Magnetic Field Rotating Cancer Research Results

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

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

Primary mechanisms (ranked):

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

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

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

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

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

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

- Selectivity: Cancer Cells vs Normal Cells

Rotating Magnetic Field Cancer Mechanisms

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

P: 0–30 min    R: 30 min–3 hr    G: >3 hr

MPTP: opening represents a mitochondrial commitment event integrating ROS and Ca²⁺ stress; sustained opening indicates irreversible bioenergetic failure.



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

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

Rotating Magnetic Field Alzheimer’s Mechanisms

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


Scientific Papers found: Click to Expand⟱
203- MFrot,  MF,    Rotating Magnetic Field Induced Oscillation of Magnetic Particles for in vivo Mechanical Destruction of Malignant Glioma
- vitro+vivo, GBM, U87MG
lysoMP↓, TumVol↓, eff↑, Apoptosis↑, Ca+2↑,
202- MFrot,  MF,    Systematic simulation of tumor cell invasion and migration in response to time-varying rotating magnetic field
- Analysis, Var, MDA-MB-231
TumCG↓, MMPs↓, ECM/TCF↓,
201- MFrot,  MF,    Gradient Rotating Magnetic Fields Impairing F-Actin-Related Gene CCDC150 to Inhibit Triple-Negative Breast Cancer Metastasis by Inactivating TGF-β1/SMAD3 Signaling Pathway
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549 - in-vitro, BC, MDA-MB-468
CCDC150↓, TGF-β↓, SMAD3↓,
200- MFrot,  MF,    Moderate intensity low frequency rotating magnetic field inhibits breast cancer growth in mice
- in-vivo, BC, MDA-MB-231 - in-vivo, BC, MCF7
ALAT↓, TumVol↓, TumCCA↑, TumCG↓, TumMeta↓, Imm↑, P53↑, ALAT↓, AST↓,
215- MFrot,  MF,    Magneto-mechanical destruction of cancer-associated fibroblasts using ultra-small iron oxide nanoparticles and low frequency rotating magnetic fields
- in-vitro, PC, CAF
TumVol↓, lysoMP↑, CAFs/TAFs↓, eff↑,
198- MFrot,  MF,    Biological effects of rotating magnetic field: A review from 1969 to 2021
- Review, Var, NA
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↓,
195- MFrot,  MF,    Application of Rotating Magnetic Fields Increase the Activity of Antimicrobials Against Wound Biofilm Pathogens
- Human, Wounds, NA
Bacteria↓,
193- MFrot,  MF,    Rotating Magnetic Field Mitigates Ankylosing Spondylitis Targeting Osteocytes and Chondrocytes via Ameliorating Immune Dysfunctions
- in-vivo, Arthritis, NA
BMD↑, Cartilage↑, IL17↓, IL22↓, IL23↓, IL28↓, CD4+↓, CD8+↓, LAMB3↑, COL4↓, THBS2↓, ITGA11↓, PPARγ↑, ACAA1↓, PLIN1↓, FABP4↓, PCK1↓, UCP1↓, TNF-α↓,
191- MFrot,  MF,    Early exposure of rotating magnetic fields promotes central nervous regeneration in planarian Girardia sinensis
- in-vivo, Nor, NA
*EGR4↑, *Netrins↑, *NSE↑, *NPY↑,
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↑, *GM-CSF↑, *TREM-1↓, QoL↑, Ca+2↑, ROS↑, Apoptosis↑, OS↑,
189- MFrot,  MF,    Cancer treatment by magneto-mechanical effect of particles, a review
- Review, Var, NA
CellMemb↑, lysoMP↑, ERK↑, Apoptosis↑,
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↑, 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, NA
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 - in-vitro, Lung, NA
mt-ROS↑, Casp3↑, selectivity↑, TumCD↑, ETC↓, H2O2↑, eff↓, GSH↑, MMP↓,
185- MFrot,  MF,    Case Report: End-Stage Recurrent Glioblastoma Treated With a New Noninvasive Non-Contact Oncomagnetic Device
- Human, GBM, NA
TumVol↓, Dose↝, cognitive↑,
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↓,
2259- MFrot,  MF,    Method and apparatus for oncomagnetic treatment
- in-vitro, GBM, NA
MMP↓, Bcl-2↓, BAX↑, Bak↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, ROS↑, lactateProd↑, Apoptosis↑, MPT↑, *selectivity↑, ChemoSen↑, 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↓,
