Database Query Results : Magnetic Field Rotating, , ROS

MFrot, Magnetic Field Rotating: Click to Expand ⟱
Features:
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 Fields
Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 ROS (tumor-selective oxidative stress) ↑ ROS (P→R); sustained to cytotoxicity (G) ↔ minimal change or transient ↑ without injury (P→R) P, R, G Primary stress amplifier Oncomagnetic reports emphasize selective tumor ROS increase with normal-cell sparing in comparable exposure conditions
2 Mitochondrial ETC inhibition (Complex I/NADH:ubiquinone) ↓ Complex I / respiration (P→R) ↔ limited effect (P→R) P, R Bioenergetic collapse trigger Rotating/spinning fields are proposed to disrupt mitochondrial electron flow, driving ROS elevation upstream of ΔΨm loss
3 Ca²⁺ signaling (ER–mitochondria Ca²⁺ transfer / mitochondrial Ca²⁺ load) ↑ Ca²⁺ dysregulation (P→R) contributing to mitochondrial failure (G) ↔ buffered Ca²⁺ homeostasis (P→R) P, R, G Amplifies ETC/ROS-driven toxicity RMF-driven mitochondrial stress can propagate via Ca²⁺ transfer to accelerate ΔΨm loss and pro-death ER stress in tumor cells while sparing normal cells
4 Mitochondrial permeability transition pore (MPTP) ↑ sustained MPTP opening (R→G) ↔ resistant to opening P, R, G Mitochondrial point-of-no-return RMF-enhanced ROS and Ca²⁺ loading promote persistent MPTP opening in tumor mitochondria, driving energetic collapse and apoptosis while normal cells remain below the opening threshold
5 ΔΨm / mitochondrial membrane integrity ↓ ΔΨm (R); progresses (G) ↔ preserved R, G Mitochondrial failure threshold Matches the “energy factory” targeting concept described in Oncomagnetic mechanism narratives
6 GSH depletion ↓ GSH (R→G) ↔ maintained R, G Loss of redox buffering Cancer-selective inability to restore GSH is a key discriminator vs normal cells
7 NRF2 response (selectivity gate) ↔ delayed/insufficient NRF2 (R→G) ↑ NRF2 (R→G) R, G Adaptive protection Normal-cell sparing is consistent with competent NRF2-driven antioxidant defense
8 ER stress / UPR (CHOP commitment) ↑ ER stress (R); CHOP/apoptotic UPR (G) ↑ adaptive UPR (R); resolves (G) R, G Proteostasis failure ETC/ROS stress propagates to ER; commitment vs resolution diverges by cell robustness
9 DNA damage (oxidative; checkpoint markers) ↑ DNA damage (R→G) ↔ or repaired (G) R, G Checkpoint stress Interpreted as ROS-mediated consequence; reported as increased damage markers in some translational datasets
10 LDH / glycolytic vulnerability ↓ LDH performance / ↓ glycolytic flux (R→G) ↔ metabolic flexibility R, G Metabolic choke Cancer glycolysis becomes unstable when NADH/NAD+ and redox buffering are stressed
11 TrxR / thioredoxin system overload ↓ reserve (R→G) ↔ preserved R, G Parallel antioxidant collapse Useful when GSH data are mixed; TrxR can be the limiting system under sustained ROS 
Time-Scale Flag: TSF = P / R / G
  P: 0–30 min (physical / electron / radical effects)
  R: 30 min–3 hr (redox signaling & stress response)
  G: >3 hr (gene-regulatory adaptation)
MPTP: opening represents a mitochondrial commitment event integrating ROS and Ca²⁺ stress; sustained opening indicates irreversible bioenergetic failure.
ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)

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

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

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

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

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

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

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

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




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






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






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






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






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






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






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
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.

