Magnetic Field Rotating Cancer Research Results

MFrot, Magnetic Field Rotating: Click to Expand ⟱
Features:

Magnetic Field Rotating — Rotating magnetic field (RMF) is a dynamic magnetic-field modality in which the magnetic-field vector rotates spatially with time, generated either by mechanically rotating permanent magnets or by phase-shifted orthogonal electromagnetic coils. Related implementations include spinning oscillating magnetic fields (sOMF/OMF), gradient rotating magnetic fields, rotating static magnetic fields, and nanoparticle-coupled magnetomechanical RMF. The Oncomagnetic platform is an important cancer-specific implementation in which rapidly rotating permanent magnets generate patterned sOMF without requiring magnetic nanoparticles. RMF should be distinguished from generic static magnetic fields, conventional alternating magnetic fields, pulsed electromagnetic fields, and transcranial magnetic stimulation because field geometry, rotation, frequency, amplitude, temporal pattern, and mechanical coupling substantially affect biological responses.

Primary mechanisms (ranked):

  1. Mitochondrial electron-transport disruption, particularly persistent inhibition of Complex I in Oncomagnetic sOMF-treated cancer cells.
  2. Tumor-selective mitochondrial ROS generation and oxidative stress downstream of disturbed electron transport.
  3. Mitochondrial depolarization, respiratory failure, mitochondrial permeability transition, and subsequent apoptotic signaling.
  4. Oxidative DNA damage, G1 cell-cycle arrest, and caspase-dependent apoptosis following sustained Oncomagnetic exposure.
  5. F-actin and cytoskeletal mechanotransduction, reducing migration, invasion, and metastasis with moderate-intensity or gradient RMF.
  6. ECM-integrin signaling modulation, including COL11A1/ITGB1/FAK/YAP and CCDC150/TGF-β1/SMAD3 pathways in triple-negative breast cancer models.
  7. Magnetomechanical membrane, cytoskeletal, lysosomal, or organelle disruption when RMF is combined with internalized magnetic nanoparticles; this mechanism requires magnetic material and is mechanistically distinct from particle-free Oncomagnetic therapy.

Bioavailability / PK relevance: Not concentration-driven. RMF is a physical-field modality and therefore has no conventional absorption, plasma concentration, metabolism, or elimination. Therapeutic exposure instead depends on field strength, rotation frequency, spatial gradient, vector geometry, temporal pattern, tissue penetration, distance from the field source, and treatment duration. Nanoparticle-assisted RMF additionally depends on particle biodistribution, tumor uptake, intracellular localization, retention, clearance, and magnetic susceptibility.

In-vitro vs systemic exposure relevance: Conventional concentration comparisons are not applicable. Translation depends on reproducing the relevant magnetic-field waveform and geometry within tissue. Oncomagnetic sOMF is specifically designed for non-contact field exposure without injected magnetic material, whereas many magnetomechanical RMF studies require nanoparticles and therefore should not be extrapolated to particle-free RMF. Field parameters from one RMF platform should not automatically be generalized to another.

Clinical evidence status: Preclinical evidence is substantial but heterogeneous, including cultured cancer cells, glioma and breast-cancer animal models, and nanoparticle-assisted magnetomechanical systems. Human evidence remains limited. Historical small clinical studies have evaluated rotating magnetic-field approaches in advanced cancers, and published Oncomagnetic compassionate-use case reports describe prolonged treatment of individual malignant glioma patients. A prospective multicenter Oncomagnetic study in newly diagnosed glioblastoma is currently recruiting, making the modality investigational rather than an established cancer treatment. The strongest contemporary mechanistic evidence is for glioma Oncomagnetic sOMF and for metastasis-modulating RMF in breast-cancer models.

Rotary Magnetic field can be generated by a spinning magnet or magnets. Or it can be implemented with 2 or more coils, power with a phase shift between them (90 deg for 2 coil implementation) (60deg for 3 coil implementation)
Targets affected are mostly the same as for Magnet fields
Main differences
- may enhance the EPR effect allowing targeting of drugs to cancer cells
- acts as wireless stirrer, especially on magnetic particles(inducing eddy currents in water media)
- research for use in nano surgery, and mechanical destruction of cancer cells
- continue to highlight ability to raise ROS in cancer cell and lower ROS in normal cells
- RMF may be responsible for Ca2+ distribution to pass across the plasma membrane(differental affected for cancer and normal cells)

Pathways:
- induce ROS production in cancer cells, while decreasing ROS in normal cells. Ca2+ is critical and the Ca2+ balance is increased in cancer cells while decreased in normal cells (example for wound healing)
- ROS↑ related: MMP↓(ΔΨm), Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx">Prx,
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : TNF-α↓, IL-6↓,
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, RhoA↓, NF-κB↓, TGF-β↓, ERK↓
- cause Cell cycle arrest : TumCCA↑,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, ERK↓,
- Others: PI3K↓, AKT↓, Wnt↓, AMPK, ERK↓, JNK,
- Synergies: < Others(review target notes), Neuroprotective, Cognitive,

- Selectivity: Cancer Cells vs Normal Cells

Rotating Magnetic Field Cancer Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Mitochondrial Complex I and electron transport ↓ Complex I activity; ↓ NADH:ubiquinone oxidoreductase function; ↓ mitochondrial electron transport ↔ no comparable persistent inhibition demonstrated in tested normal astrocytes and astroglial cells P, R Upstream metabolic disruption Current Oncomagnetic sOMF evidence identifies ROS-dependent persistent Complex I inhibition as an immediate intracellular mechanism. This provides a mechanistic link between the rotating field and subsequent oxidative injury.
2 Mitochondrial ROS and oxidative stress ↑ superoxide; ↑ intracellular ROS; ↑ oxidative stress ↔ substantially smaller response in tested normal-cell models P, R Selective oxidative injury A core Oncomagnetic mechanism. Rotation plus field oscillation produces substantially greater ROS than comparable static-field exposure in glioma models. Antioxidant rescue strongly supports a causal role for ROS.
3 Mitochondrial membrane integrity and permeability ↓ mitochondrial function; ↓ membrane integrity; ↑ permeability transition and mitochondrial injury (context-dependent) ↔ comparatively resistant in tested normal cells R Bioenergetic collapse Occurs downstream of disturbed respiratory-chain redox chemistry and ROS. Strength of direct evidence varies by RMF implementation.
4 Glutathione redox system ↓ reduced GSH availability; ↑ GSH oxidation; ↑ GSSG/GSH ratio; ↓ reducing capacity ↔ lower oxidative burden in tested normal-cell models R Weakens antioxidant buffering Directly relevant to the oxidative mechanism. GSH oxidation means reduced GSH is consumed as it is converted toward GSSG; this should not automatically be interpreted as a decrease in total cellular glutathione unless total glutathione was measured.
5 DNA oxidative damage and cell-cycle control ↑ oxidative DNA damage; ↑ G1 arrest; ↓ proliferation ↔ little comparable damage reported in tested normal astroglial cells R, G Cytostatic and genotoxic response Downstream of sOMF-induced oxidative stress rather than evidence for a direct magnetic interaction with DNA.
6 Caspase-dependent apoptosis ↑ caspase activation; ↑ apoptosis; ↓ clonogenic survival ↔ comparatively low toxicity in tested normal-cell systems R, G Cancer-cell death Oncomagnetic sOMF produces ROS-dependent loss of clonogenic survival and delayed caspase activation. Antioxidant rescue supports oxidative stress as the upstream driver.
7 F-actin and cytoskeletal mechanotransduction ↓ F-actin organization; ↓ spreading; ↓ migration; ↓ invasion ↔ insufficient comparative evidence R, G Suppresses invasive behavior Particularly relevant to moderate-intensity and gradient RMF studies in triple-negative breast cancer. This represents a mechanomechanical branch distinct from the mitochondrial Oncomagnetic mechanism.
8 Mechanosensitive Ca²⁺ signaling ↑ or altered Ca²⁺ influx and oscillatory dynamics (context-dependent); altered Ca²⁺-dependent signaling ↔ insufficient comparative cancer-specific evidence P, R Mechanotransduction and signaling modulation Rotating fields can alter predicted Ca²⁺ oscillatory dynamics through mechanosensitive-channel coupling. Direct experimental cancer-specific RMF evidence remains less mature than the ROS and mitochondrial evidence, so Ca²⁺ should be retained but ranked as secondary.
9 CCDC150 TGF-β1 SMAD3 axis ↓ CCDC150; ↓ TGF-β1/SMAD3 signaling; ↓ migration; ↓ invasion; ↓ metastasis ↔ insufficient comparative evidence G Antimetastatic signaling Directly demonstrated with gradient RMF in triple-negative breast cancer models and closely linked to RMF-induced F-actin disruption.
10 COL11A1 ITGB1 FAK YAP axis ↓ COL11A1; ↓ ITGB1 signaling; ↓ FAK/YAP activation; ↓ tumor growth; ↓ lung metastasis ↔ insufficient comparative evidence G Suppresses ECM-driven metastatic signaling Recent RMF-specific TNBC work identifies COL11A1 as an RMF-responsive extracellular-matrix component upstream of ITGB1/FAK/YAP signaling.
11 Magnetomechanical nanoparticle actuation ↑ mechanical membrane, cytoskeletal, lysosomal, or organelle injury (requires external trigger) ↔ strongly dependent on nanoparticle uptake and intracellular localization P, R Mechanical tumor-cell injury Requires magnetic nanoparticles, nanomotors, or related magnetic structures. It is a genuine rotating-field mechanism but should be distinguished from particle-free Oncomagnetic sOMF.
12 GSH GPX4 ferroptosis axis ↓ GSH; ↓ GPX4; ↑ lipid ROS; ↑ lipid peroxidation; ↑ ferroptosis (requires external trigger) ↔ model-dependent R, G Ferroptotic cell death Relevant primarily to RMF-driven magnetic nanoparticle and nanorobot systems. Current evidence does not establish GPX4 suppression as a general particle-free Oncomagnetic mechanism.
13 NRF2 antioxidant response Potential ↑ compensatory NRF2 signaling following oxidative stress (context-dependent) ↔ insufficient RMF-specific comparative evidence R, G Adaptive antioxidant defense NRF2 is mechanistically relevant to the oxidative-stress response, but direct rotating-field-specific evidence remains limited. ROS elevation should not be interpreted as NRF2 suppression; compensatory NRF2 activation is biologically plausible.
14 Tumor microenvironment mechanics ↓ matrix stiffness; altered CAF mechanics; ↑ immune-cell infiltration (model-dependent) (requires external trigger) ↔ model-dependent R, G Microenvironment remodeling Reported mainly in RMF-driven magnetic nanomotor systems rather than particle-free RMF.
15 Chemosensitization ↑ treatment response in selected combination systems (context-dependent) (requires external trigger) ↔ insufficient comparative evidence R, G Combination-treatment enhancement Evidence is currently stronger for nanoparticle-mediated RMF combinations than for particle-free Oncomagnetic therapy. RMF should not yet be described as a general chemosensitizer.
16 Clinical Translation Constraint Response depends on waveform, rotation, field amplitude, frequency, gradient, geometry, treatment duration, tumor type, and nanoparticle use Long-term human safety and comparative normal-tissue data remain limited P, R, G Limits cross-platform extrapolation Oncomagnetic sOMF, gradient RMF, moderate-intensity RMF, and nanoparticle-assisted magnetomechanical RMF are related but mechanistically non-equivalent. ER stress and TrxR effects are not included as independent rows because current rotating-field-specific cancer evidence is insufficient to establish them as direct RMF mechanisms.

