular Microenvironment(tgid=17) ⓘ

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Cellular Microenvironment(tgid=17) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Protein Aggregation(tgid=19) ⓘ

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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