tbResList Print — MFrot Magnetic Field Rotating

Filters: qv=192, qv2=%, rfv=%

Product

MFrot Magnetic Field Rotating
Description: <p><b>Magnetic Field Rotating</b> — 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.</p>

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

<p><b>Bioavailability / PK relevance:</b> 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.</p>

<p><b>In-vitro vs systemic exposure relevance:</b> 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.</p>

<p><b>Clinical evidence status:</b> 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.</p>


<b>Rotary Magnetic field</b> 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)<br>
Targets affected are mostly the same as for <a href="tbResList.php?qv=172&exPr=open">Magnet fields</a><br>
Main differences<br>
- may enhance the EPR effect allowing targeting of drugs to cancer cells<br>
- acts as wireless stirrer, especially on magnetic particles(inducing eddy currents in water media)<br>
- research for use in nano surgery, and mechanical destruction of cancer cells<br>
- continue to highlight ability to raise ROS in cancer cell and lower ROS in normal cells<br>
- RMF may be responsible for Ca2+ distribution to pass across the plasma membrane(differental affected for cancer and normal cells) <br>

<br>
Pathways:<br>

<!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑-->
- induce
<a href="tbResList.php?qv=192&tsv=275&wNotes=on">ROS</a> 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)<br>
- ROS↑ related:
<a href="tbResList.php?qv=192&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm),
<!-- <a href="tbResList.php?qv=192&tsv=103&wNotes=on">ER Stress↑</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=459&wNotes=on">UPR↑</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=356&wNotes=on">GRP78↑</a>, -->
<a href="tbResList.php?qv=192&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>,
<a href="tbResList.php?qv=192&tsv=77&wNotes=on">Cyt‑c↑</a>,
<a href="tbResList.php?qv=192&wNotes=on&word=Casp">Caspases↑</a>,
<a href="tbResList.php?qv=192&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>,
<a href="tbResList.php?qv=192&tsv=239&wNotes=on">cl-PARP↑</a>,
<a href="tbResList.php?qv=192&wNotes=on&word=HSP">HSP↓</a>,
<a href="tbResList.php?qv=192&wNotes=on&word=Prx">Prx</a>,<!-- mitochondrial antioxidant enzyme-->

<br>

<!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, -->
<!--
- Lowers AntiOxidant defense in Cancer Cells:
<a href="tbResList.php?qv=192&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>,
<a href="tbResList.php?qv=192&word=Trx&wNotes=on">TrxR↓**</a>,
<a href="tbResList.php?qv=192&tsv=298&wNotes=on&word=SOD↓">SOD↓</a>,
<a href="tbResList.php?qv=192&tsv=137&wNotes=on&word=GSH↓">GSH↓</a>
<a href="tbResList.php?qv=192&tsv=46&wNotes=on">Catalase↓</a>
<a href="tbResList.php?qv=192&tsv=597&wNotes=on">HO1↓</a>
<a href="tbResList.php?qv=192&wNotes=on&word=GPx">GPx↓</a>
<br> -->

- Raises
<a href="tbResList.php?qv=192&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a>
defense in Normal Cells:
<a href="tbResList.php?qv=192&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>,
<a href="tbResList.php?qv=192&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>,
<a href="tbResList.php?qv=192&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>,
<a href="tbResList.php?qv=192&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>,
<a href="tbResList.php?qv=192&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>,
<!-- genes involved in the oxidative stress-antioxidant defense system PRNP, NQO1, and GCLM -->
<br>

<!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, -->
- lowers
<a href="tbResList.php?qv=192&tsv=953&wNotes=on&word=Inflam">Inflammation</a> :
<a href="tbResList.php?qv=192&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>,
<a href="tbResList.php?qv=192&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>,
<a href="tbResList.php?qv=192&tsv=235&wNotes=on&word=p38↓">p38↓</a>, Pro-Inflammatory Cytokines :
<!-- <a href="tbResList.php?qv=192&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>, -->
<a href="tbResList.php?qv=192&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>,
<a href="tbResList.php?qv=192&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>,
<!-- <a href="tbResList.php?qv=192&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> -->
<br>



<!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓
inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.-->
- inhibit Growth/Metastases :
<a href="tbResList.php?qv=192&tsv=604&wNotes=on">TumMeta↓</a>,
<a href="tbResList.php?qv=192&tsv=323&wNotes=on">TumCG↓</a>,
<!-- <a href="tbResList.php?qv=192&tsv=96&wNotes=on">EMT↓</a>, -->
<a href="tbResList.php?qv=192&tsv=204&wNotes=on">MMPs↓</a>,
<a href="tbResList.php?qv=192&tsv=201&wNotes=on">MMP2↓</a>,
<a href="tbResList.php?qv=192&tsv=203&wNotes=on">MMP9↓</a>,
<!-- <a href="tbResList.php?qv=192&tsv=308&wNotes=on">TIMP2</a>, -->
<a href="tbResList.php?qv=192&tsv=415&wNotes=on">IGF-1↓</a>,
<!-- <a href="tbResList.php?qv=192&tsv=428&wNotes=on">uPA↓</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=334&wNotes=on">VEGF↓</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=1284&wNotes=on">ROCK1↓</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=110&wNotes=on">FAK↓</a>, -->
<a href="tbResList.php?qv=192&tsv=273&wNotes=on">RhoA↓</a>,
<a href="tbResList.php?qv=192&tsv=214&wNotes=on">NF-κB↓</a>,
<!-- <a href="tbResList.php?qv=192&tsv=79&wNotes=on">CXCR4↓</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=1247&wNotes=on">SDF1↓</a>, -->
<a href="tbResList.php?qv=192&tsv=304&wNotes=on">TGF-β↓</a>,
<!-- <a href="tbResList.php?qv=192&tsv=719&wNotes=on">α-SMA↓</a>, -->
<a href="tbResList.php?qv=192&tsv=105&wNotes=on">ERK↓</a>
<!-- <a href="tbResList.php?qv=192&tsv=1178&wNotes=on">MARK4↓</a> --> <!-- contributing to tumor growth, invasion, and metastasis-->
<br>