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: Moderate-intensity rotating magnetic fields have shown disease-modifying effects in mouse models of Alzheimer’s disease. Reported effects include direct inhibition of Aβ fibril formation, reduced cerebral amyloid deposition, reduced microglial activation and oxidative stress, improved cognition and memory, and increased autophagic signaling with suppression of the PI3K/AKT/mTOR pathway. These findings are preclinical; they do not establish clinical efficacy in human Alzheimer’s disease.

Clinical status: Preclinical animal evidence only for the specifically rotating-field studies. Generic rTMS, PEMF, static-field, and other non-rotating magnetic-field studies should remain under the separate Magnetic Fields category rather than being used to establish RMF clinical efficacy.

Rotating Magnetic Field Alzheimer’s Mechanisms

Rank Pathway / Axis AD Modulation Primary Effect Notes / Interpretation
1 Aβ aggregation and amyloid deposition ↓ Aβ fibril formation; ↓ amyloid plaques Reduces amyloid burden RMF can directly interfere with Aβ aggregation in vitro and reduced amyloid deposition in APP/PS1 mice.
2 Autophagy PI3K AKT mTOR ↑ autophagy; ↓ PI3K/AKT/mTOR signaling Promotes proteostatic clearance Long-term RMF exposure in APP/PS1 mice improved cognition and was associated with activation of autophagy-related pathways.
3 Microglial activation and neuroinflammation ↓ pathological microglial activation; polarization shifted toward protective phenotype Reduces neuroinflammatory injury Observed in both familial and sporadic mouse AD models.
4 Oxidative stress ↓ oxidative stress Neuroprotection Direction differs from the deliberate ROS increase observed in Oncomagnetic cancer cells, illustrating strong disease- and cell-state dependence.
5 Neuronal integrity ↑ neuronal survival and functional preservation Neuroprotection Associated with reduced neuronal damage in RMF-treated AD mice.
6 Cognition and memory ↑ spatial memory; ↑ recognition memory; ↑ cognitive performance Functional improvement Repeatedly reported in RMF-treated mouse models, but human efficacy remains unestablished.


Scientific Papers found: Click to Expand⟱
3491- MFrot,  MF,    Magnetically controlled cyclic microscale deformation of in vitro cancer invasion models
- in-vitro, BC, MDA-MB-231
Ca+2↑, Intracellular calcium influx was observed in response to cyclic actuation, as well as an influence on cancer cell invasion from 3D spheroids, as compared to unactuated controls.
ATF3↑, 15 fold increase, fig 6
FOSB↑,

3567- MFrot,  MF,    The Effect of Extremely Low-Frequency Magnetic Field on Stroke Patients: A Systematic Review
- Review, Stroke, NA
*eff↑, All included studies showed a beneficial effect of ELF-MFs on stroke patients
*ROS↓, Improvements were observed in domains such as oxidative stress, inflammation, ischemic lesion size, functional status, depressive symptoms and cognitive abilities.
*Inflam↓,
*cognitive↑, An improvement in cognitive abilities reported in some of the included studies [25,26,27,28] is in line with other researchers’ finding
*Catalase↑, Cichoń et al. [27] also showed that catalase activity in erythrocytes and superoxide dismutase were significantly higher in the experimental group than in the control group.
*SOD↑,
*SOD1↑, similar effect was observed in regard to SOD1 and SOD2 mRNA levels.
*SOD2↑,
*GPx1↑, ELF-MFs impacted also the expression of GPx1 and GPx4 mRNA, which increased in the experimental group about 160% (p < 0.001) and 140% (p < 0.001), respectively.
*GPx4↑,
*IL1β↑, blood samples of IL-1β in the experimental group after 10 sessions of rehabilitation which involved ELF-MFs were significantly higher than in the control group
*neuroP↑, majority of the articles included in this study, a neuroprotective effect of ELF-MFs was indicated
*toxicity∅, Particularly noteworthy is the fact that none of the studies included in this review reported any negative side effects of ELF-MFs.

3535- MFrot,  MF,    Pulsed Electromagnetic Field Stimulation in Osteogenesis and Chondrogenesis: Signaling Pathways and Therapeutic Implications
- Review, Nor, NA
*eff↑, Pulsed electromagnetic fields (PEMFs) are currently used as a safe and non-invasive treatment to enhance bone healing and to provide joint protection.
*COL2A1↑, exposure to PEMFs induced increased collagen type II (Col2) expression and glycosaminoglycan (GAG) content
*SOX9↑, PEMFs significantly increased the expression of chondrogenic genes (SOX9, collagen type II, and aggrecan) and the deposition of cartilaginous matrix (sulphated GAG)
*Ca+2↑, Intracellular Ca2+ increase
*FAK↑, FAK activation
*F-actin↑, increased F-actin network formation
*Inflam↓, anti-inflammatory effect of PEMFs exposure has been extensively described above
*other↑, PEMFs exert a strong anti-inflammatory effect protecting cartilage tissue from the catabolic activity of pro-inflammatory cytokines.
*Diff↑, commonly recognized that PEMFs exposure induces osteogenic differentiation of MSCs
*BMD↑, Emerging evidence shows that PEMFs stimulation represents a safe non-invasive approach to favor bone repair and optimize bone tissue engineering

