Magnetic Field Rotating / ROS 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):

Mitochondrial electron-transport disruption, particularly persistent inhibition of Complex I in Oncomagnetic sOMF-treated cancer cells.
Tumor-selective mitochondrial ROS generation and oxidative stress downstream of disturbed electron transport.
Mitochondrial depolarization, respiratory failure, mitochondrial permeability transition, and subsequent apoptotic signaling.
Oxidative DNA damage, G1 cell-cycle arrest, and caspase-dependent apoptosis following sustained Oncomagnetic exposure.
F-actin and cytoskeletal mechanotransduction, reducing migration, invasion, and metastasis with moderate-intensity or gradient RMF.
ECM-integrin signaling modulation, including COL11A1/ITGB1/FAK/YAP and CCDC150/TGF-β1/SMAD3 pathways in triple-negative breast cancer models.
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↓">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.

ROS, Reactive Oxygen Species: Click to Expand ⟱

Source: HalifaxProj (inhibit)

Type:

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

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

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

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

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

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

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

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

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy

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


Item  ROS↑  NRF2  Condition  Mechanism Class  Remarks  

ROS">Piperlongumine
+++  ↓  [D][T]  ROS-dominant
Selective <span class="wphighlight">ROS</span> stressor, Prevents compensatory upregulation of NRF2, ie GSH↓



ROS">Shikonin
+++ ↓/± [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + glycolysis + GPX4 inhibition



ROS">Vitamin K3 (menadione)
+++ ↓ [D] ROS-dominant
Quinone redox cycler; toxicity limits use



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



ROS">Sodium Selenite
+++ ↓ [D] ROS-dominant
Pro-oxidant, depletes GSH



ROS">Juglone
+++ ↓ [D] ROS-dominant
Strong quinone <span class="wphighlight">ROS</span> chemistry



ROS">Auranofin
+++ ↓ [D] ROS-dominant
TrxR inhibition → redox collapse



ROS">Photodynamic Therapy (PDT)
+++ 0 [L][O₂] ROS-dominant
Singlet oxygen is core cytotoxic mechanism



ROS">Radiotherapy / Radiation
+++ 0 [O₂] ROS-dominant
DNA damage largely via <span class="wphighlight">ROS</span>



ROS">Doxorubicin
+++ ↓ [D] ROS-dominant
Chemo; redox cycling + mitochondrial <span class="wphighlight">ROS</span>



ROS">Cisplatin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> contributes to DNA/protein damage



ROS">Salinomycin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated CSC toxicity



ROS">Artemisinin / DHA
++ ↓ [Fe][T] ROS-dominant
Iron-activated radical generation



ROS">Sulfasalazine
++ ↓ [C][T] ROS-dominant
Ferroptosis; xCT inhibition → lipid <span class="wphighlight">ROS</span>



ROS">FMD / fasting
++ ↓ [M][C][O₂] ROS-dominant
Metabolic stress → mitochondrial <span class="wphighlight">ROS</span>



ROS">Vitamin C (pharmacologic)
++ ↓ [Fe][D] ROS-dominant
Extracellular H₂O₂ at high dose



ROS">Silver nanoparticles
++ ± [F][D] ROS-dominant
<span class="wphighlight">ROS</span> common; selectivity unreliable



ROS">Gambogic acid
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Parthenolide
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + NF-κB suppression



ROS">Plumbagin
++ ↓ [D] ROS-dominant
Quinone <span class="wphighlight">ROS</span> driver



ROS">Allicin
++ ↓ [D] ROS-dominant
Thiol-reactive oxidative stress



ROS">Ashwagandha (Withaferin A)
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Berberine
++ ↓ [D][M] ROS-dominant
Mitochondrial <span class="wphighlight">ROS</span> induction



ROS">PEITC
++ ↓ [D][C] ROS-dominant
GSH depletion + <span class="wphighlight">ROS</span>



ROS">Methionine restriction
+ ↓ [M][C][T] ROS-secondary
Redox vulnerability increased; <span class="wphighlight">ROS</span> indirect



ROS">DCA
+ ± [M][T] ROS-secondary
<span class="wphighlight">ROS</span> via forced OXPHOS



ROS">Capsaicin
+ ± [D][T] ROS-secondary
Ca²⁺ stress → <span class="wphighlight">ROS</span>



ROS">Galloflavin
+ 0 [D] ROS-secondary
<span class="wphighlight">ROS</span> not primary driver



ROS">Piperine
+ ± [D][F] ROS-secondary
Weak <span class="wphighlight">ROS</span> induction



