Magnetic Fields Cancer Research Results

MF, Magnetic Fields: Click to Expand ⟱
Features: Therapy

Magnetic Fields — externally applied static or time-varying magnetic fields used to alter cellular signaling, redox state, ion handling, membrane behavior, metabolism, or neural activity without introducing a chemical agent. They are a physical therapeutic modality and include static magnetic fields (SMF), extremely-low-frequency magnetic fields (ELF-MF), pulsed electromagnetic fields (PEMF), and other non-rotating oscillating/time-varying magnetic fields. Common abbreviations include MF, SMF, ELF-MF, EMF, and PEMF. Biological effects are strongly dependent on field strength, frequency, waveform, gradient, duty cycle, exposure duration, and tissue or cell type. Rotating magnetic fields are excluded here because they are represented separately as pid 192; magnetic-nanoparticle-dependent magnetothermal or magnetomechanical effects are also better assigned primarily to the magnetic nanoparticle product.

Primary mechanisms (ranked):

  1. Redox modulation and ROS perturbation, including radical-pair and mitochondrial mechanisms; cancer cells may develop sustained oxidative stress whereas normal cells frequently show adaptive antioxidant responses.
  2. Ca²⁺ and ion-channel modulation, particularly TRPC, voltage-gated channels, intracellular Ca²⁺ handling, and ER–mitochondrial Ca²⁺ communication.
  3. Mitochondrial and bioenergetic modulation, including membrane potential, electron transport, ATP production, mitochondrial permeability, and metabolic reprogramming.
  4. Cell proliferation, cell-cycle, apoptosis, and senescence signaling through pathways including EGFR/PI3K/AKT/mTOR, MAPK/ERK, caspases, PARP, Bax and survivin.
  5. Membrane permeability and drug-uptake modulation, producing context-dependent chemosensitization to agents including doxorubicin, etoposide and methotrexate.
  6. Inflammatory and stress-response modulation including NF-κB, cytokine signaling, HSPs, ER stress and adaptive antioxidant pathways.
  7. Migration, invasion, angiogenesis and tumor-microenvironment modulation; effects are field-parameter and tumor-model dependent.

Bioavailability / PK relevance: Conventional pharmacokinetic concepts do not apply because the intervention is a physical field rather than an absorbed drug. Relevant exposure variables are magnetic flux density, field gradient, frequency, waveform, pulse width, repetition rate, duty cycle, spatial distribution, treatment duration and tissue depth. Magnetic fields can penetrate tissue without the concentration gradients characteristic of drugs, but induced electric fields and biological coupling vary markedly with geometry and frequency.

In-vitro vs systemic exposure relevance: Effects are not concentration-driven. Many experimental results cannot be generalized between devices because apparently small differences in waveform, frequency, flux density, orientation, gradient and exposure duration can change the biological response. Static fields ranging from millitesla to tesla and PEMF/ELF protocols ranging from weak fields to substantially stronger stimulation should therefore be treated as distinct exposure regimens rather than as a single dose-response continuum.

Clinical evidence status: Cancer treatment remains predominantly preclinical, with cell-culture and animal evidence plus limited supportive or adjunctive human use. Evidence supports parameter-dependent anticancer effects and chemosensitization, but non-rotating magnetic-field exposure alone is not an established standard anticancer therapy. PEMF has established clinical use in several musculoskeletal applications and has been studied as supportive therapy in oncology. Repetitive transcranial magnetic stimulation has substantially stronger human evidence in neurological and psychiatric applications, including investigational use in Alzheimer’s disease, but should not be interpreted as evidence that generic magnetic-field exposure is an established systemic cancer treatment.