3499- MFrot,  MF,    Rotating magnetic field delays human umbilical vein endothelial cell aging and prolongs the lifespan of Caenorhabditis elegans
- in-vitro, Nor, HUVECs
*AntiAge↑, RMF exposure prolonged the lifespan of C. elegans and slowed the aging of HUVECs
*AMPK↑, RMF treatment of HUVECs showed that activation of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) was associated with decreased mitochondrial membrane potential (MMP) due to increased intracellular Ca2+ concentrations induced by endo
*mPGES-1↓,
*Ca+2↑,
*ER Stress↑,
*OS↑, prolonged lifespan of C. elegans was associated with decreased levels of daf-16 which related to the insulin/insulin-like growth factor signaling pathway (IIS) activity and reactive oxygen species (ROS),
*ROS↓,

3497- MFrot,  MF,    The Effect of a Rotating Magnetic Field on the Regenerative Potential of Platelets
- Human, Nor, NA
*PDGFR-BB↑, The highest concentration of PDGF-BB was observed in the samples placed in RMF for 1 h at 25 Hz
*TGF-β↑, For TGF-β1, the highest concentrations were obtained in the samples exposed to RMF for 3 h at 25 Hz and 1 h at 50 Hz.
*IGF-1↑, highest concentrations of IGF-1 and FGF-1 were shown in plasma placed in RMF for 3 h at 25 Hz.
*FGF↑,
*angioG↑, Magnetic fields have been shown to have a beneficial effect on vasodilation, angiogenesis, accelerating repair, regeneration, and healing of soft tissues, nervous tissues and bones, analgesic aspects, anti-swelling, reducing inflammation and pain, an
*Inflam↓,
*ROS↓, RMF exposure can increase resistance to heat stress, reduce levels of ROS, affect intracellular calcium ion concentrations, and contribute to cell aging deceleration

3496- MFrot,  GoldNP,  MF,    Enhancement of chemotherapy effects by non-lethal magneto-mechanical actuation of gold-coated magnetic nanoparticles
- in-vitro, Cerv, HeLa
eff↑, Here, we show how the MMA method based on magnetically-rotated gold-coated MNP boosts only the activity of an unbound antitumor drug, without physical damage of cells via MNP
tumCV↓, Au@MNP particles, slightly rotated by an external magnetic field, manages to be significantly more effective in decreasing tumor cell viability compared to chemotherapy alone.

3495- MFrot,  MF,    Synthesis of urchin-like nickel nanoparticles with enhanced rotating magnetic field-induced cell necrosis and tumor inhibition
- in-vivo, BC, NA
TumCG↓, UNNPs showed obvious suppression against tumor cell growth in a mouse model of malignant breast cancer under the induction of low-frequency RMF.

3494- MFrot,  MF,    Magnetically switchable mechano-chemotherapy for enhancing the death of tumour cells by overcoming drug-resistance
- in-vitro, Var, NA
eff↑, RMF exposure induces a mechanical movement to this nanomaterial, which can be exploited for (i) controllably releasing the anti-cancer drug for chemotherapy,
TumCD↑, (ii) promoting the death of tumour cells by means of mechanical forces exerted onto their membranes

3493- MFrot,  MF,    Mechanical nanosurgery of chemoresistant glioblastoma using magnetically controlled carbon nanotubes
- in-vivo, GBM, NA
TumCD↑, We show that GBM cells internalize mCNTs, the mobilization of which by rotating magnetic field results in cell death.
MMP↓, We detected the dissipation of mitochondria membrane potential of GBM cells upon mCNT + magnetic treatment
Cyt‑c↑, When mitochondria integrity is compromised, mitochondrial cytochrome C is released into the cytosol to initiate caspases-dependent apoptosis
Apoptosis↑,
OS↑, Consistent with tumor burden reduction, mCNT + magnetic field treatment significantly extended the survival of GBM-bearing mice (median survival: 22.2 ± 4.0 versus 26.8 ± 6.0 days, P = 0.0072; Fig. 3F).
DNAdam↑, Tumor cells in the treatment group also exhibited increased DNA damage

3492- MFrot,  Chemo,  MF,    Synergistic Effect of Chemotherapy and Magnetomechanical Actuation of Fe-Cr-Nb-B Magnetic Particles on Cancer Cells
eff↑, efficient cancer cell destruction by exploiting the magnetomechanical actuation (MMA) of Fe-Cr-Nb-B magnetic particles (MPs), which are loaded with clinically approved chemotherapeutic drugs.
TumCD↑, The parallelepipedic shape grants magnetic shape anisotropy to the particles, resulting in a significant rotational torque in the rotating magnetic field, which leads to the destruction of cancer cells.

3745- MFrot,  MF,    The neurobiological foundation of effective repetitive transcranial magnetic brain stimulation in Alzheimer's disease
- Review, AD, NA
*neuroP↑, neuroprotective actions aimed at mitigatingoxidative stress and inflammation, and intense stimulation of neu-rotrophic factors
*ROS↓,
*Inflam↓,
*5HT↑, increase in serotoninand its metabolites and a change in the properties of serotonergicreceptors.
*cFos↑, in rats, a single session of bothLF- (1 Hz) and HF-rTMS (10 Hz) enhanced c-Fos expression in all exam-ined cortical areas
*Aβ↓, rTMS enhances neuronal viability and counteracts oxidative stressors, such as Aβ and glutamate toxicity, in vitro
*memory↑, downregulation results in memory impairments
*BDNF↑, long-term change in synaptic proteinexpression due to BDNF-TrkB pathway activation following rTMSprotocols
*Ach↑, rTMSincreases ACh levels by modulating AChE activity.
*AChE↓,
*cognitive↑, HF-rTMS (20 Hz) and LF-rTMS (1 Hz)—in termsof neurotransmitter circuits and neurogenic signaling. 142 While bothprotocols improved cognition-related behaviors
*BDNF↑, Notably, rTMS could enhance BDNF and NGF expression irrespec-tive of frequency,
*NGF↑,
*β-catenin/ZEB1↑, both LF-rTMS (1 Hz) and HF-rTMS (10 Hz)protocols enhanced cognitive performance through the activation of β-catenin via the regulation of glycogen synthase kinase-3β (GSK-3β) andTau
*p‑Akt↓, 3 weeks, iTBS reducedinflammation and increased anti-inflammatory molecules, specificallylinked to reversing the downregulation of phosphorylated forms ofAkt and the mammalian target of rapamycin.
*mTOR↓,
*MMP1↓, 6 months, patients showed significant reductions in plasma levels of MMP1, MMP9, and MMP10, along with increases in TIMP1 and TIMP2
*MMP9↓,
*MMP-10↓,
*TIMP1↑,
*TIMP2↑,

3489- MFrot,  MF,    Rotating magnetic field inhibits Aβ protein aggregation and alleviates cognitive impairment in Alzheimer's disease mice.
- in-vivo, AD, NA
*Aβ↓, RMF directly inhibited Aβ amyloid fibril formation and reduced Aβ-induced cytotoxicity in neural cells .
*motorD↑, RMF restored motor abilities to healthy control levels and significantly alleviated cognitive impairments, including exploration and spatial and non-spatial memory abilities.
*cognitive↑,
*memory↑,
*ROS↓, reduced oxidative stress in the APP/PS1 mouse brain.

