Magnetic Fields / toxicity Cancer Research Results

MF, Magnetic Fields: Click to Expand ⟱
Features: Therapy
Magnetic Fields can be Static, or pulsed. The most common therapy is a pulsed magnetic field in the uT or mT range.
The main pathways affected are:
Calcium Signaling: -influence the activity of voltage-gated calcium channels.
Oxidative Stress and Reactive Oxygen Species (ROS) Pathways
Heat Shock Proteins (HSPs) and Cellular Stress Responses
Cell Proliferation and Growth Signaling: MAPK/ERK pathway.
Gene Expression and Epigenetic Modifications: NF-κB
Angiogenesis Pathways: VEGF (improving VEGF for normal cells)
PEMF was found to have a 2-fold increase in drug uptake compared to traditional electrochemotherapy in rat melanoma models

Pathways:
- most reports have ROS production increasing in cancer cells , while decreasing in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, 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↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, VEGF↓(mostly regulated up in normal cells),
- cause Cell cycle arrest : TumCCA↑,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, GLUT1↓, LDH↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- Others: PI3K↓, AKT↓, STAT↓, Wnt↓, β-catenin↓, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, cytoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Non-Static Magnetic Fields (AC / Pulsed / Oscillating MF)
Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Reactive oxygen species (ROS) ↑ ROS (P→R); often sustained (G) ↑ ROS (P); ↔/↓ net ROS (R→G) P, R, G Upstream redox perturbation MF perturbs electron/radical dynamics: normal cells often adapt (ROS setpoint ↓), cancer cells less so
2 NRF2 antioxidant response ↔ / insufficient NRF2 induction (R→G) ↑ NRF2 activation (R→G) R, G Adaptive redox defense Explains mixed ROS direction in normal cells (initial ↑ then adaptive ↓)
3 Glutathione (GSH) homeostasis ↓ GSH (R→G) ↔ or transient ↓ (R) with recovery (G) R, G Redox buffering capacity GSH depletion reflects sustained oxidative load; recovery indicates successful adaptation
4 Superoxide dismutase (SOD) / antioxidant enzymes ↔ or inadequate enzyme upshift (G) ↑ SOD/GPx/CAT capacity (G) G Longer-term antioxidant remodeling Often the “endpoint” readout that correlates with ROS-normalization in normal tissue
5 Mitochondrial ETC / respiration ↓ ETC efficiency; ↑ electron leak (P→R) ↔ mild, reversible ETC perturbation (P→R) P, R Bioenergetic destabilization ETC perturbation is a mechanistic bridge between MF exposure and ROS/ΔΨm changes
6 Mitochondrial membrane potential (ΔΨm / MMP) ↓ ΔΨm (R); may progress (G) ↔ preserved or reversible dip (R) R, G Mitochondrial dysfunction thresholding ΔΨm loss typically follows ROS/ETC disruption rather than preceding it
7 Ca²⁺ signaling (VGCC / ER–mitochondria Ca²⁺ flux) ↑ dysregulated Ca²⁺ influx/transfer (P→R); overload may persist (G) ↑ transient Ca²⁺ signaling (P); homeostasis restored (R→G) P, R, G Stress signal amplification Ca²⁺ dysregulation links ROS/ETC perturbation to ER stress and mitochondrial dysfunction (amplifies ΔΨm loss and UPR commitment)
8 Mitochondrial permeability transition pore (MPTP) ↑ MPTP opening propensity (R); sustained opening possible (G) ↔ transient or closed (R→G) P, R, G Commitment point for mitochondrial failure MPTP opening integrates ROS, Ca²⁺ overload, and ΔΨm loss; acts as a threshold event converting reversible stress into irreversible mitochondrial dysfunction
9 ER stress / UPR ↑ ER stress (R); CHOP-commitment possible (G) ↑ adaptive UPR (R); resolves (G) R, G Proteostasis stress Often downstream of ROS + Ca²⁺ handling perturbations
10 DNA damage (oxidative) ↑ damage markers (R→G) ↔ or repaired (G) R, G Checkpoint pressure Generally secondary to ROS; interpret as stress consequence not “direct genotoxicity”
11 LDH / glycolytic flux ↓ glycolytic performance (R→G) ↔ flexible substrate switching (R→G) R, G Metabolic vulnerability Redox imbalance can destabilize high-rate glycolysis in cancer-biased contexts
12 Thioredoxin system (Trx / TrxR) ↓ functional reserve / overload (R→G) ↔ preserved capacity (G) R, G Parallel antioxidant system stress Useful when GSH-only does not explain redox phenotype 
Time-Scale Flag: TSF = P / R / G
  P: 0–30 min (physical / electron / radical effects)
  R: 30 min–3 hr (redox signaling & stress response)
  G: >3 hr (gene-regulatory adaptation)
MPTP: opening represents a mitochondrial commitment event integrating ROS and Ca²⁺ stress; sustained opening indicates irreversible bioenergetic failure.
toxicity, toxicity: Click to Expand ⟱
Source:
Type:
Toxicity
Scientific Papers found: Click to Expand⟱
2260- MF,    Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
- in-vitro, GBM, U87MG - in-vitro, GBM, LN229 - in-vivo, NA, NA
TumCP↓, TumCG↓, OS↑, ROS↑, SOD2↑, eff↓, ECAR↓, OCR↑, selectivity↑, *toxicity∅, TumVol↓, PGC-1α↑, OXPHOS↑, Glycolysis↓, PKM2↓,
3536- MF,    Targeting Mesenchymal Stromal Cells/Pericytes (MSCs) With Pulsed Electromagnetic Field (PEMF) Has the Potential to Treat Rheumatoid Arthritis
- Review, Arthritis, NA - Review, Stroke, NA
*Inflam↓, *Diff↑, *toxicity∅, *other↑, *SOX9↑, *COL2A1↑, *NO↓, *PGE2↓, *NF-kB↓, *TNF-α↓, *IL1β↓, *IL6↓, *IL10↑, *angioG↑, *MSCs↑, *VEGF↑, *TGF-β↑, *angioG↝, *VEGF↓, Ca+2↝,
3478- MF,    One Month of Brief Weekly Magnetic Field Therapy Enhances the Anticancer Potential of Female Human Sera: Randomized Double-Blind Pilot Study
- Trial, BC, NA - in-vitro, BC, MCF-7 - in-vitro, Nor, C2C12
TumCP↓, TumCMig↓, TumCI↓, *toxicity∅, TGF-β↓, Twist↓, Slug↓, β-catenin/ZEB1↓, Vim↓, p‑SMAD2↓, p‑SMAD3↓, angioG↓, VEGF↓, selectivity↑, LIF↑,
3475- MF,    A Pulsed Electromagnetic Field Protects against Glutamate-Induced Excitotoxicity by Modulating the Endocannabinoid System in HT22 Cells
- in-vitro, Nor, HT22 - Review, AD, NA
*Apoptosis↓, *LDH↓, *neuroP↑, *toxicity∅, *IL1β↓, *Inflam↓, *IL10↑, *TNF-α↓,
3567- MFrot,  MF,    The Effect of Extremely Low-Frequency Magnetic Field on Stroke Patients: A Systematic Review
- Review, Stroke, NA
*eff↑, *ROS↓, *Inflam↓, *cognitive↑, *Catalase↑, *SOD↑, *SOD1↑, *SOD2↑, *GPx1↑, *GPx4↑, *IL1β↑, *neuroP↑, *toxicity∅,
2259- MFrot,  MF,    Method and apparatus for oncomagnetic treatment
- in-vitro, GBM, NA
MMP↓, Bcl-2↓, BAX↑, Bak↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, ROS↑, lactateProd↑, Apoptosis↑, MPT↑, *selectivity↑, eff↑, MMP↓, selectivity↑, TCA?, H2O2↑, eff↑, *antiOx↑, H2O2↑, eff↓, GSH/GSSG↓, *toxicity∅, OS↑,
187- MFrot,  MF,    Method for noninvasive whole-body stimulation with spinning oscillating magnetic fields and its safety in mice
- in-vivo, GBM, NA
selectivity↑, ROS↑, *ROS∅, *toxicity∅, ETC↓, TumVol↓, Dose↝,
516- MFrot,  immuno,  MF,    Anti-tumor effect of innovative tumor treatment device OM-100 through enhancing anti-PD-1 immunotherapy in glioblastoma growth
- vitro+vivo, GBM, U87MG
TumCP↓, Apoptosis↑, TumCMig↓, ROS↑, PD-L1↑, TumVol↓, eff↑, *toxicity∅, eff↑, *toxicity∅, Dose↝, tumCV↓, TumCI↓,

Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH/GSSG↓, 1,   H2O2↑, 2,   OXPHOS↑, 1,   ROS↑, 4,   SOD2↑, 1,  

Mitochondria & Bioenergetics ⓘ

ETC↓, 1,   MMP↓, 2,   MPT↑, 1,   OCR↑, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

ECAR↓, 1,   Glycolysis↓, 1,   lactateProd↑, 1,   PKM2↓, 1,   TCA?, 1,  

Cell Death ⓘ

Apoptosis↑, 2,   Bak↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Migration ⓘ

Ca+2↝, 1,   Slug↓, 1,   p‑SMAD2↓, 1,   p‑SMAD3↓, 1,   TGF-β↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 3,   Twist↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

LIF↑, 1,   PD-L1↑, 1,  

Drug Metabolism & Resistance ⓘ

Dose↝, 2,   eff↓, 2,   eff↑, 4,   selectivity↑, 4,  

Clinical Biomarkers ⓘ

PD-L1↑, 1,  

Functional Outcomes ⓘ

OS↑, 2,   TumVol↓, 3,  
Total Targets: 47

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx1↑, 1,   GPx4↑, 1,   ROS↓, 1,   ROS∅, 1,   SOD↑, 1,   SOD1↑, 1,   SOD2↑, 1,  

Core Metabolism/Glycolysis ⓘ

LDH↓, 1,  

Cell Death ⓘ

Apoptosis↓, 1,  

Kinase & Signal Transduction ⓘ

SOX9↑, 1,  

Transcription & Epigenetics ⓘ

other↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,   MSCs↑, 1,  

Migration ⓘ

COL2A1↑, 1,   TGF-β↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↑, 1,   angioG↝, 1,   NO↓, 1,   VEGF↓, 1,   VEGF↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL10↑, 2,   IL1β↓, 2,   IL1β↑, 1,   IL6↓, 1,   Inflam↓, 3,   NF-kB↓, 1,   PGE2↓, 1,   TNF-α↓, 2,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

cognitive↑, 1,   neuroP↑, 2,   toxicity∅, 9,  
Total Targets: 37

Scientific Paper Hit Count for: toxicity, toxicity
8 Magnetic Fields
4 Magnetic Field Rotating
1 immunotherapy
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#:172  Target#:1025  State#:%  Dir#:6
  wNotes=0  sortOrder:rid,rpid

 

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