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

Magnetic Field Mechanisms in Cancer

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 ROS and redox homeostasis ↑ ROS (context-dependent); ↑ oxidative stress ↑ transient ROS followed by ↔ or ↓ ROS in adaptive protocols P, R, G Redox perturbation One of the most recurrent MF mechanisms. Direction is strongly field- and cell-dependent; sustained ROS elevation is reported in several cancer models and during chemotherapy sensitization.
2 Ca²⁺ and ion-channel signaling ↑ Ca²⁺ signaling or dysregulation; altered TRPC and voltage-sensitive channel activity ↑ transient signaling with homeostatic recovery (context-dependent) P, R Electrophysiological signal transduction Ca²⁺ is a major mechanistic bridge between membrane sensing, mitochondria, ROS, proliferation and apoptosis. Response depends strongly on waveform and frequency.
3 Mitochondrial function and membrane potential ↓ ΔΨm; altered respiration; ↑ mitochondrial stress ↔ or reversible modulation (context-dependent) P, R, G Bioenergetic destabilization Mitochondrial effects can arise downstream of ROS and Ca²⁺ signaling and contribute to apoptotic commitment.
4 Apoptosis and caspase signaling ↑ apoptosis; ↑ caspases; ↑ PARP cleavage; ↑ Bax; ↓ survivin ↔ or substantially weaker response in selective protocols R, G Programmed cell death Reported with several PEMF and time-varying field protocols and can be amplified when combined with chemotherapy.
5 EGFR PI3K AKT mTOR signaling ↓ EGFR/AKT/mTOR signaling (model-dependent) ↔ or mixed R, G Growth-signal suppression Particularly supported in static-field experiments; response varies with cell type, cell density and field intensity.
6 Cell cycle and proliferation ↓ proliferation; ↑ cell-cycle arrest or mitotic disruption ↔ or mixed G Growth suppression Effects are highly protocol-specific. Some exposures are neutral or can stimulate proliferation, so suppression should not be treated as universal.
7 DNA damage and DNA-damage response ↑ DNA damage; ↑ ATM/p53/p21 signaling (context-dependent) ↔ or mixed; protective responses reported with some protocols R, G Genotoxic stress and repair modulation Often secondary to ROS and particularly evident during combination treatment with chemotherapy or radiation. Magnetic fields alone are not consistently genotoxic, and some static-field protocols can reduce radiation-associated DNA damage.
8 Chemosensitization and drug uptake ↑ chemotherapy response; ↑ drug uptake or cytotoxicity ↔ or ↑ toxicity (drug-dependent) R, G Adjunctive anticancer effect Documented with doxorubicin, etoposide and other agents. Selectivity is not guaranteed; normal-cell toxicity must be evaluated for each field-drug combination.
9 Glutathione and antioxidant buffering ↓ GSH reserve or altered GSH/GSSG balance (context-dependent) ↑ GSH or antioxidant adaptation in some protocols R, G Redox buffering modulation GSH depletion is best interpreted as a consequence of oxidative load rather than a universal direct MF target.
10 NRF2 antioxidant response ↔ / mixed; inadequate adaptive response in some oxidative protocols ↑ NRF2 and antioxidant-response signaling in some protective protocols R, G Adaptive antioxidant defense NRF2 direction is not uniform enough to classify MF globally as either an NRF2 activator or inhibitor.
11 ER stress and unfolded protein response ↑ ER stress and UPR (model-dependent) ↑ adaptive stress response or ↔ R, G Proteostasis stress Can develop secondary to ROS, altered Ca²⁺ handling and mitochondrial dysfunction.
12 Mitochondrial permeability transition ↑ MPTP opening propensity ↔ or reversible opening R Mitochondrial death commitment Supported mechanistically for specific ELF-MF exposures through ROS-sensitive pathways; should not be generalized to all magnetic fields.
13 Glycolysis and cellular energetics ↓ glycolytic flux or altered ATP production (model-dependent) ↔ or metabolic adaptation R, G Metabolic reprogramming Some frequency-tuned exposures suppress glycolysis, but this is substantially less universal than ROS or Ca²⁺ modulation.
14 HIF-1α and angiogenic signaling ↓ HIF-1α / VEGF in selected models ↑ VEGF or tissue-repair signaling in some regenerative protocols G Angiogenesis modulation Potential cancer-versus-normal-tissue divergence is attractive but remains highly exposure- and model-specific.
15 NF-κB and inflammatory signaling ↓ NF-κB and inflammatory signaling in selected models ↓ inflammatory cytokines in many regenerative PEMF applications R, G Inflammation modulation Better established as an anti-inflammatory/regenerative PEMF effect than as a universal cancer-cell mechanism.
16 Migration invasion and angiogenesis ↓ migration; ↓ invasion; ↓ angiogenic signaling in selected models ↔ or pro-repair angiogenesis (context-dependent) G Metastatic phenotype modulation Direction varies substantially with field protocol and normal-versus-tumor context.
17 Radiosensitization ↑ radiation-induced ROS and DNA damage in selected protocols Mixed; radioprotection has also been reported with other protocols R, G Modification of radiation response Both radiosensitizing and radioprotective responses have been reported; field parameters and tissue context determine direction.
18 Clinical Translation Constraint Field-specific response; substantial tumor heterogeneity Potential tissue-specific physiological effects G Translation limitation No pharmacokinetic dose metric exists. Field strength, frequency, waveform, geometry, gradients, duration and induced electric fields must be specified. Most anticancer evidence remains preclinical and protocols are poorly standardized.

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: Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive magnetic neuromodulation modality with randomized human evidence for modest improvement in global cognition in mild cognitive impairment and Alzheimer’s disease. The strongest recent evidence supports excitatory stimulation of cortical cognitive-network regions, particularly the dorsolateral prefrontal cortex. The mechanism is principally neural-network and synaptic modulation rather than the systemic ROS-based mechanism often discussed for low-intensity PEMF. Meta-analyses generally report cognitive benefit, but protocol heterogeneity, small trials and uncertain durability remain important limitations. rTMS should therefore be classified as investigational or adjunctive for AD rather than an established disease-modifying treatment.

Clinical evidence status: Multiple RCTs and meta-analyses support a modest short-term cognitive signal. Longer-term benefit remains less certain, optimal frequency/intensity/site protocols are not standardized, and evidence does not establish prevention or reversal of Alzheimer pathology.

Magnetic Stimulation in Alzheimer’s Disease

Rank Pathway / Axis Modulation TSF Primary Effect Notes / Interpretation
1 Cortical network excitability ↑ P, R Neuromodulation High-frequency rTMS and excitatory stimulation of cortical network hubs can increase cortical responsiveness.
2 Synaptic plasticity ↑ R, G Plasticity enhancement Repeated stimulation can produce LTP-like network effects and is a leading explanation for persistence beyond the stimulation session.
3 Cognitive-network connectivity ↑ G Network normalization DLPFC and related cortical networks are the most consistently studied targets.
4 Global cognition ↑ G Clinical cognitive improvement Recent meta-analyses show modest improvement in MMSE, MoCA or ADAS-Cog outcomes, although heterogeneity remains substantial.
5 Neuroinflammation and neurotrophic signaling ↓ inflammation; ↑ neurotrophic signaling (context-dependent) G Secondary neurobiological effects Supported mainly by mechanistic and preclinical studies; less directly established than cortical-network effects in human AD.
6 Clinical Translation Constraint ↔ G Protocol heterogeneity Optimal stimulation site, frequency, intensity, pulse count, session number and maintenance schedule remain unresolved; long-term disease modification has not been demonstrated.