<!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, -->
<!--
- reactivate genes thereby inhibiting cancer cell growth :
<a href="tbResList.php?qv=192&tsv=140&wNotes=on">HDAC↓</a>,
<a href="tbResList.php?qv=192&wNotes=on&word=DNMT">DNMTs↓</a>,
<a href="tbResList.php?qv=192&tsv=108&wNotes=on">EZH2↓</a>,
<a href="tbResList.php?qv=192&tsv=236&wNotes=on">P53↑</a>,
<a href="tbResList.php?qv=192&wNotes=on&word=HSP">HSP↓</a>,
<a href="tbResList.php?qv=192&tsv=506&wNotes=on">Sp proteins↓</a>,
<a href="tbResList.php?qv=192&wNotes=on&word=TET">TET↑</a>
<br> -->

<!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ -->
- cause Cell cycle arrest :
<a href="tbResList.php?qv=192&tsv=322&wNotes=on">TumCCA↑</a>,
<!-- <a href="tbResList.php?qv=192&tsv=73&wNotes=on">cyclin D1↓</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=378&wNotes=on">cyclin E↓</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=467&wNotes=on">CDK2↓</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=894&wNotes=on">CDK4↓</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=895&wNotes=on">CDK6↓</a>, -->
<br>

<!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, -->
- inhibits Migration/Invasion :
<a href="tbResList.php?qv=192&tsv=326&wNotes=on">TumCMig↓</a>,
<a href="tbResList.php?qv=192&tsv=324&wNotes=on">TumCI↓</a>,
<a href="tbResList.php?qv=192&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis -->
<!-- <a href="tbResList.php?qv=192&tsv=110&wNotes=on">FAK↓</a>, -->
<a href="tbResList.php?qv=192&tsv=105&wNotes=on">ERK↓</a>,
<!-- <a href="tbResList.php?qv=192&tsv=96&wNotes=on">EMT↓</a>, -->
<!-- <a href="tbResList.php?qv=192&wNotes=on&word=TOP">TOP1↓</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=657&wNotes=on">TET1</a>, -->
<br>

<!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS -->
<!--
- inhibits
<a href="tbResList.php?qv=192&tsv=129&wNotes=on">glycolysis</a>
/<a href="tbResList.php?qv=192&tsv=947&wNotes=on">Warburg Effect</a> and
<a href="tbResList.php?qv=192&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> :
<a href="tbResList.php?qv=192&tsv=143&wNotes=on">HIF-1α↓</a>,
<a href="tbResList.php?qv=192&tsv=772&wNotes=on">PKM2↓</a>,
<a href="tbResList.php?qv=192&tsv=35&wNotes=on">cMyc↓</a>,
<a href="tbResList.php?qv=192&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>,
<a href="tbResList.php?qv=192&tsv=906&wNotes=on">LDH↓</a>,
<a href="tbResList.php?qv=192&tsv=175&wNotes=on&word=LDH">LDHA↓</a>,
<a href="tbResList.php?qv=192&tsv=773&wNotes=on">HK2↓</a>,
<a href="tbResList.php?qv=192&wNotes=on&word=PFK">PFKs↓</a>,
<a href="tbResList.php?qv=192&wNotes=on&word=PDK">PDKs↓</a>,
<a href="tbResList.php?qv=192&tsv=847&wNotes=on">ECAR↓</a>,
<a href="tbResList.php?qv=192&tsv=230&wNotes=on">OXPHOS↓</a>,
<a href="tbResList.php?qv=192&tsv=356&wNotes=on">GRP78↑</a>,
<a href="tbResList.php?qv=192&tsv=1278&wNotes=on">Glucose↓</a>,
<a href="tbResList.php?qv=192&tsv=623&wNotes=on">GlucoseCon↓</a>
<br>
-->

<!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)-->
<!--
- inhibits
<a href="tbResList.php?qv=192&tsv=447&wNotes=on">angiogenesis↓</a> :
<a href="tbResList.php?qv=192&tsv=334&wNotes=on">VEGF↓</a>,
<a href="tbResList.php?qv=192&tsv=143&wNotes=on">HIF-1α↓</a>,
<a href="tbResList.php?qv=192&wNotes=on&word=NOTCH">Notch↓</a>,
<a href="tbResList.php?qv=192&wNotes=on&word=FGF">FGF↓</a>,
<a href="tbResList.php?qv=192&wNotes=on&word=PDGF">PDGF↓</a>,
<a href="tbResList.php?qv=192&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>,
<a href="tbResList.php?qv=192&&wNotes=on&word=ITG">Integrins↓</a>,
<br> -->

<!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, -->
<!--
- inhibits Cancer Stem Cells :
<a href="tbResList.php?qv=192&tsv=795&wNotes=on">CSC↓</a>,
<a href="tbResList.php?qv=192&tsv=524&wNotes=on">CK2↓</a>,
<a href="tbResList.php?qv=192&tsv=141&wNotes=on">Hh↓</a>,
<a href="tbResList.php?qv=192&tsv=434&wNotes=on">GLi↓</a>,
<a href="tbResList.php?qv=192&tsv=124&wNotes=on">GLi1↓</a>,
<a href="tbResList.php?qv=192&tsv=677&wNotes=on">CD133↓</a>,
<a href="tbResList.php?qv=192&tsv=655&wNotes=on">CD24↓</a>,
<a href="tbResList.php?qv=192&tsv=342&wNotes=on">β-catenin↓</a>,
<a href="tbResList.php?qv=192&tsv=357&wNotes=on">n-myc↓</a>,
<a href="tbResList.php?qv=192&tsv=656&wNotes=on">sox2↓</a>,
<a href="tbResList.php?qv=192&wNotes=on&word=NOTCH">Notch2↓</a>,
<a href="tbResList.php?qv=192&tsv=1024&wNotes=on">nestin↓</a>,
<a href="tbResList.php?qv=192&tsv=508&wNotes=on">OCT4↓</a>,
<br> -->