3488- MFrot,  MF,    Rotating magnetic field improves cognitive and memory impairments in APP/PS1 mice by activating autophagy and inhibiting the PI3K/AKT/mTOR signaling pathway
- in-vivo, AD, NA
*cognitive↑, RMF treatment significantly ameliorated their cognitive and memory impairments, attenuated neuronal damage, and reduced amyloid deposition.
*memory↑,
*neuroP↑,
*Aβ↓,
*PI3K↓, RMF improves cognitive and memory dysfunction in APP/PS1 mice by activating autophagy and inhibiting the PI3K/AKT/mTOR signaling pathway, thus highlighting the potential of RMF as a clinical treatment for hereditary AD.
*Akt↓,
*mTOR↓,

2311- MFrot,  MF,    Magnetic fields as a potential therapy for diabetic wounds based on animal experiments and clinical trials
- in-vivo, Nor, HaCaT
*COX2/PTGS2↓, ELF‐EMF exposure enhances the proliferation of keratinocyte HaCaT cells and improves early NOS activity, while decreases cyclooxygenase 2 (COX‐2) which indicates its role in accelerating the transition from inflammation phase to remodelling phase.
*Inflam↓,
*MMP9↑, Exposure to ELF‐EMF with frequency of 50 Hz and intensity of 1 mT increases cytokine release and activates the expression of MMP‐9 in human immortalized keratinocytes
*GPx↑, On the contrary, ELF‐EMF activates glutathione peroxidase with decrease in malondialdehyde in the live tissue of rats during wound healing process
*Diff↑, ELF‐EMF promotes the proliferation and differentiation of transplanted epidermal stem cells in the full‐thickness defect nude mice

2262- MFrot,  MF,    Effects of 0.4 T Rotating Magnetic Field Exposure on Density, Strength, Calcium and Metabolism of Rat Thigh Bones
- in-vivo, ostP, NA
*BMD↑, strong magnetic field (MF) exposure could effectively increase bone density and might be used to treat osteoporosis
*eff↓, calcium supplement tended to increase the indexes of thigh bone density, energy absorption, maximum load, maximum flexibility, and elastic deformation
*ALP↑, alkaline phosphatase (ALP), serum phosphate, and serum calcium were higher in rats exposed to RMF with calcium
*other↑, RMF is in fact capable of increasing density, strength, calcium, and metabolism in bones

2259- MFrot,  MF,    Method and apparatus for oncomagnetic treatment
- in-vitro, GBM, NA
MMP↓, Oncomagnetic patent Fig 2
Bcl-2↓,
BAX↑,
Bak↑,
Cyt‑c↑,
Casp3↑, caspase staining rises progressively until after 30 min most of the cells fluoresce positive for caspase, revealing activation of this enzyme
Casp9↑,
DNAdam↑,
ROS↑, applying the oscillating magnetic field to the tissue increases the production of reactive oxygen species (ROS )
lactateProd↑,
Apoptosis↑,
MPT↑, opening of the mitochondrial membrane permeability transition pore
*selectivity↑, repetitive magnetic stimulation has shown decreased apoptosis in non -cancerous cells .
eff↑, oncomagnetic therapy may be performed in conjunction with other forms of therapy such as with chemotherapy, other forms of radiative therapy, with drugs and prescriptions, etc
MMP↓, OMF which in turn produces rapidly fluctuating or sustained depolarizations of the mitochondrial membrane potential (MMP) in the tissue .
selectivity↑, Because normal cells have a larger amount of mitochondria, have lower demand for ATP, and are not under stress, disruption of electron flow and small amount of ROS formation and MMP depolarization does not trigger apoptosis
TCA?, decrease in Krebs cycle metabolites
H2O2↑, increase in peroxide levels in GBM cells following stimulation by the system 100 using a rotating magnet
eff↑, combine the administration of BHB , or acetoacetate , or free fatty acid, or branched chain amino acid, or cryptochrome agonist , or MGMT inhibitor, or DNA alkylating agent, or DNA methylating agent, and OMF as a more effective treatment of cancer
*antiOx↑, upregulation of antioxidant mechanisms due to the application of OMFs further protects non -cancerous cells from any ROS -mediated apoptosis
H2O2↑, The experiments showed rapid increases in the levels of superoxide and H2O2 in GBM cells
eff↓, To test whether cell death is caused by the OMF - induced increase in ROS , a potent antioxidant Trolox was used to counteract it, while measuring the decrease in GBM cell count due to 4 h exposure to OMF.
GSH/GSSG↓, GSH/GSSG ratio almost exactly half that seen in control cells
*toxicity∅, No Cytotoxic Effect in Normal Cells
OS↑, OMF -Induced Prolongation of Survival in a Mouse Xenograft Model of GBM

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↓, GBM patient reversed the progression of his recurrent tumor causing >30% reduction in its contrast-enhanced volume within 4 weeks of treatment
OS↑, Mice with implanted mouse glioma cells in their brains also showed marked reduction in tumor size, increased survival (p< 0.05, n = 10)
γH2AX↑, higher DNA damage (g-H2AX foci) after sOMF treatment with a whole-body stimulation method developed by us
DNAdam↑,
selectivity↑, Normal mice exposed to sOMF for 4 months had no adverse effects on the brain and other organs
ROS↑, sOMF markedly increased reactive oxygen species (ROS) levels in cancer cells leading to the selective death of these cells, while sparing normal neurons and astrocytes
TumCD↑,
eff↑, sOMF exposure for just 2 h resulted in >40% loss of surviving GBM and DIPG cell colonies detected by clonogenic cell survival assay, similar to that produced by 2 Gy radiation dose.
eff↓, This loss was rescued by the antioxidant Trolox

1737- MFrot,  Fe,  MF,    Feature Matching of Microsecond-Pulsed Magnetic Fields Combined with Fe3O4 Particles for Killing A375 Melanoma Cells
- in-vitro, MB, A375
Dose∅, current amplitude of 1640 A, a pulse width of 28 μs and a frequency of 1 Hz nanorods, with a length of about 100 nm and a diameter of about 20 nm strongest magnetic flux density at the center of the coil reaching 1.96 T.
tumCV↓, killing rate of μs-PMF with nanorods was 39.6% higher than that of μs-PMF alone

595- MFrot,  VitC,  MF,    The Effect of Alternating Magnetic Field Exposure and Vitamin C on Cancer Cells
- in-vitro, PC, MIA PaCa-2 - in-vitro, CRC, SW-620 - in-vitro, NA, HT1080 - in-vitro, Pca, PC3 - in-vitro, OS, U2OS - in-vitro, BC, MCF7 - in-vitro, Nor, CCD-18Co
TumCD↑, An 80 percent cell death (20 percent survival) was achieved with 160 mg/dL of vitamin C in the magnetic field treatment group. It required 360 mg/dL to achieve the same effect with vitamin C only treatment group.
eff↑, vitamin C combined with low frequency magnetic field or rotating magnetic field reduces the amount of vitamin C to induce 50 percent inhibition of tumor cells.
*TumCG∅, For normal cell line of colon fibroblast magnetic field did not potentiate inhibition of cell growth. These are all mono-layer cell culture.

7382- MFrot,    Inhibition of mitochondrial NADH:ubiquinone oxidoreductase by spinning oscillating magnetic fields causes toxicity in cancer cells
- vitro+vivo, GBM, NA
ROS↑, (sOMF) produced by this device is reactive oxygen species-dependent persistent inhibition of mitochondrial complex I.
compI↓,
DNAdam↑, Steps downstream of this mechanism involve the production of oxidative stress, DNA damage, G1 phase cell cycle arrest, and caspase-dependent apoptosis.
TumCCA↑,
Casp↓,
Apoptosis↑,
mt-NADH↓, Inhibition of mitochondrial NADH
selectivity?, We also show that sOMF does not produce these effects in normal human astrocytes and astroglial cells. These data provide a rationale for safe clinical use of OMD.
*toxicity?,

8482- MFrot,    Polyhedral magnetic nanoparticles induce apoptosis in gastric cancer stem cells and suppressing tumor growth through magnetic force generation
- vitro+vivo, GC, NA
*Apoptosis↑, Under a rotating magnetic field of 15 Hz, PMNPs induced apoptosis and ferroptosis in MCSCs by disrupting cellular structures.
*Ferroptosis↑,
*Dose?, utilizing polyhedral magnetic nanoparticles (PMNPs) functionalized with CD44 antibodies and cell-penetrating peptides (CPPs) to improve uptake by gastric cancer stem cells (MCSCs).
*CellMemb↑, Functionalization enhanced their uptake capabilities. Under a rotating magnetic field (RMF) of 15 Hz, PMNPs disrupted cellular structure, leading to apoptosis and ferroptosis in MCSCs
*tumCV↓, in vitro studies showed significant reduction in MCSCs viability, while in vivo studies demonstrated tumor growth suppression with minimal side effects and high biocompatibility.
*TumCG↓,

8481- MFrot,    Therapeutic Magnetic Fields in Oncology: A Systematic Review of Safety and Supportive Clinical Use
- Review, Var, NA
*toxicity↓, Current evidence does not support the assumption that therapeutic magnetic fields are inherently harmful in oncological patients
*PFS∅, Low-frequency rotating static magnetic field (0.4 T; 7.5 Hz). No significant differences were observed between groups in PFS, ORR, or DCR
*ORR∅,
*DCR∅,
*other↝, Hand-held device (MAGCELL MICROCIRC): rotating magnetic disc 4-12 Hz, 5-min cycles; surface flux density ~420 mT peak-to-peak . NCV(Nerve Conduction) improved at T3 in MFT. CTCAE(adverse events)improved vs placebo
*TumCG↓, may even be associated with reduced tumor growth compared with controls [30].