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

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↓,

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 - in-vitro, Lung, A549
TumCG↓,
miR-486↑, decreased expression of miR-486 and an increased expression of BCAP were found in tumor tissues of lung cancer patients
BCAP↓,
Apoptosis↑,
ROS↑,
TumAuto↑, miR-486 is required for LF-MFs triggered autophagy
LC3II↑,
ATG5↑,
Beclin-1↑,
p62↑, blocked p62 degradation
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, NA
MMP2↓,
MMP9↓,
FOXP3↓,
ROS↑,
p‑Akt↓,

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

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↓,

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.

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↑,

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.

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

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↑,

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)
*ARG↑, 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

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.

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

188- MFrot,  MF,    Spinning magnetic field patterns that cause oncolysis by oxidative stress in glioma cells
- in-vitro, GBM, GBM115 - in-vitro, GBM, DIPG
ROS↑, both GBM and DIPG cells ROS generated by sOMF
SDH↓, Complex II succinate dehydrogenase
eff↓, antioxidant Trolox reverses the cytotoxic effect of sOMF on glioma cells indicating that ROS play a causal role in producing the effect
RPM↑, we hypothesized that the interaction of weak and intermediate strength magnetic fields with the RPM mechanism in the mitochondrial ETC can perturb the electron transfer process (MEP hypothesis) to generate superoxide.
eff↓, We observed that Helmholtz coil did not produce any significant increase in ROS at 2 and 4 h during stimulation or 2 h poststimulation in GBM and DIPG cells
eff↑, oscillating field alone is not sufficient to induce ROS and that the changing angle of the magnetic field axis is also required to achieve this effect.
eff↝, repeated pulse trains rising to and declining from the peak frequency with intervening pauses are sufficient to achieve near maximum level of increase in ROS
eff↝, One spinning magnet or three spinning magnets generate similar cellular ROS levels and the effect of variation of the stimulus off period.
Casp3↑, caspase 3 activation
eff↝, This indicates that the total amount of energy delivered to cancer cells is clearly not the determinant of the potency of stimulation. Instead, it appears that the longer Toff between stimuli of 750 ms in the 4-h stimulation, as opposed to 250 ms in
SOD↓, critical rise in superoxide in two types of human glioma cells (implies SOD capacity exceeded)
ETC↓, found support for the hypothesis that the sOMF-induced increase in ROS is likely due to perturbation of the electron transfer process in the mitochondrial electron transport chain (ETC)

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, NA
*IP-10/CXCL-10↑, MF group patients had higher concentrations of IP-10 and GM-CSF, and lower concentration of sTREM-1 in plasma
*GM-CSF↑, in PLASMA
*TREM-1↓, sTREM-1, in PLASMA
QoL↑, Comparing to CON group, more patients in MF group (66.7% vs 25.9%) were experiencing life quality improvement on day 21. significantly higher increase of FACT-L,TOI and LCS scores
Ca+2↑, MF treated cells were found to have higher intracellular Ca2+ concentration and Reactive Oxygen Species (ROS) reaction level, which led to higher apoptosis rates(Zhang et al. 2010;
ROS↑,
Apoptosis↑,
OS↑, median survival time for MF group and CON group was 6.7 months and 6.07 month respectively

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↓,

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

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)

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.

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

220- MFrot,  MF,    Effect of low frequency magnetic fields on melanoma: tumor inhibition and immune modulation
- in-vitro, Melanoma, B16-F10
OS↑, prolonged the mouse survival rate
DCells↑,
T-Cell↑,
Apoptosis↑,
IL1↑,
IFN-γ↓, most of cytokines were decreased
IL10↑,
TumCG↓, grow slowed
ROS↑, Phagocyte activity, ROS release and interleukin-1β (IL-1β) production were significantly promoted after continuous exposure to 50 Hz LF-MF (1mT)
TumCP↓, LF-MF inhibits the proliferation of B16-F10 cells
TumCCA↑, the S-phase rate was significantly decreased from 40.76% to 37.24% and the G2/M-phase rate was significantly increased from 8.9% to 11.6%
ChrMod↑, Compared with control cells, the treated cells were characterized by the breaking down of chromatin (white arrow) and black granule accumulation (black arrow).
CXCL9↓, in tumor-bearing mice groups, most of cytokines were decreased after LF-MF exposure, including KC, CCL1, IFN-γ, CXCL9, CXCL12, TREM-1, CCL12, IL-1rα and IL-16.
CXCL12↓,
CD4+↑, After LF-MF exposure, the proportions of CD3+, CD3 + CD4+ and CD3 + CD8+ T cells in tumor-bearing mice were increased to 24.0%, 13.28% and 7.46%, respectively
CD8+↑,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 24