<!-- OTHERS : -->
- Others: <a href="tbResList.php?qv=192&tsv=252&wNotes=on">PI3K↓</a>,
<a href="tbResList.php?qv=192&tsv=4&wNotes=on">AKT↓</a>,
<!-- <a href="tbResList.php?qv=192&wNotes=on&word=JAK">JAK↓</a>, -->
<!-- <a href="tbResList.php?qv=192&wNotes=on&word=STAT">STAT↓</a>, -->
<a href="tbResList.php?qv=192&tsv=377&wNotes=on">Wnt↓</a>,
<!-- <a href="tbResList.php?qv=192&tsv=342&wNotes=on">β-catenin↓</a>, -->
<a href="tbResList.php?qv=192&tsv=9&wNotes=on">AMPK</a>,
<!-- <a href="tbResList.php?qv=192&tsv=475&wNotes=on">α↓</a>, -->
<a href="tbResList.php?qv=192&tsv=105&wNotes=on">ERK↓</a>,
<!-- <a href="tbResList.php?qv=192&tsv=1014&wNotes=on">5↓</a>, -->
<a href="tbResList.php?qv=192&tsv=168&wNotes=on">JNK</a>,

<!-- - <a href="tbResList.php?qv=192&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol). --><br>


<!-- SYNERGIES : -->
- Synergies:
<!-- <a href="tbResList.php?qv=192&tsv=1106&wNotes=on">chemo-sensitization</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=1171&wNotes=on">chemoProtective</a>, -->
<<!-- a href="tbResList.php?qv=192&tsv=1107&wNotes=on">RadioSensitizer</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=1185&wNotes=on">RadioProtective</a>, -->
<a href="tbResList.php?qv=192&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>,
<a href="tbResList.php?qv=192&tsv=1105&wNotes=on">Neuroprotective</a>,
<a href="tbResList.php?qv=192&tsv=557&wNotes=on">Cognitive</a>,
<!-- <a href="tbResList.php?qv=192&tsv=1175&wNotes=on">Renoprotection</a>, -->
<!-- <a href="tbResList.php?qv=192&tsv=1179&wNotes=on">Hepatoprotective</a>, -->
<!-- <a href="tbResList.php?&qv=192&tsv=1188&wNotes=on">CardioProtective</a>, -->

<br>
<br>
<!-- SELECTIVE: -->
- Selectivity:
<a href="tbResList.php?qv=192&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a><br>
<br>


<h3>Rotating Magnetic Field Cancer Mechanisms</h3>
<table border="1" cellspacing="0" cellpadding="4">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer Cells</th>
<th>Normal Cells</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>

<tr>
<td>1</td>
<td>Mitochondrial Complex I and electron transport</td>
<td>↓ Complex I activity; ↓ NADH:ubiquinone oxidoreductase function; ↓ mitochondrial electron transport</td>
<td>↔ no comparable persistent inhibition demonstrated in tested normal astrocytes and astroglial cells</td>
<td>P, R</td>
<td>Upstream metabolic disruption</td>
<td>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.</td>
</tr>

<tr>
<td>2</td>
<td>Mitochondrial ROS and oxidative stress</td>
<td>↑ superoxide; ↑ intracellular ROS; ↑ oxidative stress</td>
<td>↔ substantially smaller response in tested normal-cell models</td>
<td>P, R</td>
<td>Selective oxidative injury</td>
<td>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.</td>
</tr>

<tr>
<td>3</td>
<td>Mitochondrial membrane integrity and permeability</td>
<td>↓ mitochondrial function; ↓ membrane integrity; ↑ permeability transition and mitochondrial injury (context-dependent)</td>
<td>↔ comparatively resistant in tested normal cells</td>
<td>R</td>
<td>Bioenergetic collapse</td>
<td>Occurs downstream of disturbed respiratory-chain redox chemistry and ROS. Strength of direct evidence varies by RMF implementation.</td>
</tr>

<tr>
<td>4</td>
<td>Glutathione redox system</td>
<td>↓ reduced GSH availability; ↑ GSH oxidation; ↑ GSSG/GSH ratio; ↓ reducing capacity</td>
<td>↔ lower oxidative burden in tested normal-cell models</td>
<td>R</td>
<td>Weakens antioxidant buffering</td>
<td>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.</td>
</tr>

<tr>
<td>5</td>
<td>DNA oxidative damage and cell-cycle control</td>
<td>↑ oxidative DNA damage; ↑ G1 arrest; ↓ proliferation</td>
<td>↔ little comparable damage reported in tested normal astroglial cells</td>
<td>R, G</td>
<td>Cytostatic and genotoxic response</td>
<td>Downstream of sOMF-induced oxidative stress rather than evidence for a direct magnetic interaction with DNA.</td>
</tr>

<tr>
<td>6</td>
<td>Caspase-dependent apoptosis</td>
<td>↑ caspase activation; ↑ apoptosis; ↓ clonogenic survival</td>
<td>↔ comparatively low toxicity in tested normal-cell systems</td>
<td>R, G</td>
<td>Cancer-cell death</td>
<td>Oncomagnetic sOMF produces ROS-dependent loss of clonogenic survival and delayed caspase activation. Antioxidant rescue supports oxidative stress as the upstream driver.</td>
</tr>

<tr>
<td>7</td>
<td>F-actin and cytoskeletal mechanotransduction</td>
<td>↓ F-actin organization; ↓ spreading; ↓ migration; ↓ invasion</td>
<td>↔ insufficient comparative evidence</td>
<td>R, G</td>
<td>Suppresses invasive behavior</td>
<td>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.</td>
</tr>