8480- MFrot,    Neuroprotective effect of RMF in a mouse model of sporadic Parkinson's disease
- in-vivo, Park, NA
*Dose↝, CblC mice were injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (30 mg/kg, i.p., once daily for 5 days), followed by RMF treatment at a frequency and intensity of 4 Hz and 0.4 T, respectively.
*Dose↝, The daily 2-h RMF treatment was continued for a period of 6 months.
*motorD↑, Our results showed that exposure to RMF improved motor functions, enhanced neuronal cell viability and protected neuronal integrity in a PD mouse model.
*ROS↓, We further showed that RMF diminishes the number of aggregated Lewy bodies in neurons and reduces ROS production.

8479- MFrot,  doxoR,    Dual-targeting by rotating magnetic field-driven superparamagnetic bionic nanorobots for enhanced triple-negative breast cancer therapy
- vitro+vivo, BC, 4T1
Dose?, we engineered rotating magnetic field-driven nanorobots (MFDNs) comprising DOX-loaded hollow mesoporous iron oxide nanoparticles
EPR↑, Under a rotating magnetic field (RMF; 5 Hz, 100 mT), MFDNs self-assemble into dynamic chains, evading the aggregation that plagues static magnetic field approaches and enabling deep intratumoral penetration.
BioEnh↑, active navigation via RMF, delivers a three-fold higher intracellular DOX concentration than uncoated carriers
GSH↓, Mechanistically, MFDNs depleted intracellular glutathione by 70%, suppressed glutathione peroxidase-4 (GPX4), and elevated Fe2+ , reactive oxygen species (ROS), and lipid peroxidation, thereby triggering robust ferroptosis
GPx4↓,
Iron↑, This finding supports the hypothesis that MFDNs effectively induce ferroptosis by increasing intracellular Fe2+ levels and subsequent ROS production.
ROS↑,
lipid-P↑,
Ferroptosis↑,
TumVol↓, In 4T1 tumor-bearing mice, intravenous MFDNs plus RMF shrank tumors by 90% compared with 45% for free DOX, without systemic toxicity or weight loss.
Fenton↑, enhancing the Fenton reaction, and promoting lipid peroxidation in tumor cells

8478- MFrot,    Dynamic magneto-mechanical force in lysosomes induces durable macrophage repolarization for antitumor immunity
- vitro+vivo, Lung, NA
Dose↝, Here, we developed a magneto-mechanical force-triggered lysosomal membrane permeabilization (MagLMP) strategy to induce durable macrophage repolarization for in vivo applications.
Dose↝, Self-assembled magnetic nanomotors are driven by rotational magnetic fields, facilitating dynamic damage to the lysosomal membrane by a finely tuned torque-induced vortex
AMPK↑, Intriguingly, galectin 9 (Gal9) was found to be critical for sensing cyclic MagLMP, which dynamically activated AMP-activated protein kinase (AMPK), enhanced activation of nuclear factor kappa B (NF-κB),
NF-kB↑,
pol-M1↝, and induced metabolic alterations for sustained M1-like macrophage repolarization, followed by mounting of antitumor immunity.
OS?, In a mouse model of lung adenocarcinoma in situ, overall survival was extended after intravenous administration of nanomotors followed by cyclic MagLMP, and one third of mice survived for more than 300 days.
Dose↝, A cubical MNM (25.0 ± 2.6 nm) was designed to passively target lysosomes; it consisted of a magnetic nanoparticle (MNP) coated on the surface with polylysine (PLL) and had the ability to self-assemble into elongated rod-like microstructures
Dose↝, significant increase in rotational activity was observed when the field strength increased from 4 mT to 20 mT
eff↝, The results suggested that the self-assembly behavior of MNMs was frequency dependent, consistent with the results of mathematical models (Fig. 1e; Supplementary information, Fig. S1k).
eff↑, These results demonstrated that the optimal stimulation frequency for reversible LMP was ~1 Hz, as this frequency produced the desired permeabilization effect without causing permanent damage to the lysosomes.

8477- MFrot,    Urchin-like magnetic nanoparticles loaded with type X collagen siRNA and Stattic to treat triple negative breast cancer under rotating magnetic field like an "enchanted micro-scalpel"
- Study, BC, NA
TumCD↑, Urchin-like magnetic nanoparticles (UMN) with abundant spike-like structures exhibit superior magneto-mechanical force to destroy tumor cells compared with other shapes of magnetic nanoparticles.
Dose↝, Stattic (STAT3 inhibitor) and COL10A1 siRNA were loaded onto the UMN@PEI to form UMNP/St/si.
CellMemb↑, The RMF drove UMNP/St/si disrupted the cell membrane, promoted cell death.

8476- MFrot,    Actin-Targeted Magnetic Nanomotors Mechanically Modulate the Tumor Mechanical Microenvironment for Cancer Treatment
- in-vitro, Var, NA
Dose↝, Here, we propose an actin-binding protein-modified magnetic nanomotor (ABP-MN) coupled with the rotating magnetic field (MF) to dynamically regulate the actin cytoskeleton for remodeling the TMME.
TumCG↓, Cancer-associated fibroblasts (CAFs) and tumor cells, which internalize ∼69.3% of ABP-MNs, are significantly tuned under MF with signs of a 7-fold decrease in tumor matrix stiffness, increased immune cell infiltration, and 95.8% tumor growth inhibi
other↝, This strategy unlocks a fresh field to reshape the TMME with the intracellular mechanical approach, thereby providing an effective mechano-based therapy in treating solid tumors

7388- MFrot,    Magnetoporation and magnetolysis of cancer cells via carbon nanotubes induced by rotating magnetic fields
- in-vitro, BC, MCF7
EPR↑, Weak magnetic fields (40 and 75 mT) were used either to enhance cell membrane poration
Dose?, Rotation speed of the visible MWCNT (5% impurity) bundles ranged from 12 to 20 rpm; the rotation of MWCNTs with 9% impurity was faster (18 to 28 rpm)

7386- MFrot,    ONCOSCILLATORS: INDUCTION OF THE MITOCHONDRIAL PERMEABILITY TRANSITION IN CANCER CELLS
- in-vitro, Var, NA
ETC↓, Using OMF of appropriate field strength, frequency and on/off acceleration/deceleration profiles we can completely arrest electron transport in isolated respiring rat liver mitochondria.
H2O2↑, Parallel to this inhibition of electron flux, we also independently observe an increase in superoxide and hydrogen peroxide
MPT↑, OMF generated by oncoscillators can induce mitochondrial permeability transition in primary cultured malignant meningioma, diffuse intrinsic pontine glioma and GBM cells.

516- MFrot,  immuno,  MF,    Anti-tumor effect of innovative tumor treatment device OM-100 through enhancing anti-PD-1 immunotherapy in glioblastoma growth
- vitro+vivo, GBM, U87MG
TumCP↓,
Apoptosis↑,
TumCMig↓,
ROS↑, treatment with OM-100 led to an increase in intracellular ROS levels
PD-L1↑, upregulating PD-L1 expression, thereby enhancing the efficacy of anti-PD-1 immunotherapy
TumVol↓, in mice
eff↑, enhance the efficacy of anti‑PD‑1 immunotherapy in vivo
*toxicity∅, OM-100 did not result in noteworthy changes in the blood routine parameters (Gran, HCT, HGB, Lymph, MCH, MCV, PLT, RBC, MPV, and WBC) and biochemical indicators (ALT, AST, T-BIL, CREA, TG, TC, HDL-c, and LDL-c) in normal mice
eff↑, Particularly, there was a more pronounced response to anti-PD-1 therapy in patients whose tumors expressed PD-L1 3
*toxicity∅, OM-100 treatment in healthy mice showed no adverse effects, indicating its safety for normal tissues.
Dose↝, 24-day treatment with a magnetic field intensity of 1.066 mT and a frequency of 100 kHz (figure shows motor driven 120Hz, 7200rpm pulsed
tumCV↓, anti-tumor efficacy of OM-100 treatment, which by impairing cell viability, increasing apoptosis, inhibiting cell migration, and invasion capabilities, as well as promoting oxidative stress.
TumCI↓,

5535- MFrot,    Spatiotemporal magnetic fields enhance cytosolic Ca2+ levels and induce actin polymerization via activation of voltage-gated sodium channels in skeletal muscle cells
- in-vitro, Nor, NA
*Dose↝, We used complex spatiotemporal magnetic fields (17–70 mT) to control intracellular signaling in skeletal muscle cells
*Vm/CMP↑, By changing different parameters of the alternating magnetic field (amplitude, inversion time, rotation frequency), we induced transient depolarization of cellular membranes
*Na+↑, leading to i) Na+ influx through voltage-gated sodium channels (VGSC), ii) cytosolic calcium increase, and iii) VGSC- and ryanodine receptor-dependent increase of actin polymerization.
*VGSC↑, ion fluxes occurred only, when the field was applied and returned to baseline after the field was turned off.
*Vm/CMP↑, mediates a local change in the membrane potential triggering the activation of VGSC.