ROS">Propyl gallate
+ ↓ [D] ROS-secondary
Pro-oxidant at high dose



ROS">Scoulerine
+ ? [D][T] ROS-secondary
Sparse <span class="wphighlight">ROS</span> data



ROS">Thymoquinone
± ± [D][T] Dual redox
Antioxidant ↔ pro-oxidant switch



ROS">Emodin
± ± [D][T] Dual redox
Not cancer-exclusive



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



ROS">Curcumin
± ↑/↓ [D][F] NRF2-dominant
Hormetic redox behavior



ROS">EGCG
± ↑/↓ [D][O₂] NRF2-dominant
Auto-oxidation artifacts common



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



ROS">Resveratrol
± ↑ [D][M] NRF2-dominant
<span class="wphighlight">ROS</span> only at high dose



ROS">Sulforaphane
± ↑↑ [D] NRF2-dominant
Strong NRF2 activator



ROS">Lycopene
0 ↑ — Antioxidant
Consistently antioxidant



ROS">Rosmarinic acid
0 ↑ — Antioxidant
Primarily antioxidant



ROS">Citrate
0 0 — Neutral
Metabolic; not a <span class="wphighlight">ROS</span> agent

Scientific Papers found: Click to Expand⟱

3567-

MFrot,

MF,

The Effect of Extremely Low-Frequency Magnetic Field on Stroke Patients: A Systematic Review

Review,

Stroke,

*eff↑, *ROS↓, *Inflam↓, *cognitive↑, *Catalase↑, *SOD↑, *SOD1↑, *SOD2↑, *GPx1↑, *GPx4↑, *IL1β↑, *neuroP↑, *toxicity∅,

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↑, *AMPK↑, *mPGES-1↓, *Ca+2↑, *ER Stress↑, *OS↑, *ROS↓,

3497-

MFrot,

MF,

The Effect of a Rotating Magnetic Field on the Regenerative Potential of Platelets

Human,

Nor,

30 healthy female and male volunteers

*PDGFR-BB↑, *TGF-β↑, *IGF-1↑, *FGF↑, *angioG↑, *Inflam↓, *ROS↓,

3745-

MFrot,

MF,

The neurobiological foundation of effective repetitive transcranial magnetic brain stimulation in Alzheimer's disease

Review,

AD,

*neuroP↑, *ROS↓, *Inflam↓, *5HT↑, *cFos↑, *Aβ↓, *memory↑, *BDNF↑, *Ach↑, *AChE↓, *cognitive↑, *BDNF↑, *NGF↑, *β-catenin/ZEB1↑, *p‑Akt↓, *mTOR↓, *MMP1↓, *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,

mice

*Aβ↓, *motorD↑, *cognitive↑, *memory↑, *ROS↓,

2259-

MFrot,

MF,

Method and apparatus for oncomagnetic treatment

in-vitro,

GBM,

Oncomagnetic patent

MMP↓, Bcl-2↓, BAX↑, Bak↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, ROS↑, lactateProd↑, Apoptosis↑, MPT↑, *selectivity↑, eff↑, MMP↓, selectivity↑, TCA?, H2O2↑, eff↑, *antiOx↑, H2O2↑, eff↓, GSH/GSSG↓, *toxicity∅, OS↑,

2258-

MFrot,

MF,

EXTH-68. ONCOMAGNETIC TREATMENT SELECTIVELY KILLS GLIOMA CANCER CELLS BY INDUCING OXIDATIVE STRESS AND DNA DAMAGE

in-vitro,

GBM,

GBM

in-vitro,

Nor,

SVGp12

TumVol↓, OS↑, γH2AX↑, DNAdam↑, selectivity↑, ROS↑, TumCD↑, eff↑, eff↓,

7382-

MFrot,

Inhibition of mitochondrial NADH:ubiquinone oxidoreductase by spinning oscillating magnetic fields causes toxicity in cancer cells

vitro+vivo,

GBM,

ROS↑, compI↓, DNAdam↑, TumCCA↑, Casp↓, Apoptosis↑, mt-NADH↓, selectivity?, *toxicity?,

8480-

MFrot,

Neuroprotective effect of RMF in a mouse model of sporadic Parkinson's disease

in-vivo,

Park,

*Dose↝, *Dose↝, *motorD↑, *ROS↓,

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?, EPR↑, BioEnh↑, GSH↓, GPx4↓, Iron↑, ROS↑, lipid-P↑, Ferroptosis↑, TumVol↓, Fenton↑,

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

1mT, 120Hz (7200rpm), 24, 48, and 72 h

OM‑100 device (motor driven pulses)