P: 0–30 min     R: 30 min–3 hr     G: >3 hr
Scientific Papers found: Click to Expand⟱
8489- MF,    Pulsed electromagnetic fields induce ferroptosis in osteosarcoma cells and promote osteogenic differentiation
- in-vitro, OS, U2OS - in-vitro, OS, MG63
TumCP↓, TumCMig↓, Ferroptosis↑, GPx4↓, xCT/SLC7A11↓, BMD↑, selectivity↑, Dose↝, TumCG↓, Dose↝, OS↑, ROS↑, MDA↑, Iron↑, ChemoSen↑, TOP2↑, radioP↑,
8488- MF,    Efficacy and Durability of Repetitive Transcranial Magnetic Stimulation on Cognitive Function in Patients With Mild-to-Moderate Alzheimer's Disease: A Systematic Review and Meta-Analysis
- Review, AD, NA
*eff↑, *cognitive↑, *Dose↝,
8487- MF,    The effect of repetitive transcranial magnetic stimulation on immediate and long-term cognitive functions in Alzheimer's dementia and mild cognitive impairment: a meta-analysis
- Review, AD, NA
*cognitive↑, *Dose↝, *Dose↝, *BDNF↑, *neuroP↑,
8486- MF,    Silent forces, hidden currents: the influence of static magnetic field stimulation on tumor biophysics
- Review, Var, NA
Ca+2↑, TumCG↓, MMP↓, CellMemb↑, SOX2↓, Nanog↓, cMyc↓, CD44↓, CD133↓, P53↑, ROS↑, DNAdam↑, CDK1↓, CycB/CCNB1↓, TumCCA↑, TumCP↓, pH↓, TumCP↓, Telomerase↓, ChemoSen↑, TRPV1↝, Bax:Bcl2↑, Casp3↑, Akt↓, mTOR↓, mitA↑, ROS↓, P-gp/ABCB1↓, MDR1↓, RadioS↑, Apoptosis↑, GSH↓, lipid-P↑, Iron↑, Iron↓, Fenton↑,
8485- MF,  doxoR,    Static magnetic field promotes the doxorubicin toxicity effects on osteosarcoma cells
- in-vitro, OS, G292
tumCV↓, Dose↝, Apoptosis↑, ROS↑, i-Iron↓, *Ca+2↓, *Iron↑, *chemoP↑, ROS↓, ChemoSen↑, selectivity↑,
8484- MF,  doxoR,    Pulsed Electromagnetic Field Increases Doxorubicin-induced Mitotic Slippage in MDA-MB-231 Breast Cancer Cells
- in-vitro, BC, MDA-MB-231
ChemoSen↑, Dose↝, eff↑, CDK1?, p‑H3↓, survivin↓, PLK1↓,
8483- MF,    Magnetic Fields in Cancer Therapy: Mechanistic Insights, Signaling Pathways, and Evidence from Clinical and In Vitro Studies
- Review, Var, NA
Apoptosis↑, TumCP↓, Ferroptosis↑, TumCMig↓, EMT↓, ROS↝, ChemoSen↑, RadioS↑, Telomerase↓, selectivity↑, ROS↑, DNAdam↑, Casp↑, Ca+2↑, MMP↓, lysoMP↑, lipid-P↑, NA↑, other↑, ChemoSen↑, P53↑,
7391- MF,    The effects of pulsed magnetic field exposure on the permeability of leukemia cancer cells
- in-vitro, AML, K562
Dose↝, Ca+2↓, eff↑,
7390- MF,    A 60-Hz sinusoidal magnetic field induces apoptosis of prostate cancer cells through reactive oxygen species
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP
TumCG↓, Apoptosis↑, TumCCA↑, cl‑Casp3↑, ROS↑, eff↓, Dose↝, Dose↝, H2O2↑,
4106- MF,    Cognitive Decline: Current Intervention Strategies and Integrative Therapeutic Approaches for Alzheimer's Disease
- Review, AD, NA
*cognitive↑, *memory↑, *Aβ↓, *neuroP↑,
7387- MF,    Effects of Sinusoidal Magnetic Field Observed on Cell Proliferation, Ion Concentration, and Osmolarity in Two Human Cancer Cell Lines
- in-vitro, AML, HL-60 - in-vitro, adrenal, SK-HEP-1
Dose↝, TumCG↓, Na+↑, K+↑,
7384- MF,    Reactive oxygen species (ROS) production in HepG2 cancer cell line through the application of localized alternating magnetic field
- in-vitro, Liver, HepG2
ROS↑, tumCV↓, mtDam↑, Dose↝, ER Stress↑,
7383- MF,    Magneto mitochondrial dysfunction mediated cancer cell death using intracellular magnetic nano-transducers
- vitro+vivo, Var, NA
mtDam↑, Apoptosis↑, MitoP↑, Dose↝, Dose↝, eff↑, PINK1↑, PARK2↑,
6942- MF,    Emerging techniques in ‘truly’ minimal-invasive treatment options of benign prostatic obstruction
- Review, BPH, NA
PV↓,