5245- MFrot,  Rad,    The hemoprotective effects of a rotary magnetic field in mice exposed to γ irradiation
- in-vivo, Nor, NA
*OS↑, The RMF treatment increased the survival rate and survival days among the irradiated mice
*radioP↑, RMF treatment had an obvious protective effect against the effects of irradiation and it accelerated the recovery of hematopeiesis and the hematopoietic microenvironment in mouse bone marrow

5244- MFrot,    The growth dynamics of Walker carcinosarcoma during exposure to a magnetic eddy field
- in-vitro, Var, NA
TumCG↓, The influence of rotational magnetic field on Walker's carcinosarcoma growth was studied. The antitumor effect of the field was established. In some cases, tumor growth was inhibited by more than 80-90%. The antitumor effect was related to induction

5243- MFrot,    The assessment of the efficacy of the effect of a rotational magnetic field on the course of the tumor process in patients with generalized breast cancer
- Human, BC, NA
OS↑, A significant response was achieved in 27 of 51 patients.
eff↑, A significant response was achieved in 27 of 51 patients.

5242- MFrot,    Rotating magnetic field downregulating type XI collagen to suppress triple-negative breast cancer metastasis by inactivating the ITGB1/FAK/YAP signaling pathway
- in-vitro, BC, NA
TumCI↓, RMF can significantly inhibit the invasion and metastasis of TNBC cells.
COL11A1↓, Notably, COL11A1 was reduced following exposure to RMF.
TumCG↓, both COL11A1 siRNA and RMF effectively suppressed tumor growth and lung metastasis, an effect reversed by ITGB1 agonist.
TumMeta↓,
ITGB1↓, suppress triple-negative breast cancer metastasis by inactivating the ITGB1/FAK/YAP signaling pathway
FAK↓,
YAP/TEAD↓,
Dose↝, we selected two magnetic field frequencies (2.5 and 5 Hz) and three magnetic induction intensities (0.04, 0.2, and 0.41 T) for investigation.

4569- MFrot,    Case Report: A new noninvasive device-based treatment of a mesencephalic H3 K27M glioma
- Case Report, GBM, NA
Dose↝, treatment was for 2 hours on the first day with a 5-min break between the first and the second hour.
Dose↑, On the second day, two 2-hour sessions were conducted with a 1-hour break between the sessions.
Dose↑, 2-hour sessions was increased to three on the third day
OS↑, The longest documented survival for an adult with H3K27A brainstem DMG is 23 months (6). The patient in the present study survived for 30 months
toxicity↓, OMT was well tolerated by the patient
ETC↓, underlying mechanism of action of sOMF in DMG is analogous to that in GBM, involving disruption of electron transport in the mitochondrial respiratory chain, with release of ROS producing cancer cell oncolysis ()
ROS↑,

4567- MFrot,    Oncogenic pathways and the electron transport chain: a dangeROS liaison
- Review, Var, NA
ROS↑, In this review, we focus on the ETC as a source of ROS and its modulation by oncogenic pathways, which generates a vicious cycle that resets ROS levels to a higher homoeostatic set point, sustaining the cancer cell phenotype.
ETC↓, Electrons leaking from the ETC can prematurely react with oxygen, resulting in the generation of reactive oxygen species (ROS).
other↝, ETC-derived ROS are pivotal regulators of cell fate, given the central role of mitochondria in life and death.
Fenton↑, The hydroxyl radical (•OH) is a highly damaging ROS with an extremely short half-life that is generated from H2O2 in the presence of iron or copper through the Fenton reaction.
RNS↑, O2•– can also interact with nitric oxide (NO), generating the reactive nitrogen species (RNS) peroxynitrite (ONOO−), which controls signalling molecules through the nitration of tyrosine residues

4566- MFrot,    On the mitochondrial aspect of reactive oxygen species action in external magnetic fields
- Study, Var, NA
ROS↑, formation of reactive oxygen species requires electron leakage from the normal route in the respiratory chain.
ETC↓, leakage
selectivity↑, For all those reasons, it can be expected that coapplication of a low external magnetic field and mitochondrial inducers of reactive oxygen species should damage cancer cells without any detriment to the normal cells.

195- MFrot,  MF,    Application of Rotating Magnetic Fields Increase the Activity of Antimicrobials Against Wound Biofilm Pathogens
- Human, Wounds, NA
Bacteria↓, Our results suggest that RMF as an adjunct to antiseptic wound care can significantly improve antibiofilm activity

209- MFrot,  MF,    The effect of a rotating magnetic field on the antioxidant system in healthy volunteers - preliminary study
- Human, NA, NA
*SOD↑, RFM can reduce oxidative stress, as evidenced by higher SOD and CAT activities in the CG than in samples placed in the RFM.
*Catalase↑,
*ROMO1↑, required 3hrs
*MDA↓, Too long a stay in the RMF at the frequency of 50 Hz increased the level
*TAC↑, RFM at 50 Hz increased the TAC level,
*ROS↓, In the case of ROMO1, it is stated that 1 h 25 Hz are the optimal conditions for no increased production of ROS.

205- MFrot,  MF,    Intermittent F-actin Perturbations by Magnetic Fields Inhibit Breast Cancer Metastasis
- vitro+vivo, BC, MDA-MB-231
OS↑, 31-46% prolonged survival
F-actin↓, decrease F-actin formation in vitro and in vivo
TumCI↓,
TumCMig↓, >4.5hrs
Rho↓,
selectivity↑, F-actin in noncancerous breast cells is much less sensitive than that in breast cancer cells, which indicate that the normal cells in our human bodies are less likely to be agitated by these magnetic fields.
TumMeta↓, Using an intermittent treatment modality, low-frequency rotating magnetic fields could significantly reduce mouse breast cancer metastasis, prolong mouse survival by 31.5 to 46.0% (P < 0.0001), and improve their overall physical condition.

204- MFrot,  MF,    Rotating magnetic field improved cognitive and memory impairments in a sporadic ad model of mice by regulating microglial polarization
- in-vivo, AD, NA
*NF-kB↓, RMF improves memory and cognitive impairments in a sporadic AD model, potentially by promoting the M1 to M2 transition of microglial polarization through inhibition of the NF-кB/MAPK signaling pathway.
*MAPK↓,
*TLR4↓,
*memory↑,
*cognitive↑,
*TGF-β1↑, RMF treatment promoted the expression of anti-inflammatory cytokines (TGF-β1, Arg-1, IL-4, IL-10)
*ARG1/2↑, Arg-1
*IL4↑,
*IL10↑,
*IL6↓,
*IL1↓, IL-1β
*TNF-α↓,
*iNOS↓,
*ROS↓, in mice brain
*NO↓, in serum
*MyD88↓,
*p‑IKKα↓, phosphorylated IKKα/β, IкBα, NF-кB p65, JNK, p38,
*p‑IκB↓, IкBα
*p‑p65↓,
*p‑JNK↓,
*p‑p38↓,
*ERK↓,
*neuroP↑, RMF treatment resulted in reduced aluminum deposition in the brains of AD mice.
*Aβ↓, RMF treatment reduced Aβ deposition in the AD model mice

203- MFrot,  MF,    Rotating Magnetic Field Induced Oscillation of Magnetic Particles for in vivo Mechanical Destruction of Malignant Glioma
- vitro+vivo, GBM, U87MG
lysoMP↓, tear the lysosomal membrane
TumVol↓, 1hr, 40% distroyed
eff↑, MPs can be internalized into the glioma cells and induce apoptosis under a rotating magnetic field
Apoptosis↑, Intratumoral MPs induces apoptosis
Ca+2↑, induce chemical ionic signal such as calcium to nitiate programmed cell death upon exposure to an alternating field [9].

