Magnetic Field Rotating / TumCG 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.


TumCG, Tumor cell growth: Click to Expand ⟱
Source:
Type:
Normal cells grow and divide in a regulated manner through the cell cycle, which consists of phases (G1, S, G2, and M).
Cancer cells often bypass these regulatory mechanisms, leading to uncontrolled proliferation. This can result from mutations in genes that control the cell cycle, such as oncogenes (which promote cell division) and tumor suppressor genes (which inhibit cell division).
Scientific Papers found: Click to Expand⟱
3495- MFrot,  MF,    Synthesis of urchin-like nickel nanoparticles with enhanced rotating magnetic field-induced cell necrosis and tumor inhibition
- in-vivo, BC, NA
TumCG↓, UNNPs showed obvious suppression against tumor cell growth in a mouse model of malignant breast cancer under the induction of low-frequency RMF.

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

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

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

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

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

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

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

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

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↓,

221- MFrot,  MF,    Low Frequency Magnetic Fields Enhance Antitumor Immune Response against Mouse H22 Hepatocellular Carcinoma
- in-vivo, Liver, NA
OS↑,
TumCG↓, inhibit
IL6↓,
GM-CSF↓,
CXCc↓, keratinocyte-derived chemokine (KC)
Macrophages↑,
DCells↑,
CD4+↑,
CD8+↑,
IL12↑,

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/ATG6↑,
p62↑, blocked p62 degradation
TumCP↓,

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, NA, 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↑, enhanced miR-34a transcription
E2Fs↓, E2F1/E2F3
P53↑,
TfR1/CD71↓, TfR1 protein levels
Ferritin↓, inhibits iron metabolism

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+↑,


Showing Research Papers: 1 to 15 of 15

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 15

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 3,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↓, 1,   TfR1/CD71↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ETC↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 2,   BCAP↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 2,   Casp3↑, 1,   TumCD↑, 2,   YAP/TEAD↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

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

Autophagy & Lysosomes(tgid=9) ⓘ

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

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 2,  

Cell Cycle & Senescence(tgid=11) ⓘ

E2Fs↓, 1,   TumCCA↑, 4,  

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

miR-34a↑, 1,   TumCG↓, 12,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   COL11A1↓, 1,   CXCL12↓, 1,   FAK↓, 1,   ITGB1↓, 1,   miR-486↑, 1,   MMPs↓, 1,   TumCI↓, 1,   TumCP↓, 2,   TumMeta↓, 4,  

Angiogenesis & Vasculature(tgid=14) ⓘ

ECM/TCF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 3,   CXCc↓, 1,   CXCL9↓, 1,   DCells↑, 3,   GM-CSF↓, 1,   IFN-γ↓, 1,   IL1↑, 1,   IL10↑, 1,   IL12↑, 1,   IL6↓, 2,   Imm↑, 2,   Macrophages↑, 1,   T-Cell↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 2,   eff↑, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 2,   AST↓, 1,   Ferritin↓, 1,   IL6↓, 2,  

Functional Outcomes(tgid=23) ⓘ

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

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 3,  
Total Targets: 72

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

DCR∅, 1,   ORR∅, 1,   PFS∅, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Ferroptosis↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   Ferroptosis↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,   tumCV↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↓, 1,  

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

mTOR↓, 1,   TumCG↓, 2,   TumCG∅, 1,  

Migration(tgid=13) ⓘ

β-Endo↑, 1,  

Barriers & Transport(tgid=15) ⓘ

CellMemb↑, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose?, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BMD↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,   OS↑, 1,   toxicity↓, 1,  
Total Targets: 22

Scientific Paper Hit Count for: TumCG, Tumor cell growth
15 Magnetic Field Rotating
10 Magnetic Fields
1 Vitamin C (Ascorbic Acid)
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#:323  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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