6941- MF,  Ex,    The effects of pulsed electromagnetic field therapy on muscle strength and pain in patients with end-stage knee osteoarthritis: a randomized controlled trial
- Trial, Arthritis, NA
*Strength↑, *Pain↓, *eff↑, *Dose↝,
6940- MF,    Meta-analysis of the effectiveness and safety of magnetic stimulation for chronic pelvic pain
- Review, BPH, NA
*UFR↑, *other?, *Pain↓, *BloodF↑, *other↑, *Inflam↓, *QoL↑,
6939- MF,    A prospective, randomized, placebo controlled, double-blind study of pelvic electromagnetic therapy for the treatment of chronic pelvic pain syndrome with 1 year of followup
- Trial, Nor, NA
*Pain↓,
6938- MF,    Effect of pulsed electromagnetic field therapy on prostate volume and vascularity in the treatment of benign prostatic hyperplasia: a pilot study in a canine model
- in-vivo, BPH, NA
*Dose↝, *toxicity↓, *BloodF↑, *Dose↝, *PV↓, *Inflam↓,
6937- MF,    Noninvasive treatment for men suffering from enlarged prostate
- Review, BPH, NA
*PV↓, *Inflam↓, *BloodF↑, *Dose↝,
6936- MF,  Ex,    Pulsed electromagnetic field with or without exercise therapy in the treatment of benign prostatic hyperplasia
- Trial, BPH, NA
*eff↑, *Synergy↑, *BloodF↑, *Diff↝, *Dose↝, *Dose↝, *Dose↝, *Dose↝, *Dose↝, *Dose↝, *Dose↝, *UFR↑, *UR↓, *PSA↓, *other↑, *Inflam↓,
5534- MF,    Targeted Osmotic Lysis of Highly Invasive Breast Carcinomas Using Pulsed Magnetic Field Stimulation of Voltage-Gated Sodium Channels and Pharmacological Blockade of Sodium Pumps
- vitro+vivo, BC, MDA-MB-231 - in-vitro, Nor, MCF10
TumVol↓, VGSC↑, OS↑, selectivity↑, eff↑,
5533- MF,    Magnetic field-induced drug permeability in liposome vesicles
- in-vitro, Nor, NA
*Dose↝, *CellMemb↑, *other↝,
5532- MF,    Magnetoporation: New Method for Permeabilization of Cancerous Cells to Hydrophilic Drugs
- in-vivo, BC, NA
Dose↑, CellMemb↑, eff↝, other↝, TumCG↓,
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↝,
3737- MF,    The Effect of Time-Dependence of 10 Hz Electromagnetic Field on Spatial Learning and Memory in Rats
- in-vivo, AD, NA
*memory↑, *BDNF↑, *BBB↑,
3735- MF,    Examining the effects of extremely low-frequency magnetic fields on cognitive functions and functional brain markers in aged mice
- in-vivo, AD, NA
*APP∅, *Aβ∅, *Inflam∅, *memory∅,
3734- MF,    Extremely low frequency electromagnetic fields promote cognitive function and hippocampal neurogenesis of rats with cerebral ischemia
- in-vivo, AD, NA
*cognitive↑, *NOTCH1↑,
3728- MF,    Long-term exposure to ELF-MF ameliorates cognitive deficits and attenuates tau hyperphosphorylation in 3xTg AD mice
- in-vivo, AD, NA
*cognitive↑, *neuroP↑, *Apoptosis↓, *ROS↓, *p‑tau↓, *GSK‐3β↓, *CDK5↓,
3727- MF,    RKIP-Mediated NF-κB Signaling is involved in ELF-MF-mediated improvement in AD rat
- in-vivo, AD, NA
*cognitive↑, *RKIP↑, *p‑IKKα↓,
3479- MF,    Evaluation of Pulsed Electromagnetic Field Effects: A Systematic Review and Meta-Analysis on Highlights of Two Decades of Research In Vitro Studies
- Review, Var, NA
*eff↓, eff↝, *Hif1a↑, *VEGF↑, *TIMP1↑, *E2Fs↑, *MMP2↑, *MMP9↑, Apoptosis↑,
3725- MF,    Short-term effects of extremely low frequency electromagnetic fields exposure on Alzheimer's disease in rats
- in-vivo, AD, NA
*Weight∅, *memory∅, *cognitive∅, *Aβ∅,
3724- MF,  RF,    Electromagnetic Field in Alzheimer's Disease: A Literature Review of Recent Preclinical and Clinical Studies
- Review, AD, NA
*memory↑, *neuroP↑,
3569- MF,    Current Evidence Using Pulsed Electromagnetic Fields in Osteoarthritis: A Systematic Review