202- MFrot,  MF,    Systematic simulation of tumor cell invasion and migration in response to time-varying rotating magnetic field
- Analysis, Var, MDA-MB-231
TumCG↓, inhibit tumor progression
MMPs↓,
ECM/TCF↓,

201- MFrot,  MF,    Gradient Rotating Magnetic Fields Impairing F-Actin-Related Gene CCDC150 to Inhibit Triple-Negative Breast Cancer Metastasis by Inactivating TGF-β1/SMAD3 Signaling Pathway
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549 - in-vitro, BC, MDA-MB-468
CCDC150↓, magnetic field response gene
TGF-β↓,
SMAD3↓,

200- MFrot,  MF,    Moderate intensity low frequency rotating magnetic field inhibits breast cancer growth in mice
- in-vivo, BC, MDA-MB-231 - in-vivo, BC, MCF7
ALAT↓,
TumVol↓, reduced tumor size in LF-RMF group. In the end of the experiment on day 11, the tumor was removed and weighted, which showed a 35% reduction in tumor weigh
TumCCA↑, They found that RMF could disturb the cell cycle and change midkine (MK) expression in cancer cells
TumCG↓, 0.4 T, 7 Hz LF-RMF inhibited the growth and metastasis of melanoma cancer B16-F10 cells and improved immune function of tumor-bearing mice
TumMeta↓,
Imm↑,
P53↑, LF-RMF inhibits iron metabolism and suppresses lung cancer through activation of P53-miR-34a-E2F1/E2F3 pathway in mice
ALAT↓, However, it was interesting that we observed reduced ALT (118.70 ± 95.81 to 62.83 ± 44.33, a 47% reduction, p = 0.2243) and AST (187.50 ± 46.54 to 155.70 ± 66.61, a 17% reduction, p = 0.3599) (Table 2), although statistically not significant
AST↓,

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↝, (i) WMF can evoke new tissue production/regeneration (stem cell proliferation and subsequent differentiation) due to manipulation of ROS levels and also downstream heat shock protein 70 (Hsp70) expression
*other↝, (ii) The magnetic field causes changes in membrane potential and temporary membrane permeabilization that affects sodium content and potassium-efflux or the transmembrane voltage
*other↝, (iii) The calcium gradient between the extracellular and intracellular fluid is a transduction second messenger [28], and its gradient could potentially be affected by EMFs and MFs.
*other↝, (iv) MF may induce changes in enzymatic activities (e.g., enzymes involved in mitochondrial metabolism).
*other↝, (v) MF may cause cytoskeletal organization (due to reorganization of the electrostatically negative charged actin filaments), and those changes may affect the cellular shape, endoplasmic reticulum, mitotic apparatus
*other?, vi) Finally, the RMF creates the mixing process at the micro-level and may affect the energy level; some of the selected molecules strongly influence the transfer processes between the living cells and the culture medium

198- MFrot,  MF,    Biological effects of rotating magnetic field: A review from 1969 to 2021
- Review, Var, NA
AntiCan↑, RMF can inhibit the growth of various types of cancer cells in vitro and in vivo and improve clinical symptoms of patients with advanced cancer.
breath↑, 0.4T, 7Hz RMF was applied to treat 13 advanced non-small cell lung cancer patients (2 h/day, 5 days per week, for 6–10 weeks)
Pain↓, Decreased pleural effusion (2 patients, 15.4%), remission of shortness of breath (5 patients, 38.5%), relief of cancer pain (5 patients, 38.5%), increased appetite (6 patients, 46.2%), improved physical strength (9 patients, 69.2%), regular bowel mov
Appetite↑,
Strength↑,
BowelM↑,
TumMeta↓, The same RMF (2 h/day, for 43 days) can also suppress the growth and metastasis of B16-F10 cells in vivo
TumCCA↑, The up-regulated transcription of miR-34a induced cell proliferation inhibition, cell cycle arrest, and cell senescence by targeting E2F1/E2F3, two members of E2F family which are major regulators of the cell cycle,
ETC↓, 2h exposure) effectively inhibited the growth of two types of cultured brain cancer cells, glioblastoma cells and diffuse intrinsic pontine glioma cells. They found that the mitochondrial electron transport chain was significantly disturbed by RMF,
MMP↓, which caused loss of mitochondrial integrity, decreased mitochondrial carbon flux in cancer cells, and eventual cancer cell death (Sharpe et al., 2021).
TumCD↑,
selectivity↑, same group further reported that the same RMF can also selectively kill cultured human glioblastoma and non-small cell lung cancer cells, and leave normal cells unharmed
ROS↑, Mechanistic studies revealed that RMF can increase the mitochondrial ROS level, which further activated the caspase-3 and disturbed the electron fflow in the respiratory chain pathway in cancer cells. (Helekar et al., 2021).
Casp3↑,
TumCG↓, 0.4T, 7.5Hz RMF (2 h/day, for 5 days) inhibited the growth of mouse melanoma cell line B16–F10 in vitro,
TumCCA↑, and its mechanism involved cell cycle arrest and decomposition of chromatins.
ChrMod↑,
TumMeta↓, (2 h/day, for 43 days) can also suppress the growth and metastasis of B16–F10 cells in vivo,
Imm↑, benefiting from improved immune function, including decreased regulatory T cells, increased T cells, and dendritic cells
DCells↑,
Akt↓, inhibiting the activation of the AKT pathway (Tang et al., 2016). T
OS⇅, 51 women with advanced breast cancer underwent RMF treatment. The results showed that 27 patients among them achieved signicant therapeutic effects, and there were no side-effects
toxicity↓,
QoL↑, 13 advanced non-small cell lung cancer patients the quality of life was improved in different degrees. Median survival and 1-year survival rate was 50% and 100% longer
hepatoP↑, In addition, it seems that the RMF can also attenuate liver damage in mice bearing MCF7 and GIST-T1 cells (Zha et al., 2018)
Pain↓, The results showed that the RMF treatment reduced abdominal pain by 42.9% (9/21), nausea/vomiting by 19.0% (4/21), weight loss by 52.4% (11/21), ongoing blood loss by 9.5% (2/21), improved physical strength by 23.8% (5/21) and sleep quality by 19.0%
Weight↑,
Strength↑,
Sleep↑,
IL6↓, Furthermore, decreased levels of interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and keratinocyte-derived chemokine (KC) were observed
CD4+↑, it was discovered that macrophages and dendritic cells were activated, CD4+ T and CD8+ T lymphocytes increased, and the ratio of Th17/Treg was balanced.
CD8+↑,
Ca+2↑, effects of RMF were strongly associated with increased calcium tunnel activity and intracellular Ca2+ level in CNS
radioP↑, These results suggest that RMF may be helpful to alleviate the damage of hematopoietic function caused by radiotherapy and chemotherapy
chemoP↑,
*BMD↑, 0.4T, 8Hz RMF treatment (30min/day, for 30 days) along with calcium supplement, synergistically improved bone density
*AntiAge↑, In 2019, Xu et al. reported that a 4h exposure to a 0.2T, 4Hz RMF delayed the aging of human umbilical vein endothelial cells (HUVEC)
*AMPK↑, Mechanistic research revealed that RMF treatment increased the expression of AMPK while reducing the expression of p21, p53 and mTOR.
*P21↓,
*P53↓,
*mTOR↓,
*OS↑, They also discovered that the RMF (2 h/day, for 6, 10 or 14days) can prolong the health status lifespan of Caenorhabditis elegans.
*β-Endo↑, 0.1–0.8T, 0.33Hz RMF treatment signicantly increased the β-endorphin level in the blood of rabbits and humans (23 times higher than before). Moreover, it decreased serotonin (5-HT) in brains, small intestine tissue and serum of mice.
*5HT↓,

212- MFrot,  MF,    Rotating magnetic field inhibits Aβ protein aggregation and alleviates cognitive impairment in Alzheimer’s disease mice
- in-vivo, AD, SH-SY5Y
*β-Amyloid↓, Aβ amyloid fibril formation
*cognitive↑,
*motorD↑, RMF improves motor and exploration abilities in APP/PS1 mice
*ROS↓, RMF reduces oxidative stress in APP/PS1 mouse brains and lipid deposition in the liver
*memory↑, RMF significantly alleviates spatial memory impairments in APP/PS1 mice
*Aβ?, 0.4 T RMF inhibits Aβ amyloid fibril formation in vitro