1737- MFrot,  Fe,  MF,    Feature Matching of Microsecond-Pulsed Magnetic Fields Combined with Fe3O4 Particles for Killing A375 Melanoma Cells
- in-vitro, MB, A375
Dose∅, tumCV↓,
595- MFrot,  VitC,  MF,    The Effect of Alternating Magnetic Field Exposure and Vitamin C on Cancer Cells
- in-vitro, PC, MIA PaCa-2 - in-vitro, CRC, SW-620 - in-vitro, NA, HT1080 - in-vitro, Pca, PC3 - in-vitro, OS, U2OS - in-vitro, BC, MCF7 - in-vitro, Nor, CCD-18Co
TumCD↑, Synergy↑, *TumCG∅,
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↑, PD-L1↑, TumVol↓, eff↑, *toxicity∅, eff↑, *toxicity∅, Dose↝, tumCV↓, TumCI↓,
230- MFrot,  MF,    Study on the Effect of Rotating Magnetic Field on Cellular Response of Mammalian Cells
- in-vitro, Nor, L929
*ALDH↑,
229- MFrot,  MF,    Molecular mechanism of effect of rotating constant magnetic field on organisms
- in-vivo, Nor, NA
*NO↑, *5HT↓, *eff↝, *eff↝, *β-Endo↑, *other↓,
228- MFrot,  MF,    Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17
- in-vitro, MS, NA
*CD4+↑, *MCP1/CCL2↓, RANTES↓, *MIP‑1α/CCL3↓, *Treg lymp↓, *IFN-γ↓, *IL17↓, *CXCc↓,
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↑, BCAP↓, Apoptosis↑, ROS↑, TumAuto↑, LC3II↑, ATG5↑, Beclin-1/ATG6↑, p62↑, TumCP↓,
226- MFrot,  MF,    Involvement of midkine expression in the inhibitory effects of low-frequency magnetic fields on cancer cells
- in-vitro, Lung, A549 - in-vitro, NA, LoVo
TumCP↓, eff↝,
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↑, mitResp↓, mtDam↑, Dose↝, MMP?, OCR↓, mt-H2O2↑, eff↓, SDH↓, Thiols↓, GSH↓, TumCD↑, Casp3↑, Casp7↑, MPT↑, Cyt‑c↑, selectivity↑, GSH/GSSG↓, ETC↓,
224- MFrot,  MF,    A pilot study of extremely low-frequency magnetic fields in advanced non-small cell lung cancer: Effects on survival and palliation of general symptoms
- Human, NSCLC, NA
PleEff↓, breath↑, Pain↓, Appetite↑, Strength↑, BowelM↑, OS↑,
223- MFrot,  MF,    The effect of rotating magnetic fields on the growth of Deal's guinea pig sarcoma transplanted subcutaneously in guinea pigs
- in-vivo, sarcoma, NA
TumCG↓,
222- MFrot,  MF,    LF-MF inhibits iron metabolism and suppresses lung cancer through activation of P53-miR-34a-E2F1/E2F3 pathway
- in-vitro, Lung, A549
TumCG↓, OS↑, miR-34a↑, E2Fs↓, P53↑, TfR1/CD71↓, Ferritin↓,
221- MFrot,  MF,    Low Frequency Magnetic Fields Enhance Antitumor Immune Response against Mouse H22 Hepatocellular Carcinoma
- in-vivo, Liver, NA
OS↑, TumCG↓, IL6↓, GM-CSF↓, CXCc↓, Macrophages↑, DCells↑, CD4+↑, CD8+↑, IL12↑,
220- MFrot,  MF,    Effect of low frequency magnetic fields on melanoma: tumor inhibition and immune modulation
- in-vitro, Melanoma, B16-F10
OS↑, DCells↑, T-Cell↑, Apoptosis↑, IL1↑, IFN-γ↓, IL10↑, TumCG↓, ROS↑, TumCP↓, TumCCA↑, ChrMod↑, CXCL9↓, CXCL12↓, CD4+↑, CD8+↑,
219- MFrot,  MF,    The expression and intranuclear distribution of nucleolin in HL-60 and K-562 cells after repeated, short-term exposition to rotating magnetic fields
- in-vitro, AML, HL-60 - in-vitro, AML, K562
nucleolin↑,
218- MFrot,  MF,    Extremely low frequency magnetic fields inhibit adipogenesis of human mesenchymal stem cells
- in-vitro, Nor, NA
*PPARγ↓, *p‑JNK↑, *Wnt↑, *ALP∅, *COL1∅, *RUNX2∅, *OCN∅, *FABP4↓, *p‑JNK↑, *Diff↓,
217- MFrot,  MF,    Effect of low-frequency rotary magnetic fields on advanced gastric cancer
- in-vivo, GC, HL-60 - in-vivo, GC, SK-HEP-1
OS↑, Pain↓, ChemoSideEff↓, Weight↑, Strength↑, Sleep↑,
216- MFrot,  MF,    Elongated Nanoparticle Aggregates in Cancer Cells for Mechanical Destruction with Low Frequency Rotating Magnetic Field
- in-vitro, GBM, U87MG
lysoMP↓, CellMemb↑,

Showing Research Papers: 51 to 86 of 86
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 86

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Fenton↑, 2,   GPx4↓, 1,   GSH↓, 2,   GSH↑, 1,   GSH/GSSG↓, 2,   H2O2↑, 4,   mt-H2O2↑, 1,   Iron↑, 1,   lipid-P↑, 1,   mt-NADH↓, 1,   RNS↑, 1,   ROS↑, 19,   mt-ROS↑, 1,   RPM↑, 1,   SOD↓, 1,   Thiols↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↓, 1,   TfR1/CD71↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

compI↓, 2,   compII↓, 1,   ETC↓, 9,   mitResp↓, 1,   mitResp⇅, 1,   mtDam↑, 1,   OCR↓, 1,   PleEff↓, 1,   SDH↓, 2,   UCP1↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

