Magnetic Field Rotating / selectivity 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,
- 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.


selectivity, selectivity: Click to Expand ⟱
Source:
Type:
The selectivity of cancer products (such as chemotherapeutic agents, targeted therapies, immunotherapies, and novel cancer drugs) refers to their ability to affect cancer cells preferentially over normal, healthy cells. High selectivity is important because it can lead to better patient outcomes by reducing side effects and minimizing damage to normal tissues.

Achieving high selectivity in cancer treatment is crucial for improving patient outcomes. It relies on pinpointing molecular differences between cancerous and normal cells, designing drugs or delivery systems that exploit these differences, and overcoming intrinsic challenges like tumor heterogeneity and resistance

Factors that affect selectivity:
1. Ability of Cancer cells to preferentially absorb a product/drug
-EPR-enhanced permeability and retention of cancer cells
-nanoparticle formations/carriers may target cancer cells over normal cells
-Liposomal formations. Also negatively/positively charged affects absorbtion

2. Product/drug effect may be different for normal vs cancer cells
- hypoxia
- transition metal content levels (iron/copper) change probability of fenton reaction.
- pH levels
- antiOxidant levels and defense levels

3. Bio-availability
Scientific Papers found: Click to Expand⟱
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

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?,

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.

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.

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↓,

187- MFrot,  MF,    Method for noninvasive whole-body stimulation with spinning oscillating magnetic fields and its safety in mice
- in-vivo, GBM, NA
selectivity↑, Our in vitro experiments demonstrated selective cancer cell death while sparing normal cells by sOMF-induced increase in intracellular reactive oxygen species (ROS) levels due to magnetic perturbation of mitochondrial electron transport.
ROS↑,
*ROS∅,
*toxicity∅, no significant adverse effects of chronic or acute sOMF stimulation on the health, behavior, electrocardiographic and electroencephalographic activities, hematologic profile, and brain and other tissue and organ morphology of treated mice
ETC↓, We have evidence that its mechanism of action involves alteration of electron transport in the mitochondrial respiratory chain leading to the production of reactive oxygen species (ROS)(
TumVol↓, In a case report published recently we reported that 36-day treatment with this device caused a > 30% shrinkage of the contrast-enhanced tumor volume of a left frontal GBM in a 53-year-old male patient
Dose↝, rrangement of oncoscillators generates a magnetic field strength of >1 mT (range 1 – ~100 mT) in each cage

186- MFrot,  MF,    Selective induction of rapid cytotoxic effect in glioblastoma cells by oscillating magnetic fields
- in-vitro, GBM, GBM - in-vitro, Lung, NA
mt-ROS↑, Cytotoxic effects of OMF may be caused by an increase in ROS
Casp3↑, Cell death is associated with activation of caspase 3
selectivity↑, OMF induces highly selective cell death of patient derived GBM cells associated with activation of caspase 3, while leaving normal tissue cells undamaged
TumCD↑, Exposure to OMF causes cancer cell death
ETC↓, The underlying mechanism is a marked increase in ROS in the mitochondria, possibly in part through perturbation of the electron flow in the respiratory chain.
H2O2↑, Figure 6A shows rapid increases in the levels of superoxide and H 2 O 2 in GBM cells,
eff↓, we used the potent antioxidant Trolox to counteract it,
GSH↑, We tested whether GSH synthesis was upregulated as a feedback protective effect in response to OMF-induced increase in ROS. An examination of GSH levels showed that there was a 20% elevation in treated cells
MMP↓, underlying mechanism involves a marked increase in ROS, mitochondrial membrane depolarization, fragmentation of mitochondrial network and activation of caspase 3.