193- MFrot,  MF,    Rotating Magnetic Field Mitigates Ankylosing Spondylitis Targeting Osteocytes and Chondrocytes via Ameliorating Immune Dysfunctions
- in-vivo, Arthritis, NA
BMD↑, loss reduced
Cartilage↑, more intact cartilage surfaces and denser proteoglycan
IL17↓,
IL22↓,
IL23↓,
IL28↓,
CD4+↓, tremendously attenuated
CD8+↓, In this investigation, data showed that RMF treatment decreased CD3-expressing proliferative cells via immunostaining and reduced CD4+/CD8+ T-cells via flow cytometry in AS mice
LAMB3↑,
COL4↓,
THBS2↓,
ITGA11↓,
PPARγ↑, mice have decreased expression of peroxisome proliferator-activated receptor γ (PPAR-γ), a ligand-activated transcription factor belonging to the nuclear hormone receptor superfamily, which RMF reverses.
ACAA1↓,
PLIN1↓,
FABP4↓,
PCK1↓,
UCP1↓,
TNF-α↓,


Showing Research Papers: 1 to 50 of 76
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 76

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

compII↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ATF3↑, 1,   compI↓, 1,   Fenton↑, 2,   Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 2,   GSH↑, 1,   GSH/GSSG↓, 2,   H2O2↑, 4,   mt-H2O2↑, 1,   Iron↑, 1,   lipid-P↑, 1,   mt-NADH↓, 1,   RNS↑, 1,   ROS↑, 16,   mt-ROS↑, 1,   RPM↑, 1,   SOD↓, 1,   Thiols↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↓, 1,   TfR1/CD71↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ETC↓, 9,   mitResp↓, 1,   MMP?, 1,   MMP↓, 5,   MPT↑, 3,   mtDam↑, 1,   OCR↓, 1,   PleEff↓, 1,   SDH↓, 2,   UCP1↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACAA1↓, 1,   ALAT↓, 2,   AMPK↑, 1,   BCAP↓, 1,   FABP4↓, 1,   GlucoseCon↓, 1,   lactateProd↑, 1,   PCK1↓, 1,   PLIN1↓, 1,   PPARγ↑, 1,   TCA?, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 9,   Bak↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp↓, 1,   Casp3↑, 5,   Casp7↑, 1,   Casp9↑, 1,   Cyt‑c↑, 3,   Ferroptosis↑, 1,   lysoMP↓, 2,   lysoMP↑, 2,   TumCD↑, 9,   YAP/TEAD↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

BowelM↑, 2,   ChrMod↑, 2,   other↝, 2,   tumCV↓, 3,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1/ATG6↑, 1,   LC3II↑, 1,   p62↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 4,   P53↑, 2,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

E2Fs↓, 1,   TumCCA↑, 5,  

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

ERK↑, 1,   miR-34a↑, 1,   TumCG↓, 12,  

Migration(tgid=13) ⓘ

Ca+2↑, 4,   CAFs/TAFs↓, 1,   Cartilage↑, 1,   CCDC150↓, 1,   COL11A1↓, 1,   COL4↓, 1,   CXCL12↓, 1,   F-actin↓, 1,   FAK↓, 1,   FOSB↑, 1,   ITGA11↓, 1,   ITGB1↓, 1,   LAMB3↑, 1,   miR-486↑, 1,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   Rho↓, 1,   SMAD3↓, 1,   TGF-β↓, 1,   THBS2↓, 1,   TumCI↓, 3,   TumCMig↓, 2,   TumCP↓, 4,   TumMeta↓, 5,  

Angiogenesis & Vasculature(tgid=14) ⓘ

ECM/TCF↓, 1,   EPR↑, 2,   nucleolin↑, 1,  

Barriers & Transport(tgid=15) ⓘ

CellMemb↑, 5,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↓, 1,   CD4+↑, 3,   CXCc↓, 1,   CXCL9↓, 1,   DCells↑, 3,   FOXP3↓, 1,   GM-CSF↓, 1,   IFN-γ↓, 1,   IL1↑, 1,   IL10↑, 1,   IL12↑, 1,   IL17↓, 1,   IL22↓, 1,   IL23↓, 1,   IL28↓, 1,   IL6↓, 2,   Imm↑, 2,   pol-M1↝, 1,   Macrophages↑, 1,   NF-kB↑, 1,   PD-L1↑, 1,   RANTES↓, 1,   T-Cell↑, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioEnh↑, 1,   Dose?, 2,   Dose↑, 2,   Dose↝, 12,   Dose∅, 1,   eff↓, 6,   eff↑, 14,   eff↝, 5,   selectivity?, 1,   selectivity↑, 8,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 2,   AST↓, 1,   BMD↑, 1,   Ferritin↓, 1,   IL6↓, 2,   PD-L1↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   Appetite↑, 2,   breath↑, 2,   chemoP↑, 1,   ChemoSideEff↓, 1,   cognitive↑, 1,   hepatoP↑, 1,   OS?, 1,   OS↑, 12,   OS⇅, 1,   Pain↓, 4,   QoL↑, 2,   radioP↑, 1,   Sleep↑, 2,   Strength↑, 4,   toxicity↓, 2,   TumVol↓, 8,   Weight↑, 2,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,   CD8+↓, 1,   CD8+↑, 3,  
Total Targets: 166

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

DCR∅, 1,   ORR∅, 1,   PFS∅, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 2,   Ferroptosis↑, 1,   GPx↑, 1,   GPx1↑, 1,   GPx4↑, 1,   MDA↓, 1,   ROMO1↑, 1,   ROS↓, 9,   ROS↑, 1,   ROS∅, 1,   SOD↑, 2,   SOD1↑, 1,   SOD2↑, 1,   TAC↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 2,   FABP4↓, 1,   PPARγ↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 1,   Ferroptosis↑, 1,   iNOS↓, 1,   p‑JNK↓, 1,   p‑JNK↑, 2,   MAPK↓, 1,   p‑p38↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

OCN∅, 1,   SOX9↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 1,   other?, 1,   other↓, 1,   other↑, 2,   other↝, 6,   TREM-1↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↓, 1,  

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

ALDH↑, 1,   cFos↑, 1,   Diff↓, 1,   Diff↑, 2,   ERK↓, 1,   FGF↑, 1,   IGF-1↑, 1,   mTOR↓, 3,   PI3K↓, 1,   RUNX2∅, 1,   TumCG↓, 2,   TumCG∅, 1,   VGSC↑, 1,   Wnt↑, 1,  

Migration(tgid=13) ⓘ

ARG1/2↑, 1,   Ca+2↓, 1,   Ca+2↑, 2,   COL1∅, 1,   COL2A1↑, 1,   F-actin↑, 1,   FAK↑, 1,   MMP-10↓, 1,   MMP1↓, 1,   MMP9↓, 1,   MMP9↑, 1,   Na+↑, 1,   Netrins↑, 1,   TGF-β↑, 1,   TGF-β1↑, 1,   TIMP1↑, 1,   TIMP2↑, 1,   Treg lymp↓, 1,   β-catenin/ZEB1↑, 1,   β-Endo↑, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 1,   EGR4↑, 1,   NO↓, 1,   NO↑, 1,   NPY↑, 1,   PDGFR-BB↑, 1,  

Barriers & Transport(tgid=15) ⓘ

CellMemb↑, 1,   Na+↑, 1,   Vm/CMP↑, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   COX2/PTGS2↓, 1,   CXCc↓, 1,   GM-CSF↑, 1,   IFN-γ↓, 1,   p‑IKKα↓, 1,   IL1↓, 1,   IL10↑, 1,   IL17↓, 1,   IL1β↑, 1,   IL4↑, 1,   IL6↓, 1,   Inflam↓, 5,   IP-10/CXCL-10↑, 1,   p‑IκB↓, 1,   MCP1/CCL2↓, 1,   MIP‑1α/CCL3↓, 1,   mPGES-1↓, 1,   MyD88↓, 1,   NF-kB↓, 1,   p‑p65↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 2,   5HT↑, 1,   AChE↓, 1,   BDNF↑, 2,   NGF↑, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ?, 1,   Aβ↓, 4,   β-Amyloid↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose?, 1,   Dose↝, 3,   eff↓, 1,   eff↑, 2,   eff↝, 2,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALP↑, 1,   ALP∅, 1,   BMD↑, 3,   IL6↓, 1,   NSE↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 2,   cognitive↑, 6,   memory↑, 5,   motorD↑, 3,   neuroP↑, 4,   OS↑, 3,   radioP↑, 1,   toxicity?, 1,   toxicity↓, 1,   toxicity∅, 5,  
Total Targets: 137

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#:192  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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