- Review, Arthritis, NA
*Pain↓, *QoL↑, *motorD↑,
3568- MF,    The Efficacy of Pulsed Electromagnetic Fields on Pain, Stiffness, and Physical Function in Osteoarthritis: A Systematic Review and Meta-Analysis
- Review, Arthritis, NA
*eff↑, *Pain↓, *motorD↑,
3566- MF,    Positive and Negative Effects of Administering a Magnetic Field to Patients with Rheumatoid Arthritis (RA)
- Study, Arthritis, NA
*Inflam↓, *QoL↑, *Pain↓, *motorD↑, *toxicity↓, *Cartilage↑, *Inflam↓,
3726- MF,    Spatial memory recovery in Alzheimer's rat model by electromagnetic field exposure
- in-vivo, AD, NA
*memory↑, *cognitive↑,
3501- MF,    Unveiling the Power of Magnetic-Driven Regenerative Medicine: Bone Regeneration and Functional Reconstruction
- Review, Nor, NA
*VEGF↑, *BMPs↓, *SMAD4↑, *SMAD5↑, *Ca+2↑,
3500- MF,    Moderate Static Magnet Fields Suppress Ovarian Cancer Metastasis via ROS-Mediated Oxidative Stress
- in-vitro, Ovarian, SKOV3
ROS↑, CSCs↓, CD44↓, SOX2↓, cMyc↓, TumMeta↓, TumCI↓, TumCMig↓, CD133↓, Nanog↓,
3498- MF,    Effect of Static Magnetic Field on Oxidant/Antioxidant Parameters in Cancerous and Noncancerous Human Gastric Tissues
- in-vitro, GC, NA
*SOD↑, *MDA↓, SOD↓, GPx↓, MDA↑, Catalase↑,
3487- MF,  Rad,    High-specificity protection against radiation-induced bone loss by a pulsed electromagnetic field
- Review, Var, NA
radioP↑, *Ca+2↑, RAS↑, MAPK↓,
3486- MF,    Pulsed electromagnetic field potentiates etoposide-induced MCF-7 cell death
- in-vitro, BC, MCF-10AT
ChemoSen↑, tumCV↓, cl‑PARP↑, Casp7↑, Casp9↑, survivin↓, BAX↑, DNAdam↑, ROS↑, eff↓,
3485- MF,    Cytoprotective effects of low-frequency pulsed electromagnetic field against oxidative stress in glioblastoma cells
- in-vitro, GBM, U87MG
*antiOx↑, *ROS↓, *cytoP↑,
3484- MF,    Extremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of •O2 − and H2O2
- in-vitro, Nor, NA
*GPx↑, *SOD2↑, *Catalase↑, *GSR↑, *ROS↓,
3483- MF,    Pulsed Electromagnetic Fields Protect Against Brain Ischemia by Modulating the Astrocytic Cholinergic Anti-inflammatory Pathway
- in-vivo, Stroke, NA
*Inflam↓, *STAT3↓, *p‑STAT3↓,
3482- MF,    Pulsed Electromagnetic Fields Increase Angiogenesis and Improve Cardiac Function After Myocardial Ischemia in Mice
- in-vitro, Nor, NA
*cardioP↑, *VEGF↑, *VEGFR2/KDR/Flk1↑, *Hif1a↑, *FGF↑, *ITGB1↑, *angioG↑,
3481- MF,    No effects of pulsed electromagnetic fields on expression of cell adhesion molecules (integrin, CD44) and matrix metalloproteinase-2/9 in osteosarcoma cell lines
- in-vitro, OS, MG63 - in-vitro, OS, SaOS2
ITGA1∅, ITGB1∅, ITGA5∅, ITGB3∅, ITGB4∅, MMP2∅, MMP9∅, eff↑,
3480- MF,    Cellular and Molecular Effects of Magnetic Fields
- Review, Nor, NA
ROS↑, *Ca+2↑, *Inflam↓, *Akt↓, *mTOR↓, selectivity↑, *memory↑, *MMPs↑, *VEGF↑, *FGF↑, *PDGF↑, *TNF-α↑, *HGF/c-Met↑, *IL1↑,
4097- MF,    Theta Frequency Electromagnetic Stimulation Enhances Functional Recovery After Stroke
- Trial, Stroke, NA
*motorD↑, *eff↑, *Dose↝,
4105- MF,    Extremely low frequency electromagnetic fields stimulation modulates autoimmunity and immune responses: a possible immuno-modulatory therapeutic effect in neurodegenerative diseases
- Review, AD, NA
*Inflam↓, *neuroP↑, *NO↑, *ROS↓, *NO↓, *MCP1/CCL2↑, *HSP70/HSPA5↑, *antiOx↑, *NRF2↑, *NF-kB↓,
4104- MF,    Effects of exposure to extremely low-frequency electromagnetic fields on spatial and passive avoidance learning and memory, anxiety-like behavior and oxidative stress in male rats
- in-vivo, Nor, NA
*memory↑, *ROS↑,