<tr>
<td>8</td>
<td>Mechanosensitive Ca²⁺ signaling</td>
<td>↑ or altered Ca²⁺ influx and oscillatory dynamics (context-dependent); altered Ca²⁺-dependent signaling</td>
<td>↔ insufficient comparative cancer-specific evidence</td>
<td>P, R</td>
<td>Mechanotransduction and signaling modulation</td>
<td>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.</td>
</tr>

<tr>
<td>9</td>
<td>CCDC150 TGF-β1 SMAD3 axis</td>
<td>↓ CCDC150; ↓ TGF-β1/SMAD3 signaling; ↓ migration; ↓ invasion; ↓ metastasis</td>
<td>↔ insufficient comparative evidence</td>
<td>G</td>
<td>Antimetastatic signaling</td>
<td>Directly demonstrated with gradient RMF in triple-negative breast cancer models and closely linked to RMF-induced F-actin disruption.</td>
</tr>

<tr>
<td>10</td>
<td>COL11A1 ITGB1 FAK YAP axis</td>
<td>↓ COL11A1; ↓ ITGB1 signaling; ↓ FAK/YAP activation; ↓ tumor growth; ↓ lung metastasis</td>
<td>↔ insufficient comparative evidence</td>
<td>G</td>
<td>Suppresses ECM-driven metastatic signaling</td>
<td>Recent RMF-specific TNBC work identifies COL11A1 as an RMF-responsive extracellular-matrix component upstream of ITGB1/FAK/YAP signaling.</td>
</tr>

<tr>
<td>11</td>
<td>Magnetomechanical nanoparticle actuation</td>
<td>↑ mechanical membrane, cytoskeletal, lysosomal, or organelle injury (requires external trigger)</td>
<td>↔ strongly dependent on nanoparticle uptake and intracellular localization</td>
<td>P, R</td>
<td>Mechanical tumor-cell injury</td>
<td>Requires magnetic nanoparticles, nanomotors, or related magnetic structures. It is a genuine rotating-field mechanism but should be distinguished from particle-free Oncomagnetic sOMF.</td>
</tr>

<tr>
<td>12</td>
<td>GSH GPX4 ferroptosis axis</td>
<td>↓ GSH; ↓ GPX4; ↑ lipid ROS; ↑ lipid peroxidation; ↑ ferroptosis (requires external trigger)</td>
<td>↔ model-dependent</td>
<td>R, G</td>
<td>Ferroptotic cell death</td>
<td>Relevant primarily to RMF-driven magnetic nanoparticle and nanorobot systems. Current evidence does not establish GPX4 suppression as a general particle-free Oncomagnetic mechanism.</td>
</tr>

<tr>
<td>13</td>
<td>NRF2 antioxidant response</td>
<td>Potential ↑ compensatory NRF2 signaling following oxidative stress (context-dependent)</td>
<td>↔ insufficient RMF-specific comparative evidence</td>
<td>R, G</td>
<td>Adaptive antioxidant defense</td>
<td>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.</td>
</tr>

<tr>
<td>14</td>
<td>Tumor microenvironment mechanics</td>
<td>↓ matrix stiffness; altered CAF mechanics; ↑ immune-cell infiltration (model-dependent) (requires external trigger)</td>
<td>↔ model-dependent</td>
<td>R, G</td>
<td>Microenvironment remodeling</td>
<td>Reported mainly in RMF-driven magnetic nanomotor systems rather than particle-free RMF.</td>
</tr>

<tr>
<td>15</td>
<td>Chemosensitization</td>
<td>↑ treatment response in selected combination systems (context-dependent) (requires external trigger)</td>
<td>↔ insufficient comparative evidence</td>
<td>R, G</td>
<td>Combination-treatment enhancement</td>
<td>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.</td>
</tr>

<tr>
<td>16</td>
<td>Clinical Translation Constraint</td>
<td>Response depends on waveform, rotation, field amplitude, frequency, gradient, geometry, treatment duration, tumor type, and nanoparticle use</td>
<td>Long-term human safety and comparative normal-tissue data remain limited</td>
<td>P, R, G</td>
<td>Limits cross-platform extrapolation</td>
<td>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.</td>
</tr>
</table>
<p>P: 0–30 min&nbsp;&nbsp;&nbsp;&nbsp;R: 30 min–3 hr&nbsp;&nbsp;&nbsp;&nbsp;G: &gt;3 hr</p>


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


<br><br>
<hr>
<br>

<p><b>Alzheimer’s disease relevance:</b> 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.</p>

<p><b>Clinical status:</b> 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.</p>



<h3>Rotating Magnetic Field Alzheimer’s Mechanisms</h3>
<table border="1" cellspacing="0" cellpadding="4">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>AD Modulation</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>

<tr>
<td>1</td>
<td>Aβ aggregation and amyloid deposition</td>
<td>↓ Aβ fibril formation; ↓ amyloid plaques</td>
<td>Reduces amyloid burden</td>
<td>RMF can directly interfere with Aβ aggregation in vitro and reduced amyloid deposition in APP/PS1 mice.</td>
</tr>

<tr>
<td>2</td>
<td>Autophagy PI3K AKT mTOR</td>
<td>↑ autophagy; ↓ PI3K/AKT/mTOR signaling</td>
<td>Promotes proteostatic clearance</td>
<td>Long-term RMF exposure in APP/PS1 mice improved cognition and was associated with activation of autophagy-related pathways.</td>
</tr>

<tr>
<td>3</td>
<td>Microglial activation and neuroinflammation</td>
<td>↓ pathological microglial activation; polarization shifted toward protective phenotype</td>
<td>Reduces neuroinflammatory injury</td>
<td>Observed in both familial and sporadic mouse AD models.</td>
</tr>

<tr>
<td>4</td>
<td>Oxidative stress</td>
<td>↓ oxidative stress</td>
<td>Neuroprotection</td>
<td>Direction differs from the deliberate ROS increase observed in Oncomagnetic cancer cells, illustrating strong disease- and cell-state dependence.</td>
</tr>

