MFrot Magnetic Field Rotating
Description: <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>
Rotating Magnetic Fields
<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>ROS (tumor-selective oxidative stress)</td>
<td>↑ ROS (P→R); sustained to cytotoxicity (G)</td>
<td>↔ minimal change or transient ↑ without injury (P→R)</td>
<td>P, R, G</td>
<td>Primary stress amplifier</td>
<td>Oncomagnetic reports emphasize selective tumor ROS increase with normal-cell sparing in comparable exposure conditions</td>
</tr>
<tr>
<td>2</td>
<td>Mitochondrial ETC inhibition (Complex I/NADH:ubiquinone)</td>
<td>↓ Complex I / respiration (P→R)</td>
<td>↔ limited effect (P→R)</td>
<td>P, R</td>
<td>Bioenergetic collapse trigger</td>
<td>Rotating/spinning fields are proposed to disrupt mitochondrial electron flow, driving ROS elevation upstream of ΔΨm loss</td>
</tr>
<tr>
<td>3</td>
<td>Ca²⁺ signaling (ER–mitochondria Ca²⁺ transfer / mitochondrial Ca²⁺ load)</td>
<td>↑ Ca²⁺ dysregulation (P→R) contributing to mitochondrial failure (G)</td>
<td>↔ buffered Ca²⁺ homeostasis (P→R)</td>
<td>P, R, G</td>
<td>Amplifies ETC/ROS-driven toxicity</td>
<td>RMF-driven mitochondrial stress can propagate via Ca²⁺ transfer to accelerate ΔΨm loss and pro-death ER stress in tumor cells while sparing normal cells</td>
</tr>
<tr>
<td>4</td>
<td>Mitochondrial permeability transition pore (MPTP)</td>
<td>↑ sustained MPTP opening (R→G)</td>
<td>↔ resistant to opening</td>
<td>P, R, G</td>
<td>Mitochondrial point-of-no-return</td>
<td>RMF-enhanced ROS and Ca²⁺ loading promote persistent MPTP opening in tumor mitochondria, driving energetic collapse and apoptosis while normal cells remain below the opening threshold</td>
</tr>
<tr>
<td>5</td>
<td>ΔΨm / mitochondrial membrane integrity</td>
<td>↓ ΔΨm (R); progresses (G)</td>
<td>↔ preserved</td>
<td>R, G</td>
<td>Mitochondrial failure threshold</td>
<td>Matches the “energy factory” targeting concept described in Oncomagnetic mechanism narratives</td>
</tr>
<tr>
<td>6</td>
<td>GSH depletion</td>
<td>↓ GSH (R→G)</td>
<td>↔ maintained</td>
<td>R, G</td>
<td>Loss of redox buffering</td>
<td>Cancer-selective inability to restore GSH is a key discriminator vs normal cells</td>
</tr>
<tr>
<td>7</td>
<td>NRF2 response (selectivity gate)</td>
<td>↔ delayed/insufficient NRF2 (R→G)</td>
<td>↑ NRF2 (R→G)</td>
<td>R, G</td>
<td>Adaptive protection</td>
<td>Normal-cell sparing is consistent with competent NRF2-driven antioxidant defense</td>
</tr>
<tr>
<td>8</td>
<td>ER stress / UPR (CHOP commitment)</td>
<td>↑ ER stress (R); CHOP/apoptotic UPR (G)</td>
<td>↑ adaptive UPR (R); resolves (G)</td>
<td>R, G</td>
<td>Proteostasis failure</td>
<td>ETC/ROS stress propagates to ER; commitment vs resolution diverges by cell robustness</td>
</tr>
<tr>
<td>9</td>
<td>DNA damage (oxidative; checkpoint markers)</td>
<td>↑ DNA damage (R→G)</td>
<td>↔ or repaired (G)</td>
<td>R, G</td>
<td>Checkpoint stress</td>
<td>Interpreted as ROS-mediated consequence; reported as increased damage markers in some translational datasets</td>
</tr>
<tr>
<td>10</td>
<td>LDH / glycolytic vulnerability</td>
<td>↓ LDH performance / ↓ glycolytic flux (R→G)</td>
<td>↔ metabolic flexibility</td>
<td>R, G</td>
<td>Metabolic choke</td>
<td>Cancer glycolysis becomes unstable when NADH/NAD+ and redox buffering are stressed</td>
</tr>
<tr>
<td>11</td>
<td>TrxR / thioredoxin system overload</td>
<td>↓ reserve (R→G)</td>
<td>↔ preserved</td>
<td>R, G</td>
<td>Parallel antioxidant collapse</td>
<td>Useful when GSH data are mixed; TrxR can be the limiting system under sustained ROS</td>
</tr>
</table>
<pre>
Time-Scale Flag: TSF = P / R / G
P: 0–30 min (physical / electron / radical effects)
R: 30 min–3 hr (redox signaling & stress response)
G: >3 hr (gene-regulatory adaptation)
</pre>
MPTP: opening represents a mitochondrial commitment event integrating ROS and Ca²⁺ stress; sustained opening indicates irreversible bioenergetic failure.<br>