Showing Research Papers: 151 to 200 of 282
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 282

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

NA↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 1,   Catalase↑, 4,   Fenton↑, 1,   GPx↓, 1,   GPx1↓, 1,   GPx1↑, 1,   GPx4↓, 1,   GSH↓, 2,   GSH↑, 1,   GSH/GSSG↓, 2,   GSR↑, 1,   H2O2↑, 7,   mt-H2O2↑, 1,   Iron↓, 1,   Iron↑, 2,   i-Iron↓, 1,   lipid-P↑, 2,   MDA↑, 3,   Prx6↑, 1,   ROS↓, 2,   ROS↑, 55,   ROS⇅, 1,   ROS↝, 3,   mt-ROS↑, 2,   RPM↑, 4,   SOD↓, 2,   SOD↑, 2,   SOD1↓, 1,   SOD1↑, 1,   SOD2↓, 1,   SOD2↑, 2,   Thiols↓, 1,   xCT/SLC7A11↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↓, 1,   TfR1/CD71↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ADP:ATP↓, 2,   compII↓, 1,   ETC↓, 5,   mitResp↓, 1,   mitResp↑, 1,   mtDam↑, 3,   OCR↓, 1,   OCR↑, 1,   OXPHOS↑, 3,   PGC-1α↑, 1,   PINK1↑, 1,   PleEff↓, 1,   SDH↓, 2,   SIRT3↑, 1,   UCP1↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACAA1↓, 1,   ALAT↓, 2,   ATP↓, 2,   ATP↑, 2,   ATP⇅, 1,   ATP∅, 1,   cAMP⇅, 1,   DHCR24↑, 1,   ECAR↓, 1,   FABP4↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 3,   Glycolysis∅, 1,   GSK‐3β↑, 1,   lactateProd↑, 1,   PCK1↓, 1,   PKM2↓, 1,   PLIN1↓, 1,   Pyruv↓, 2,   SIRT1↑, 1,   TCA?, 1,   Warburg↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 42,   p‑BAD↓, 1,   Bak↑, 1,   BAX↑, 5,   Bax:Bcl2↑, 1,   Bcl-2↓, 5,   Casp↑, 1,   Casp↝, 1,   Casp3↓, 1,   Casp3↑, 9,   cl‑Casp3↑, 2,   Casp7↓, 1,   Casp7↑, 3,   cl‑Casp7↑, 1,   Casp8↑, 1,   cl‑Casp8↑, 1,   Casp9↑, 3,   cl‑Casp9↑, 1,   Cyt‑c↑, 3,   Cyt‑c↝, 1,   Endon↑, 1,   Fas↑, 1,   Ferroptosis↑, 2,   iNOS↑, 2,   Mcl-1↓, 1,   Necroptosis↑, 1,   necrosis↑, 1,   p38↑, 3,   survivin↓, 3,   TumCD↑, 11,   TumCD∅, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 5,   p‑Akt↓, 2,   BCAP↓, 1,   EGFR↓, 1,   EGFR↝, 1,   ERK↑, 1,   p‑ERK↑, 2,   p‑ERK↝, 1,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 3,   mTOR↓, 2,   PI3K↓, 2,   PTEN↓, 1,   RAS↑, 1,   STAT3↑, 1,   p‑STAT3↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

ATF3↑, 1,   ChrMod↑, 2,   cMyc↓, 2,   p‑H3↓, 1,   miR-125b↓, 1,   miR-126↓, 1,   miR-129-5p↑, 1,   miR-155↑, 1,   miR-200c↓, 1,   miR-21↑, 1,   miR-210↑, 1,   miR-34a↑, 1,   miR-486↑, 1,   other↓, 3,   other↑, 7,   other↝, 3,   other∅, 1,   SOX2↓, 2,   tumCV↓, 8,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   ER Stress↓, 1,   ER Stress↑, 3,   GRP78/BiP↑, 1,   GRP94↑, 1,   HSP70/HSPA5↓, 2,   HSP70/HSPA5↑, 8,   HSP70/HSPA5∅, 1,   HSP90↓, 2,   HSPs↑, 1,   HSPs∅, 1,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1/ATG6↑, 2,   LC3II↑, 1,   lysoMP↓, 2,   lysoMP↑, 3,   MitoP↑, 1,   p62↑, 1,   PARK2↑, 1,   TumAuto↑, 6,  

DNA Damage & Repair(tgid=10) ⓘ

ATM↑, 1,   DNAdam↑, 14,   P53↑, 9,   P53↝, 1,   cl‑PARP↑, 3,   Telomerase↓, 2,   TOP2↑, 1,   γH2AX↑, 1,   p‑γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1?, 1,   CDK1↓, 1,   p‑CDK2↓, 1,   p‑CHK1↓, 1,   Chk2↑, 2,   CycB/CCNB1↓, 2,   cycE/CCNE↓, 1,   E2Fs↓, 1,   mitA↑, 1,   P21↑, 2,   PLK1↓, 1,   TumCCA↑, 16,  

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

CD133↓, 2,   CSCs↓, 2,   Diff↑, 1,   Nanog↓, 2,   TumCG↓, 27,   TumCP↓, 22,   TumCP∅, 1,   p‑TumCP↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↓, 2,   Ca+2↑, 30,   Ca+2↝, 3,   i-Ca+2↑, 1,   CAFs/TAFs↓, 1,   Cartilage↑, 1,   CCDC150↓, 1,   COL4↓, 1,   EMT↓, 1,   F-actin↓, 1,   FOSB↑, 1,   ITGA1∅, 1,   ITGA11↓, 1,   ITGA5∅, 1,   ITGB1∅, 1,   ITGB3∅, 1,   ITGB4∅, 1,   LAMB3↑, 1,   MMP2↓, 1,   MMP2↑, 2,   MMP2∅, 1,   MMP9↓, 1,   MMP9↑, 1,   MMP9∅, 1,   MMPs↓, 1,   Na+↑, 1,   Rho↓, 1,   Slug↓, 1,   p‑SMAD2↓, 1,   SMAD3↓, 1,   p‑SMAD3↓, 1,   TGF-β↓, 2,   THBS2↓, 1,   TumCI↓, 7,   TumCMig↓, 9,   TumMeta↓, 7,   Twist↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 8,   ECM/TCF↓, 1,   Hif1a↓, 1,   NO↑, 1,   nucleolin↑, 1,   VEGF↓, 2,   VEGFR2/KDR/Flk1↓, 2,  