<tr>
<td>5</td>
<td>Neuronal integrity</td>
<td>↑ neuronal survival and functional preservation</td>
<td>Neuroprotection</td>
<td>Associated with reduced neuronal damage in RMF-treated AD mice.</td>
</tr>

<tr>
<td>6</td>
<td>Cognition and memory</td>
<td>↑ spatial memory; ↑ recognition memory; ↑ cognitive performance</td>
<td>Functional improvement</td>
<td>Repeatedly reported in RMF-treated mouse models, but human efficacy remains unestablished.</td>
</tr>
</table>



Pathway results for Effect on Cancer / Diseased Cells

NA, unassigned(tgid=0) ⓘ

compII↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ATF3↑, 1,   compI↓, 1,   Fenton↑, 2,   Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 2,   GSH↑, 1,   GSH/GSSG↓, 2,   mt-H2O2↑, 1,   H2O2↑, 4,   Iron↑, 1,   lipid-P↑, 1,   mt-NADH↓, 1,   RNS↑, 1,   ROS↑, 16,   mt-ROS↑, 1,   RPM↑, 1,   SOD↓, 1,   Thiols↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↓, 1,   TfR1/CD71↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ETC↓, 9,   mitResp↓, 1,   MMP?, 1,   MMP↓, 5,   MPT↑, 3,   mtDam↑, 1,   OCR↓, 1,   PleEff↓, 1,   SDH↓, 2,   UCP1↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACAA1↓, 1,   ALAT↓, 2,   AMPK↑, 1,   BCAP↓, 1,   FABP4↓, 1,   GlucoseCon↓, 1,   lactateProd↑, 1,   PCK1↓, 1,   PLIN1↓, 1,   PPARγ↑, 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,   lysoMP↑, 2,   lysoMP↓, 2,   TumCD↑, 9,   YAP/TEAD↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 1,   p‑Akt↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

BowelM↑, 2,   ChrMod↑, 2,   other↝, 2,   tumCV↓, 3,  

Autophagy & Lysosomes(tgid=9) ⓘ

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

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 4,   P53↑, 2,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

E2Fs↓, 1,   TumCCA↑, 5,  

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

ERK↑, 1,   miR-34a↑, 1,   TumCG↓, 12,  

Migration(tgid=13) ⓘ

Ca+2↑, 4,   CAFs/TAFs↓, 1,   Cartilage↑, 1,   CCDC150↓, 1,   COL11A1↓, 1,   COL4↓, 1,   CXCL12↓, 1,   F-actin↓, 1,   FAK↓, 1,   FOSB↑, 1,   ITGA11↓, 1,   ITGB1↓, 1,   LAMB3↑, 1,   miR-486↑, 1,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   Rho↓, 1,   SMAD3↓, 1,   TGF-β↓, 1,   THBS2↓, 1,   TumCI↓, 3,   TumCMig↓, 2,   TumCP↓, 4,   TumMeta↓, 5,  

Angiogenesis & Vasculature(tgid=14) ⓘ

ECM/TCF↓, 1,   EPR↑, 2,   nucleolin↑, 1,  

Barriers & Transport(tgid=15) ⓘ

CellMemb↑, 5,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↓, 1,   CD4+↑, 3,   CXCc↓, 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↑, 2,   pol-M1↝, 1,   Macrophages↑, 1,   NF-kB↑, 1,   PD-L1↑, 1,   RANTES↓, 1,   T-Cell↑, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioEnh↑, 1,   Dose↝, 12,   Dose∅, 1,   Dose↑, 2,   Dose?, 2,   eff↓, 6,   eff↑, 14,   eff↝, 5,   selectivity↑, 8,   selectivity?, 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,   breath↑, 2,   chemoP↑, 1,   ChemoSideEff↓, 1,   cognitive↑, 1,   hepatoP↑, 1,   OS↑, 12,   OS⇅, 1,   OS?, 1,   Pain↓, 4,   QoL↑, 2,   radioP↑, 1,   Sleep↑, 2,   Strength↑, 4,   toxicity↓, 2,   TumVol↓, 8,   Weight↑, 2,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,   CD8+↓, 1,   CD8+↑, 3,  
Total Targets: 166

Pathway results for Effect on Normal Cells

NA, unassigned(tgid=0) ⓘ

DCR∅, 1,   ORR∅, 1,   PFS∅, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 2,   Ferroptosis↑, 1,   GPx↑, 1,   GPx1↑, 1,   GPx4↑, 1,   MDA↓, 1,   ROMO1↑, 1,   ROS∅, 1,   ROS↑, 1,   ROS↓, 9,   SOD↑, 2,   SOD1↑, 1,   SOD2↑, 1,   TAC↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 2,   FABP4↓, 1,   PPARγ↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   Ferroptosis↑, 1,   iNOS↓, 1,   p‑JNK↓, 1,   p‑JNK↑, 2,   MAPK↓, 1,   p‑p38↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 1,   p‑Akt↓, 1,   OCN∅, 1,   SOX9↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 1,   other↝, 6,   other?, 1,   other↓, 1,   other↑, 2,   TREM-1↓, 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,   ERK↓, 1,   FGF↑, 1,   IGF-1↑, 1,   mTOR↓, 3,   PI3K↓, 1,   RUNX2∅, 1,   TumCG∅, 1,   TumCG↓, 2,   VGSC↑, 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,   Treg lymp↓, 1,   β-catenin/ZEB1↑, 1,   β-Endo↑, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 1,   EGR4↑, 1,   NO↓, 1,   NO↑, 1,   NPY↑, 1,   PDGFR-BB↑, 1,  

Barriers & Transport(tgid=15) ⓘ

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

Immune & Inflammatory Signaling(tgid=16) ⓘ

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

Synaptic & Neurotransmission(tgid=18) ⓘ

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

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 4,   Aβ?, 1,   β-Amyloid↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Clinical Biomarkers(tgid=22) ⓘ

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

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 2,   cognitive↑, 6,   memory↑, 5,   motorD↑, 3,   neuroP↑, 4,   OS↑, 3,   radioP↑, 1,   toxicity∅, 5,   toxicity?, 1,   toxicity↓, 1,  
Total Targets: 137