184- MFrot,  MF,    Rotating Magnetic Fields Inhibit Mitochondrial Respiration, Promote Oxidative Stress and Produce Loss of Mitochondrial Integrity in Cancer Cells
- in-vitro, GBM, GBM
ROS↑, sOMF
mitResp↓, Inhibit Mitochondrial Respiration
mtDam↑, Produce Loss of Mitochondrial Integrity
Dose↝, Repeated intermittent sOMF was applied for 2 hours at a specific frequency, in the 200-300 Hz frequency range, with on-off epochs of 250 or 500 ms duration.
MMP?, ROS generation has been shown to be driven, in part, by elevated mitochondrial membrane chemiosmotic potential (ΔΨ) and ubiquinol (QH2)
OCR↓, Immediately after cessation of field rotation we observe a loss of mitochondrial integrity (labeled LMI), with a very rapid increase in O2 consumption
mt-H2O2↑, We have previously demonstrated that sOMF treatment of cells generates superoxide/hydrogen peroxide in the mitochondrial matrix
eff↓, we repeated the same experiment in the presence of Trolox, which protects thiols from ROS oxidation (47). sOMF treatment of RLM in State 3u pre-treated with Trolox (15 μM), show minimal inhibition,
SDH↓, SDH Inhibition by sOMF in State 3u RLM Is Caused by ROS Generation
Thiols↓, suggest that thiol oxidation in SDH may result from sOMF.
GSH↓, Glutathione in the mitochondrial matrix can provide some protection from ROS, but after solubilizing the mitochondria, this protection is lost and the SDH becomes more sensitive to sOMF.
TumCD↑, sOMF is highly effective at killing non-dividing GBM cell cultures,
Casp3↑, caspase-3 activation 1 h after sOMF
Casp7↑, rapid activation of caspase-3/7
MPT↑, OMF-treated cell that causes near simultaneous MPT, release of cytochrome c and other apoptosis-inducing factors, resulting in caspase-3/7 activation in these GBM cells.
Cyt‑c↑,
selectivity↑, differential sensitivity to sOMF of cancer cells over ‘normal’ cells becomes apparent. rapid increase in the reactive oxygen species (ROS) in the mitochondria to cytotoxic levels only in cancer cells, and not in normal human cortical neurons
GSH/GSSG↓, increasing GSSG/GSH ratio
ETC↓, completely arrest electron transport in isolated, respiring, rat liver mitochondria and patient derived glioblastoma (GBM)


Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

compI↓, 1,   GSH↓, 1,   GSH↑, 1,   GSH/GSSG↓, 2,   H2O2↑, 3,   mt-H2O2↑, 1,   mt-NADH↓, 1,   ROS↑, 7,   mt-ROS↑, 1,   Thiols↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ETC↓, 5,   mitResp↓, 1,   MMP?, 1,   MMP↓, 4,   MPT↑, 2,   mtDam↑, 1,   OCR↓, 1,   SDH↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

lactateProd↑, 1,   TCA?, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 2,   Bak↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp↓, 1,   Casp3↑, 4,   Casp7↑, 1,   Casp9↑, 1,   Cyt‑c↑, 2,   TumCD↑, 4,  

Transcription & Epigenetics(tgid=7) ⓘ

BowelM↑, 1,   ChrMod↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 3,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 3,  

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

TumCG↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   F-actin↓, 1,   Rho↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumMeta↓, 3,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   DCells↑, 1,   IL6↓, 1,   Imm↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 2,   eff↓, 4,   eff↑, 3,   selectivity?, 1,   selectivity↑, 8,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   Appetite↑, 1,   breath↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   OS↑, 3,   OS⇅, 1,   Pain↓, 2,   QoL↑, 1,   radioP↑, 1,   Sleep↑, 1,   Strength↑, 2,   toxicity↓, 1,   TumVol↓, 2,   Weight↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 1,  
Total Targets: 69

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   ROS∅, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↓, 1,  

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

mTOR↓, 1,  

Migration(tgid=13) ⓘ

β-Endo↑, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BMD↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,   OS↑, 1,   toxicity?, 1,   toxicity∅, 2,  
Total Targets: 14

Scientific Paper Hit Count for: selectivity, selectivity
9 Magnetic Field Rotating
7 Magnetic Fields
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#:1110  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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