Barriers & Transport(tgid=15) ⓘ

CellMemb↑, 9,   EPR↑, 2,   K+↑, 1,   MMP?, 1,   MMP↓, 10,   MMP↑, 1,   MPT↑, 2,   Na+↑, 1,   TRPC1↑, 1,   TRPV1↑, 1,   TRPV1↝, 1,   VGSC↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↓, 1,   CD4+↑, 3,   CD44↓, 2,   CD8+↓, 1,   CD8+↑, 3,   COX2/PTGS2↓, 1,   CXCc↓, 1,   CXCL12↓, 1,   CXCL9↓, 1,   DCells↑, 3,   FOXP3↓, 1,   GM-CSF↓, 1,   IFN-γ↓, 1,   IL1↑, 1,   IL10↑, 2,   IL12↑, 1,   IL17↓, 2,   IL22↓, 1,   IL23↓, 1,   IL28↓, 1,   IL6↓, 2,   IL6↑, 1,   Imm↑, 2,   Imm↝, 1,   Inflam↓, 1,   LIF↑, 1,   Macrophages↑, 1,   NF-kB↓, 1,   NF-kB↑, 2,   PD-L1↑, 1,   RANTES↓, 1,   T-Cell↑, 1,   TNF-α↓, 1,   TNF-α↑, 2,  

Cellular Microenvironment(tgid=17) ⓘ

pH↓, 1,   i-pH↑, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

PPARγ↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 20,   ChemoSen∅, 1,   Dose?, 1,   Dose↓, 1,   Dose↑, 1,   Dose↝, 22,   Dose∅, 1,   eff↓, 14,   eff↑, 22,   eff⇅, 1,   eff↝, 15,   MDR1↓, 1,   P-gp/ABCB1↓, 3,   RadioS↑, 7,   selectivity↑, 29,   Synergy↑, 5,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 2,   AST↓, 1,   BloodF↑, 1,   BMD↑, 2,   EGFR↓, 1,   EGFR↝, 1,   Ferritin↓, 1,   IL6↓, 2,   IL6↑, 1,   PD-L1↑, 1,   PV↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   AntiTum↑, 1,   Appetite↑, 2,   BowelM↑, 2,   breath↑, 2,   chemoP↑, 2,   ChemoSideEff↓, 1,   cognitive↑, 2,   hepatoP↑, 1,   OS↑, 16,   OS⇅, 1,   Pain↓, 6,   QoL↑, 3,   radioP↑, 3,   Sleep↑, 3,   Strength↑, 4,   toxicity↓, 1,   TumVol↓, 16,   Weight↑, 2,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 334

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 9,   Catalase↑, 8,   GPx↑, 4,   GPx∅, 1,   GPx1↑, 5,   GPx3↑, 1,   GPx4↑, 5,   GSH↑, 1,   GSH∅, 1,   GSR↑, 3,   GSSG↓, 1,   HO-1↑, 1,   Iron↑, 1,   Keap1↓, 1,   MDA↓, 5,   MDA↑, 1,   NRF2↑, 3,   ROMO1↑, 1,   ROS↓, 29,   ROS↑, 9,   ROS⇅, 2,   ROS↝, 1,   ROS∅, 1,   mt-ROS↑, 2,   RPM↓, 1,   RPM↑, 3,   SOD↓, 1,   SOD↑, 9,   SOD1↑, 5,   SOD2↓, 1,   SOD2↑, 6,   TAC↑, 1,   Trx↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ADP:ATP↓, 1,   ETC↓, 2,   Insulin↓, 1,   mitResp↓, 1,   OCR↑, 1,   mt-OCR↑, 1,   OXPHOS↓, 2,   OXPHOS↑, 2,   PGC-1α↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 2,   ATP↑, 3,   cAMP↑, 2,   ECAR↓, 1,   ECAR↑, 1,   FABP4↓, 1,   FAO↓, 1,   FAO↑, 1,   Glycolysis↓, 1,   Glycolysis↑, 2,   GSK‐3β↓, 1,   p‑GSK‐3β↑, 1,   HK2↑, 2,   lactateProd↓, 1,   LDHB↑, 1,   NAD↑, 1,   PFKL↑, 2,   PFKM↑, 2,   PFKP↑, 1,   PKM2↑, 2,   PONs↓, 1,   PPP↓, 1,   SREBP1/SREBF1↓, 1,   TCA↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 6,   BAD↓, 1,   BAX↓, 3,   Bcl-2↑, 1,   Bcl-2∅, 1,   Bcl-xL↑, 1,   Casp1↓, 1,   cl‑Casp1↓, 1,   proCasp1↓, 1,   Casp3↓, 2,   Cyt‑c↑, 2,   GSDMD?, 1,   GSDMD↓, 1,   HEY1↑, 1,   iNOS↓, 3,   iNOS↑, 1,   necrosis↓, 1,   p38↑, 2,   p‑p38↓, 1,   YAP/TEAD↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 2,   Akt↑, 2,   p‑Akt↓, 1,   p‑Akt↑, 1,   p‑CREB↑, 1,   ERK↓, 1,   ERK↑, 2,   p‑ERK↓, 1,   p‑ERK↑, 2,   HGF/c-Met↑, 1,   p‑IKKα↓, 2,   p‑IκB↓, 1,   p‑JNK↓, 1,   p‑JNK↑, 3,   MAPK↓, 1,   MAPK↑, 2,   mTOR↓, 4,   mTOR↑, 2,   mTOR↝, 1,   p‑P70S6K↑, 1,   PDGFR-BB↑, 1,   PI3K↓, 1,   PI3K↑, 1,   PKA↑, 1,   PKCδ↓, 1,   PTEN↑, 1,   RKIP↑, 1,   STAT3↓, 2,   p‑STAT3↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

miR-34b-5p↓, 1,   other?, 3,   other↓, 2,   other↑, 16,   other↝, 11,   RUNX2↑, 1,   RUNX2∅, 1,   SOX9↑, 2,   tumCV↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,   HSP70/HSPA5↑, 5,   HSPs↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK5↓, 1,   E2Fs↑, 1,   P21↓, 1,  