Research papers

Year Title Authors PMID Link Flag
2026Therapeutic Magnetic Fields in Oncology: A Systematic Review of Safety and Supportive Clinical UseSaverio ColonnaPMC12921648https://pmc.ncbi.nlm.nih.gov/articles/PMC12921648/0
2026Neuroprotective effect of RMF in a mouse model of sporadic Parkinson's diseaseUmer Anayyat41862117https://pubmed.ncbi.nlm.nih.gov/41862117/0
2026Dual-targeting by rotating magnetic field-driven superparamagnetic bionic nanorobots for enhanced triple-negative breast cancer therapyWei Song—https://link.springer.com/article/10.1631/bdm.25006560
2026Dynamic magneto-mechanical force in lysosomes induces durable macrophage repolarization for antitumor immunityYingze LiPMC12909937https://pmc.ncbi.nlm.nih.gov/articles/PMC12909937/0
2026Inhibition of mitochondrial NADH:ubiquinone oxidoreductase by spinning oscillating magnetic fields causes toxicity in cancer cellsShashank Hambarde41510612https://pubmed.ncbi.nlm.nih.gov/41510612/0
2026Rotating magnetic field downregulating type XI collagen to suppress triple-negative breast cancer metastasis by inactivating the ITGB1/FAK/YAP signaling pathwayTongyao Yu—https://www.sciencedirect.com/science/article/abs/pii/S01418130251023410
2025Urchin-like magnetic nanoparticles loaded with type X collagen siRNA and Stattic to treat triple negative breast cancer under rotating magnetic field like an "enchanted micro-scalpel"Jie Liu39864683https://pubmed.ncbi.nlm.nih.gov/39864683/0
2025Actin-Targeted Magnetic Nanomotors Mechanically Modulate the Tumor Mechanical Microenvironment for Cancer TreatmentXing Fan39915111https://pubmed.ncbi.nlm.nih.gov/39915111/0
2025Case Report: A new noninvasive device-based treatment of a mesencephalic H3 K27M gliomaSantosh A HelekarPMC12626803https://pmc.ncbi.nlm.nih.gov/articles/PMC12626803/0
2025The neurobiological foundation of effective repetitive transcranial magnetic brain stimulation in Alzheimer's diseaseAnnibale Antonioni—https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.70337?utm_source=chatgpt.com0
2025Rotating magnetic field improves cognitive and memory impairments in APP/PS1 mice by activating autophagy and inhibiting the PI3K/AKT/mTOR signaling pathwayMengqing L—https://pubmed.ncbi.nlm.nih.gov/39461710/0
2024Feature Matching of Microsecond-Pulsed Magnetic Fields Combined with Fe3O4 Particles for Killing A375 Melanoma CellsYan MiPMC11117552https://pmc.ncbi.nlm.nih.gov/articles/PMC11117552/0
2024Anti-tumor effect of innovative tumor treatment device OM-100 through enhancing anti-PD-1 immunotherapy in glioblastoma growthZhaoxian YanPMC11310191https://www.nature.com/articles/s41598-024-67437-4.pdf0
2024Rotating magnetic field inhibits Aβ protein aggregation and alleviates cognitive impairment in Alzheimer's disease mice.Ruo-Wen Guo—https://ngdc.cncb.ac.cn/openlb/publication/OLB-PM-390210810
2024Synergistic Effect of Chemotherapy and Magnetomechanical Actuation of Fe-Cr-Nb-B Magnetic Particles on Cancer CellsCristina StavilăPMC11256100https://pmc.ncbi.nlm.nih.gov/articles/PMC11256100/0
2024Enhancement of chemotherapy effects by non-lethal magneto-mechanical actuation of gold-coated magnetic nanoparticlesCristina Stavilă PhD student—https://www.sciencedirect.com/science/article/pii/S15499634240003520
2024The Effect of a Rotating Magnetic Field on the Regenerative Potential of PlateletsElżbieta Cecerska-HeryćPMC11012199https://pmc.ncbi.nlm.nih.gov/articles/PMC11012199/0
2024The Effect of Extremely Low-Frequency Magnetic Field on Stroke Patients: A Systematic ReviewRenata MarchewkaPMC11119128https://pmc.ncbi.nlm.nih.gov/articles/PMC11119128/0
2024Polyhedral magnetic nanoparticles induce apoptosis in gastric cancer stem cells and suppressing tumor growth through magnetic force generationJianhua Wang—https://www.sciencedirect.com/science/article/abs/pii/S01683659240048870
2024Rotating magnetic field inhibits Aβ protein aggregation and alleviates cognitive impairment in Alzheimer’s disease miceRuo-Wen GuoRuo-Wen Guohttps://pmc.ncbi.nlm.nih.gov/articles/PMC11298676/0
2024Gradient Rotating Magnetic Fields Impairing F-Actin-Related Gene CCDC150 to Inhibit Triple-Negative Breast Cancer Metastasis by Inactivating TGF-β1/SMAD3 Signaling PathwayGe ZhangPMC10900498https://pmc.ncbi.nlm.nih.gov/articles/PMC10900498/0
2024Systematic simulation of tumor cell invasion and migration in response to time-varying rotating magnetic fieldShilong Zhang38801615https://pubmed.ncbi.nlm.nih.gov/38801615/0
2024Rotating magnetic field improved cognitive and memory impairments in a sporadic ad model of mice by regulating microglial polarizationMengqing LiPMC11493917https://pmc.ncbi.nlm.nih.gov/articles/PMC11493917/0
2024The effect of a rotating magnetic field on the antioxidant system in healthy volunteers - preliminary studyElżbieta Cecerska-HeryćPMC11018782https://pmc.ncbi.nlm.nih.gov/articles/PMC11018782/0