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Fenton↑, 1,   GSH↓, 1,   GSH↑, 1,   GSH/GSSG↓, 2,   H2O2↑, 3,   mt-H2O2↑, 1,   RNS↑, 1,   ROS↑, 14,   mt-ROS↑, 1,   RPM↑, 1,   SOD↓, 1,   Thiols↓, 1,  

Mitochondria & Bioenergetics ⓘ

ETC↓, 8,   mitResp↓, 1,   MMP?, 1,   MMP↓, 4,   MPT↑, 2,   mtDam↑, 1,   OCR↓, 1,   SDH↓, 2,  

Core Metabolism/Glycolysis ⓘ

BCAP↓, 1,   lactateProd↑, 1,   TCA?, 1,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 5,   Bak↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 5,   Casp7↑, 1,   Casp9↑, 1,   Cyt‑c↑, 2,   TumCD↑, 4,  

Transcription & Epigenetics ⓘ

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

Autophagy & Lysosomes ⓘ

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

DNA Damage & Repair ⓘ

DNAdam↑, 2,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 3,  

Migration ⓘ

Ca+2↑, 2,   CXCL12↓, 1,   miR-486↑, 1,   MMP2↓, 1,   MMP9↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 3,   TumMeta↓, 2,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 2,   CXCL9↓, 1,   DCells↑, 2,   FOXP3↓, 1,   IFN-γ↓, 1,   IL1↑, 1,   IL10↑, 1,   IL6↓, 1,   Imm↑, 1,   PD-L1↑, 1,   T-Cell↑, 1,  

Drug Metabolism & Resistance ⓘ

Dose↑, 2,   Dose↝, 4,   eff↓, 6,   eff↑, 6,   eff↝, 3,   selectivity↑, 7,  

Clinical Biomarkers ⓘ

IL6↓, 1,   PD-L1↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   Appetite↑, 1,   breath↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   OS↑, 5,   OS⇅, 1,   Pain↓, 2,   QoL↑, 2,   radioP↑, 1,   Sleep↑, 1,   Strength↑, 2,   toxicity↓, 2,   TumVol↓, 3,   Weight↑, 1,  

Infection & Microbiome ⓘ

CD8+↑, 2,  
Total Targets: 91

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 2,   GPx1↑, 1,   GPx4↑, 1,   MDA↓, 1,   ROMO1↑, 1,   ROS↓, 8,   ROS↑, 1,   ROS∅, 1,   SOD↑, 2,   SOD1↑, 1,   SOD2↑, 1,   TAC↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 2,  

Cell Death ⓘ

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

Transcription & Epigenetics ⓘ

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

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

DNA Damage & Repair ⓘ

P53↓, 1,  

Cell Cycle & Senescence ⓘ

P21↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

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

Migration ⓘ

ARG↑, 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 ⓘ

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

Immune & Inflammatory Signaling ⓘ

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 ⓘ

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

Protein Aggregation ⓘ

Aβ?, 1,   Aβ↓, 3,   β-Amyloid↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

BMD↑, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 2,   cognitive↑, 5,   memory↑, 4,   motorD↑, 2,   neuroP↑, 3,   OS↑, 2,   toxicity∅, 5,  
Total Targets: 81

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
24 Magnetic Field Rotating
21 Magnetic Fields
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

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