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

ALDH↑, 1,   BMP2↑, 2,   BMPs↓, 1,   BMPs↑, 2,   cFos↑, 1,   Diff↓, 1,   Diff↑, 9,   Diff↝, 1,   FGF↑, 5,   IGF-1↑, 1,   MSCs↑, 1,   NOTCH↑, 1,   NOTCH1↑, 1,   TumCG↑, 1,   TumCG∅, 1,   Wnt↑, 3,  

Migration(tgid=13) ⓘ

ARG1/2↑, 1,   Ca+2↓, 6,   Ca+2↑, 10,   Ca+2↝, 2,   Ca+2∅, 1,   i-Ca+2↓, 1,   Cartilage↑, 2,   COL1↑, 1,   COL1∅, 1,   COL2A1↑, 2,   F-actin↑, 1,   FAK↑, 2,   Fibronectin↑, 1,   ITGB1↑, 1,   MMP-10↓, 2,   MMP1↓, 1,   MMP1↑, 1,   MMP2↓, 1,   MMP2↑, 2,   MMP3↓, 1,   MMP3↑, 1,   MMP9↓, 3,   MMP9↑, 2,   MMPs↑, 1,   Netrins↑, 1,   OPN↑, 1,   PDGF↑, 1,   SMAD4↑, 1,   SMAD5↑, 1,   STAC2↑, 1,   TGF-β↑, 4,   TGF-β1↑, 1,   TIMP1↑, 3,   TIMP2↑, 1,   TumCMig↑, 1,   β-catenin/ZEB1↑, 4,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 8,   angioG↝, 1,   EGR4↑, 1,   HIF-1↓, 1,   Hif1a↑, 2,   Hif1a↝, 1,   Hif1a∅, 2,   HIF2a↑, 1,   NO↓, 4,   NO↑, 5,   NPY↑, 1,   VEGF↓, 1,   VEGF↑, 13,   VEGFR2/KDR/Flk1↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   CellMemb↑, 2,   GLUT1↑, 2,   GLUT4↑, 1,   MMP↑, 3,   MMP⇅, 1,   MMP↝, 1,   MMP∅, 1,   MPT↑, 1,   TRPC1↑, 1,   VGCC↑, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   COX2/PTGS2↓, 4,   CXCc↓, 1,   GM-CSF↑, 1,   IFN-γ↓, 1,   IL1↓, 2,   IL1↑, 1,   IL10↑, 7,   IL17↓, 1,   IL1β↓, 7,   IL1β↑, 1,   IL2↑, 1,   IL4↑, 2,   IL6↓, 7,   IL6↑, 2,   IL8↓, 4,   IL9↓, 1,   Imm↑, 1,   Inflam↓, 33,   Inflam∅, 1,   IP-10/CXCL-10↑, 1,   MCP1/CCL2↓, 1,   MCP1/CCL2↑, 2,   MIP‑1α/CCL3↓, 1,   mPGES-1↓, 1,   MyD88↓, 1,   NF-kB↓, 6,   NLRP3↓, 2,   p‑p65↓, 1,   PGE2↓, 4,   PGE2↑, 1,   PSA↓, 1,   TLR4↓, 1,   TNF-α↓, 11,   TNF-α↑, 1,   Treg lymp↓, 1,   TREM-1↓, 1,  

Cellular Microenvironment(tgid=17) ⓘ

pH↑, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 2,   5HT↑, 2,   Ach↑, 1,   AChE↓, 1,   BDNF↑, 11,   NGF↑, 1,   PSD95↑, 1,   β-Endo↑, 2,  

Protein Aggregation(tgid=19) ⓘ

APP∅, 1,   Aβ?, 1,   Aβ↓, 9,   Aβ∅, 2,   BACE/β-secretase↓, 1,   p‑tau↓, 2,   β-Amyloid↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

PPARγ↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   BioEnh↑, 4,   Dose↝, 33,   Dose∅, 1,   eff↓, 6,   eff↑, 19,   eff↝, 5,   selectivity↑, 2,   Synergy↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALP↑, 2,   ALP∅, 1,   BloodF↑, 4,   BMD↑, 12,   Calcium↑, 1,   IL6↓, 7,   IL6↑, 2,   LDH↓, 1,   NSE↑, 1,   OCN↑, 1,   OCN∅, 1,   PSA↓, 1,   PV↓, 3,   UFR↑, 2,   UR↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 2,   cardioP↑, 3,   chemoP↑, 1,   cognitive↑, 21,   cognitive∅, 1,   cytoP↑, 1,   hepatoP↑, 1,   memory↑, 19,   memory∅, 2,   Mood⇅, 1,   motorD↑, 10,   neuroP↑, 19,   OS↑, 2,   Pain↓, 9,   QoL↑, 5,   Strength↑, 1,   Stroke↓, 1,   toxicity?, 1,   toxicity↓, 6,   toxicity∅, 9,   Weight∅, 1,   Wound Healing↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

GutMicro↑, 1,  
Total Targets: 309

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#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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