2023Spinning magnetic field patterns that cause oncolysis by oxidative stress in glioma cellsShashank HambardePMC10630398https://pmc.ncbi.nlm.nih.gov/articles/PMC10630398/0
2023Rotating Magnetic Field Mitigates Ankylosing Spondylitis Targeting Osteocytes and Chondrocytes via Ameliorating Immune DysfunctionsYu HanPMC10093245https://pmc.ncbi.nlm.nih.gov/articles/PMC10093245/0
2023Biological effects of rotating magnetic field: A review from 1969 to 2021Yunpeng Wei36574882https://pubmed.ncbi.nlm.nih.gov/36574882/0
2023Mechanical nanosurgery of chemoresistant glioblastoma using magnetically controlled carbon nanotubesXIAN WANG—https://www.science.org/doi/10.1126/sciadv.ade53210
2023Magnetically controlled cyclic microscale deformation of in vitro cancer invasion modelsDaphne Osk Asgeirsson—https://www.researchgate.net/publication/374768956_Magnetically_Controlled_Cyclic_Microscale_Deformation_of_In_Vitro_Cancer_Invasion_Models0
2023Intermittent F-actin Perturbations by Magnetic Fields Inhibit Breast Cancer MetastasisXinmiao JiPMC10017101https://pmc.ncbi.nlm.nih.gov/articles/PMC10017101/0
2022Rotating Magnetic Field-Assisted Reactor Enhances Mechanisms of Phage Adsorption on Bacterial Cell SurfaceBartłomiej GrygorcewiczPMC8947294https://pmc.ncbi.nlm.nih.gov/articles/PMC8947294/0
2022Method for noninvasive whole-body stimulation with spinning oscillating magnetic fields and its safety in miceShashank Hambarde36154345https://pubmed.ncbi.nlm.nih.gov/36154345/0
2022Method and apparatus for oncomagnetic treatmentHelekar et al—https://patents.google.com/patent/US12186575B2/en0
2022EXTH-68. ONCOMAGNETIC TREATMENT SELECTIVELY KILLS GLIOMA CANCER CELLS BY INDUCING OXIDATIVE STRESS AND DNA DAMAGEShashank HambardePMC9661114https://pmc.ncbi.nlm.nih.gov/articles/PMC9661114/0
2021Pulsed Electromagnetic Field Stimulation in Osteogenesis and Chondrogenesis: Signaling Pathways and Therapeutic ImplicationsKatia VaraniPMC7830993https://pmc.ncbi.nlm.nih.gov/articles/PMC7830993/0
2021Case Report: End-Stage Recurrent Glioblastoma Treated With a New Noninvasive Non-Contact Oncomagnetic DeviceDavid S BaskinPMC8341943https://pmc.ncbi.nlm.nih.gov/articles/PMC8341943/0
2021Selective induction of rapid cytotoxic effect in glioblastoma cells by oscillating magnetic fieldsSantosh A Helekar34477946https://pubmed.ncbi.nlm.nih.gov/34477946/0
2021Magneto-mechanical destruction of cancer-associated fibroblasts using ultra-small iron oxide nanoparticles and low frequency rotating magnetic fieldsSara LopezPMC9417452https://pmc.ncbi.nlm.nih.gov/articles/PMC9417452/0
2021Modulation of Cellular Response to Different Parameters of the Rotating Magnetic Field (RMF)—An In Vitro Wound Healing StudyMagdalena Jedrzejczak-SilickaPMC8199476https://pmc.ncbi.nlm.nih.gov/articles/PMC8199476/0
2021Magnetic fields as a potential therapy for diabetic wounds based on animal experiments and clinical trialsHuanhuan LvPMC7941227https://pmc.ncbi.nlm.nih.gov/articles/PMC7941227/0
2021Rotating Magnetic Fields Inhibit Mitochondrial Respiration, Promote Oxidative Stress and Produce Loss of Mitochondrial Integrity in Cancer CellsMartyn A SharpePMC8631329https://pmc.ncbi.nlm.nih.gov/articles/PMC8631329/0
2020Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17Tianying ZhanPMC7185125https://pmc.ncbi.nlm.nih.gov/articles/PMC7185125/0
2020Synthesis of urchin-like nickel nanoparticles with enhanced rotating magnetic field-induced cell necrosis and tumor inhibitionYong Qian—https://www.sciencedirect.com/science/article/abs/pii/S13858947203195130
2020Magnetically switchable mechano-chemotherapy for enhancing the death of tumour cells by overcoming drug-resistanceYao Chenyang—https://m.x-mol.net/paper/article/13077384348683182080
2020ONCOSCILLATORS: INDUCTION OF THE MITOCHONDRIAL PERMEABILITY TRANSITION IN CANCER CELLSMartyn SharpePMC7651633https://pmc.ncbi.nlm.nih.gov/articles/PMC7651633/0
2020The 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 trialMinghui Zhu32238091https://pubmed.ncbi.nlm.nih.gov/32238091/0
2020Cancer treatment by magneto-mechanical effect of particles, a reviewCécile NaudPMC9419242https://pmc.ncbi.nlm.nih.gov/articles/PMC9419242/0
2020Study on the Effect of Rotating Magnetic Field on Cellular Response of Mammalian CellsMagdalena Jędrzejczak-Silicka—https://www.researchgate.net/publication/341242877_Study_on_the_Effect_of_Rotating_Magnetic_Field_on_Cellular_Response_of_Mammalian_Cells0
2019Rotating magnetic field delays human umbilical vein endothelial cell aging and prolongs the lifespan of Caenorhabditis elegansJiangyao Xu—https://www.researchgate.net/publication/337466667_Rotating_magnetic_field_delays_human_umbilical_vein_endothelial_cell_aging_and_prolongs_the_lifespan_of_Caenorhabditis_elegans0
2019Oncogenic pathways and the electron transport chain: a dangeROS liaisonVittoria RaimondiPMC7052168https://pmc.ncbi.nlm.nih.gov/articles/PMC7052168/0
2018Spatiotemporal magnetic fields enhance cytosolic Ca2+ levels and induce actin polymerization via activation of voltage-gated sodium channels in skeletal muscle cellsMónica Rubio Ayala—https://www.sciencedirect.com/science/article/abs/pii/S01429612183011700