TumCP↓, Apoptosis↑, TumCMig↓, ROS↑, PD-L1↑, TumVol↓, eff↑, *toxicity∅, eff↑, *toxicity∅, Dose↝, tumCV↓, TumCI↓,

4569-

MFrot,

Case Report: A new noninvasive device-based treatment of a mesencephalic H3 K27M glioma

Case Report,

GBM,

Dose↝, Dose↑, Dose↑, OS↑, toxicity↓, ETC↓, ROS↑,

4567-

MFrot,

Oncogenic pathways and the electron transport chain: a dangeROS liaison

Review,

Var,

ROS↑, ETC↓, other↝, Fenton↑, RNS↑,

4566-

MFrot,

On the mitochondrial aspect of reactive oxygen species action in external magnetic fields

Study,

Var,

ROS↑, ETC↓, selectivity↑,

209-

MFrot,

MF,

The effect of a rotating magnetic field on the antioxidant system in healthy volunteers - preliminary study

Human,

NA,

 30 healthy volunteers

*SOD↑, *Catalase↑, *ROMO1↑, *MDA↓, *TAC↑, *ROS↓,

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,

 0.2T, 4Hz

 reduced aluminum deposition in the brains of AD mice

*NF-kB↓, *MAPK↓, *TLR4↓, *memory↑, *cognitive↑, *TGF-β1↑, *ARG1/2↑, *IL4↑, *IL10↑, *IL6↓, *IL1↓, *TNF-α↓, *iNOS↓, *ROS↓, *NO↓, *MyD88↓, *p‑IKKα↓, *p‑IκB↓, *p‑p65↓, *p‑JNK↓, *p‑p38↓, *ERK↓, *neuroP↑, *Aβ↓,

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

 f = 30 Hz; B from 5.9 to 28.4 mT

NA,

HaCaT

*ROS↑, *Ca+2↓, *other↝, *other↝, *other↝, *other↝, *other↝, *other?,

198-

MFrot,

MF,

Biological effects of rotating magnetic field: A review from 1969 to 2021

Review,

Var,

AntiCan↑, breath↑, Pain↓, Appetite↑, Strength↑, BowelM↑, TumMeta↓, TumCCA↑, ETC↓, MMP↓, TumCD↑, selectivity↑, ROS↑, Casp3↑, TumCG↓, TumCCA↑, ChrMod↑, TumMeta↓, Imm↑, DCells↑, Akt↓, OS⇅, toxicity↓, QoL↑, hepatoP↑, Pain↓, Weight↑, Strength↑, Sleep↑, IL6↓, CD4+↑, CD8+↑, Ca+2↑, radioP↑, chemoP↑, *BMD↑, *AntiAge↑, *AMPK↑, *P21↓, *P53↓, *mTOR↓, *OS↑, *β-Endo↑, *5HT↓,

212-

MFrot,

MF,

Rotating magnetic field inhibits Aβ protein aggregation and alleviates cognitive impairment in Alzheimer’s disease mice

in-vivo,

AD,

SH-SY5Y

 0.4T, 4.2 Hz

 mice

*β-Amyloid↓, *cognitive↑, *motorD↑, *ROS↓, *memory↑, *Aβ?,

190-

MFrot,

MF,

Chemo,

The efficacy and safety of low-frequency rotating static magnetic field therapy combined with chemotherapy on advanced lung cancer patients: a randomized, double-blinded, controlled clinical trial

Human,

Lung,

 0.4T static MF, with a rotating frequency of
7.5HZ,  2 hours per day continuously for 21 days

 human trial, 77 patients

*IP-10/CXCL-10↑, *GM-CSF↑, *TREM-1↓, QoL↑, Ca+2↑, ROS↑, Apoptosis↑, OS↑,

188-

MFrot,

MF,

Spinning magnetic field patterns that cause oncolysis by oxidative stress in glioma cells

in-vitro,

GBM,

GBM115

 0.4-58mT pulsed

  ~ 137 Hz and was large enough to generate a peak-topeak amplitude (PPA) of ~ 5 mT

in-vitro,

GBM,

DIPG

ROS↑, SDH↓, eff↓, RPM↑, eff↓, eff↑, eff↝, eff↝, Casp3↑, eff↝, SOD↓, ETC↓, compII↓,