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

Cell Death(tgid=5) ⓘ

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

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 1,   p‑Akt↓, 1,   BCAP↓, 1,   ERK↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

ATF3↑, 1,   ChrMod↑, 2,   miR-34a↑, 1,   miR-486↑, 1,   other↝, 4,   tumCV↓, 4,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1/ATG6↑, 1,   LC3II↑, 1,   lysoMP↓, 2,   lysoMP↑, 2,   p62↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 6,   P53↑, 2,   γH2AX↑, 2,  

Cell Cycle & Senescence(tgid=11) ⓘ

E2Fs↓, 1,   TumCCA↑, 7,  

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

TumCG↓, 14,   TumCP↓, 5,  

Migration(tgid=13) ⓘ

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

Angiogenesis & Vasculature(tgid=14) ⓘ

ECM/TCF↓, 1,   nucleolin↑, 1,  

Barriers & Transport(tgid=15) ⓘ

CellMemb↑, 4,   EPR↑, 2,   MMP?, 1,   MMP↓, 6,   MPT↑, 3,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↓, 1,   CD4+↑, 4,   CD8+↓, 1,   CD8+↑, 4,   CXCc↓, 1,   CXCL12↓, 1,   CXCL9↓, 1,   DCells↑, 3,   FOXP3↓, 1,   GM-CSF↓, 1,   IFN-γ↓, 1,   IL1↑, 1,   IL10↑, 1,   IL12↑, 1,   IL17↓, 1,   IL22↓, 1,   IL23↓, 1,   IL28↓, 1,   IL6↓, 2,   Imm↑, 4,   pol-M1↝, 1,   Macrophages↑, 1,   NF-kB↑, 1,   PD-1↝, 1,   PD-L1↑, 1,   RANTES↓, 1,   T-Cell↑, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

PPARγ↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioEnh↑, 1,   ChemoSen↑, 1,   Dose?, 2,   Dose↑, 2,   Dose↝, 18,   Dose∅, 1,   eff↓, 7,   eff↑, 13,   eff↝, 5,   selectivity?, 1,   selectivity↑, 10,   Synergy↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

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

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   Appetite↑, 2,   BowelM↑, 2,   breath↑, 2,   chemoP↑, 1,   ChemoSideEff↓, 1,   cognitive↑, 1,   hepatoP↑, 1,   OS?, 1,   OS↑, 14,   OS⇅, 1,   Pain↓, 4,   QoL↑, 2,   radioP↑, 1,   Sleep↑, 2,   Strength↑, 4,   toxicity↓, 3,   TumVol↓, 9,   Weight↑, 2,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 170

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 2,   GPx↑, 1,   GPx1↑, 1,   GPx4↑, 1,   MDA↓, 1,   ROMO1↑, 1,   ROS↓, 10,   ROS↑, 1,   ROS∅, 1,   SOD↑, 2,   SOD1↑, 1,   SOD2↑, 1,   TAC↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 2,   FABP4↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   Ferroptosis↑, 1,   iNOS↓, 1,   p‑p38↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 1,   p‑Akt↓, 1,   ERK↓, 1,   p‑IKKα↓, 1,   p‑IκB↓, 1,   p‑JNK↓, 1,   p‑JNK↑, 2,   MAPK↓, 1,   mTOR↓, 4,   PDGFR-BB↑, 1,   PI3K↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other?, 1,   other↓, 1,   other↑, 2,   other↝, 6,   other?, 1,   RUNX2∅, 1,   SOX9↑, 1,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↓, 1,  

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

ALDH↑, 1,   cFos↑, 1,   Diff↓, 1,   Diff↑, 2,   FGF↑, 1,   IGF-1↑, 1,   TumCG↓, 2,   TumCG∅, 1,   Wnt↑, 1,  

Migration(tgid=13) ⓘ

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

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 1,   EGR4↑, 1,   NO↓, 1,   NO↑, 1,   NPY↑, 1,  

Barriers & Transport(tgid=15) ⓘ

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

Immune & Inflammatory Signaling(tgid=16) ⓘ

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

Synaptic & Neurotransmission(tgid=18) ⓘ

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

Protein Aggregation(tgid=19) ⓘ

Aβ?, 1,   Aβ↓, 4,   β-Amyloid↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

PPARγ↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Clinical Biomarkers(tgid=22) ⓘ

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

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 2,   cognitive↑, 6,   DCR∅, 1,   memory↑, 5,   motorD↑, 5,   neuroP↑, 4,   ORR∅, 1,   OS↑, 3,   PFS∅, 1,   radioP↑, 1,   Strength↑, 1,   Stroke↓, 1,   toxicity?, 1,   toxicity↓, 1,   toxicity∅, 5,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 141

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

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

 

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