2018Application of Rotating Magnetic Fields Increase the Activity of Antimicrobials Against Wound Biofilm PathogensA. F. Junka—https://www.nature.com/articles/s41598-017-18557-70
2018Effect of low-frequency rotary magnetic fields on advanced gastric cancerChen, Zheng29970658https://journals.lww.com/cancerjournal/fulltext/2018/14040/effect_of_low_frequency_rotary_magnetic_fields_on.15.aspx0
2017LF-MF inhibits iron metabolism and suppresses lung cancer through activation of P53-miR-34a-E2F1/E2F3 pathwayJing RenPMC5429732https://pmc.ncbi.nlm.nih.gov/articles/PMC5429732/0
2017Elongated Nanoparticle Aggregates in Cancer Cells for Mechanical Destruction with Low Frequency Rotating Magnetic FieldYajing ShenPMC5436524https://pmc.ncbi.nlm.nih.gov/articles/PMC5436524/0
2017Low Frequency Magnetic Fields Induce Autophagy-associated Cell Death in Lung Cancer through miR-486-mediated Inhibition of Akt/mTOR Signaling PathwayYujun XuPMC5603574https://pmc.ncbi.nlm.nih.gov/articles/PMC5603574/0
2016Early exposure of rotating magnetic fields promotes central nervous regeneration in planarian Girardia sinensisQiang Chen27061713https://pubmed.ncbi.nlm.nih.gov/27061713/0
2016Extremely low frequency magnetic fields regulate differentiation of regulatory T cells: Potential role for ROS-mediated inhibition on AKTRuijing Tang26807660https://pubmed.ncbi.nlm.nih.gov/26807660/0
2016Moderate intensity low frequency rotating magnetic field inhibits breast cancer growth in miceMeng Zha30142006https://www.researchgate.net/publication/327213612_Moderate_intensity_low_frequency_rotating_magnetic_field_inhibits_breast_cancer_growth_in_mice0
2015Modification of bacterial cellulose through exposure to the rotating magnetic fieldKarol Fijałkowski26344254https://pubmed.ncbi.nlm.nih.gov/26344254/0
2015Rotating Magnetic Field Induced Oscillation of Magnetic Particles for in vivo Mechanical Destruction of Malignant GliomaYu ChengPMC4724455https://pmc.ncbi.nlm.nih.gov/articles/PMC4724455/0
2014Extremely low frequency magnetic fields inhibit adipogenesis of human mesenchymal stem cellsLeilei Du25196555https://pubmed.ncbi.nlm.nih.gov/25196555/0
2013Low Frequency Magnetic Fields Enhance Antitumor Immune Response against Mouse H22 Hepatocellular CarcinomaYunzhong NiePMC3835892https://pmc.ncbi.nlm.nih.gov/articles/PMC3835892/0
2013Effect of low frequency magnetic fields on melanoma: tumor inhibition and immune modulationYunzhong NiePMC4029221https://pmc.ncbi.nlm.nih.gov/articles/PMC4029221/0
2012Magnetoporation and magnetolysis of cancer cells via carbon nanotubes induced by rotating magnetic fieldsDun Liu22950948https://pubmed.ncbi.nlm.nih.gov/22950948/0
2012A pilot study of extremely low-frequency magnetic fields in advanced non-small cell lung cancer: Effects on survival and palliation of general symptomsCHENGTAO SUNPMC3499610https://pmc.ncbi.nlm.nih.gov/articles/PMC3499610/0
2011Involvement of midkine expression in the inhibitory effects of low-frequency magnetic fields on cancer cellsTingting Wang21360556https://pubmed.ncbi.nlm.nih.gov/21360556/0
2008The hemoprotective effects of a rotary magnetic field in mice exposed to γ irradiationXue-jun Xie—https://www.semanticscholar.org/paper/The-hemoprotective-effects-of-a-rotary-magnetic-in-Xie-Qi/e39cd1191f5dc087d298977871cea29f76dec0c10
2008The expression and intranuclear distribution of nucleolin in HL-60 and K-562 cells after repeated, short-term exposition to rotating magnetic fieldsMarek Masiuk18821389https://pubmed.ncbi.nlm.nih.gov/18821389/0
2006Effects of 0.4 T Rotating Magnetic Field Exposure on Density, Strength, Calcium and Metabolism of Rat Thigh BonesXiao-yun Zhang—http://www.zgkjcx.com/Article/UploadFiles/200807/20080710121302169.pdf0
2001The Effect of Alternating Magnetic Field Exposure and Vitamin C on Cancer CellsNina Mikirova, Ph.D.—https://isom.ca/wp-content/uploads/2020/01/JOM_2001_16_3_10_The_Effect_of_Alternating_Magnetic_Field_Exposure_and-.pdf0
2001Molecular mechanism of effect of rotating constant magnetic field on organismsX Zhang18726401https://pubmed.ncbi.nlm.nih.gov/18726401/0
1999On the mitochondrial aspect of reactive oxygen species action in external magnetic fieldsP. Waliszewski—https://www.sciencedirect.com/science/article/abs/pii/S1011134499900003?via%3Dihub0
1993The effect of rotating magnetic fields on the growth of Deal's guinea pig sarcoma transplanted subcutaneously in guinea pigsE Schwartz8353767https://pubmed.ncbi.nlm.nih.gov/8353767/0
1991The growth dynamics of Walker carcinosarcoma during exposure to a magnetic eddy fieldN G Bakhmutskiĭ1843148https://pubmed.ncbi.nlm.nih.gov/1843148/0
1991The assessment of the efficacy of the effect of a rotational magnetic field on the course of the tumor process in patients with generalized breast cancerN G Bakhmutskiĭ—https://pubmed.ncbi.nlm.nih.gov/1948335/0