187-

MFrot,

MF,

Method for noninvasive whole-body stimulation with spinning oscillating magnetic fields and its safety in mice

in-vivo,

GBM,

healthy mice

selectivity↑, ROS↑, *ROS∅, *toxicity∅, ETC↓, TumVol↓, Dose↝,

186-

MFrot,

MF,

Selective induction of rapid cytotoxic effect in glioblastoma cells by oscillating magnetic fields

in-vitro,

GBM,

GBM

 new device that generates oscillating magnetic fields (OMF) by rapid rotation of strong permanent magnets in specially designed patterns of frequency and timing

in-vitro,

Lung,

mt-ROS↑, Casp3↑, selectivity↑, TumCD↑, ETC↓, H2O2↑, eff↓, GSH↑, MMP↓,

227-

MFrot,

MF,

Low Frequency Magnetic Fields Induce Autophagy-associated Cell Death in Lung Cancer through miR-486-mediated Inhibition of Akt/mTOR Signaling Pathway

in-vivo,

Lung,

A549

 0.4T, 7.5 Hz, 4 h/day

 mouse

in-vitro,

Lung,

A549

TumCG↓, miR-486↑, BCAP↓, Apoptosis↑, ROS↑, TumAuto↑, LC3II↑, ATG5↑, Beclin-1/ATG6↑, p62↑, TumCP↓,

225-

MFrot,

MF,

Extremely low frequency magnetic fields regulate differentiation of regulatory T cells: Potential role for ROS-mediated inhibition on AKT

vitro+vivo,

Lung,

 0.4 T, 7.5 Hz: 2 h/day for 27 days.

 mice

MMP2↓, MMP9↓, FOXP3↓, ROS↑, p‑Akt↓,

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

 80mT pulsed

ROS↑, mitResp↓, mtDam↑, Dose↝, MMP?, OCR↓, mt-H2O2↑, eff↓, SDH↓, Thiols↓, GSH↓, TumCD↑, Casp3↑, Casp7↑, MPT↑, Cyt‑c↑, selectivity↑, GSH/GSSG↓, ETC↓,

220-

MFrot,

MF,

Effect of low frequency magnetic fields on melanoma: tumor inhibition and immune modulation

in-vitro,

Melanoma,

B16-F10

 0.4 T, 7.5 Hz

 mouse cell line

OS↑, DCells↑, T-Cell↑, Apoptosis↑, IL1↑, IFN-γ↓, IL10↑, TumCG↓, ROS↑, TumCP↓, TumCCA↑, ChrMod↑, CXCL9↓, CXCL12↓, CD4+↑, CD8+↑,

Showing Research Papers: 1 to 27 of 27

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 27

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 2,
Total Targets: 104

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1, Catalase↑, 2, 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,

Cell Death(tgid=5) ⓘ

p‑Akt↓, 1, iNOS↓, 1, p‑JNK↓, 1, MAPK↓, 1, p‑p38↓, 1,

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 1, other?, 1, other↝, 5, TREM-1↓, 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) ⓘ

cFos↑, 1, ERK↓, 1, FGF↑, 1, IGF-1↑, 1, mTOR↓, 2,

Migration(tgid=13) ⓘ

ARG1/2↑, 1, Ca+2↓, 1, Ca+2↑, 1, MMP-10↓, 1, MMP1↓, 1, MMP9↓, 1, TGF-β↑, 1, TGF-β1↑, 1, TIMP1↑, 1, TIMP2↑, 1, β-catenin/ZEB1↑, 1, β-Endo↑, 1,

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 1, NO↓, 1, PDGFR-BB↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

GM-CSF↑, 1, p‑IKKα↓, 1, IL1↓, 1, IL10↑, 1, IL1β↑, 1, IL4↑, 1, IL6↓, 1, Inflam↓, 3, IP-10/CXCL-10↑, 1, p‑IκB↓, 1, mPGES-1↓, 1, MyD88↓, 1, NF-kB↓, 1, p‑p65↓, 1, TLR4↓, 1, TNF-α↓, 1,

Synaptic & Neurotransmission(tgid=18) ⓘ

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

Protein Aggregation(tgid=19) ⓘ

Aβ?, 1, Aβ↓, 3, β-Amyloid↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 2, eff↑, 1, selectivity↑, 1,

Clinical Biomarkers(tgid=22) ⓘ

BMD↑, 1, IL6↓, 1,

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 2, cognitive↑, 5, memory↑, 4, motorD↑, 3, neuroP↑, 3, OS↑, 2, toxicity?, 1, toxicity∅, 5,
Total Targets: 83

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

27 Magnetic Field Rotating
21 Magnetic Fields
1 doxorubicin
1 immunotherapy
1 Chemotherapy

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:192  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

Magnetic Field Rotating / ROS Cancer Research Results

Rotating Magnetic Field Cancer Mechanisms

Rotating Magnetic Field Alzheimer’s Mechanisms

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

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