Magnetic Fields / TumCG 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
TumCG, Tumor cell growth: Click to Expand ⟱
Source:
Type:
Normal cells grow and divide in a regulated manner through the cell cycle, which consists of phases (G1, S, G2, and M).
Cancer cells often bypass these regulatory mechanisms, leading to uncontrolled proliferation. This can result from mutations in genes that control the cell cycle, such as oncogenes (which promote cell division) and tumor suppressor genes (which inhibit cell division).
Scientific Papers found: Click to Expand⟱
526- MF,    Inhibition of Cancer Cell Growth by Exposure to a Specific Time-Varying Electromagnetic Field Involves T-Type Calcium Channels
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF7 - in-vitro, Pca, HeLa - vitro+vivo, Melanoma, B16-BL6 - in-vitro, Nor, HEK293
TumCG↓, Exposure to Thomas-EMF inhibited tumour growth in mice
Ca+2↑, exposure of malignant cells to Thomas-EMF for > 15 min promoted Ca2+ influx
selectivity↑, but did not effect non-malignant cells
*Ca+2∅, only malignant cells showed enhanced Ca2+ uptake following exposure to Thomas-EMF.
ROS↑, EMF-dependent increases in reactive oxygen species, rapid influx of Ca2+, or activation of specific signaling pathway
HSP70/HSPA5↑, Some studies have shown increased expression of HSP70, a marker of cellular stress responses, in response to EMF exposures
AntiCan↑, These observations suggest that the Thomas-EMF could provide a potential anti-cancer therapy.

538- MF,    The extremely low frequency electromagnetic stimulation selective for cancer cells elicits growth arrest through a metabolic shift
- in-vitro, BC, MDA-MB-231 - in-vitro, Melanoma, MSTO-211H
TumCG↓, did not affect the non-malignant counterpart.
Ca+2↑,
COX2/PTGS2↓,
ATP↑, (ATP5B) and mitochondrial transcription (MT-ATP6)
MMP↑, significant enhancement of mitochondrial membrane potential (ΔΨm)
ROS↑, demonstrated for the first time the association of ROS production with the stimulation of the mitochondrial metabolism triggered by the electromagnetic field
OXPHOS↑,
mitResp↑, Mitochondrial respiration is increased by ELF-EMF exposure

3464- MF,    Progressive Study on the Non-thermal Effects of Magnetic Field Therapy in Oncology
- Review, Var, NA
AntiTum↑, frequency below 300 Hz) exert anti-tumor function, independent of thermal effects
TumCG↓, Magnetic fields (MFs) could inhibit cell growth and proliferation; induce cell cycle arrest, apoptosis, autophagy, and differentiation; regulate the immune system; and suppress angiogenesis and metastasis via various signaling pathways
TumCCA↑,
Apoptosis↑,
TumAuto↑,
Diff↑,
angioG↓,
TumMeta↓,
EPR↑, MFs not only promote the absorption of chemotherapy drugs by producing small holes on the surface of cell membrane
ChemoSen↑,
ROS↑, MF treatment has been shown to promote the generation of ROS in many studies (31, 71, 72), with exposure within a 60 Hz sinusoidal MF for 48 h in induced human prostate cancer for DU145, PC3, and LNCaP apoptoses
DNAdam↑, Repetitive exposure to LF-MFs induced DNA damage and accumulation of DSBs and triggered apoptosis in Hela and MCF7 cell lines
P53↑, PMFs could trigger apoptosis cell death by upregulating the p53 level and through the mitochondrial-dependent pathway
Akt↓, LF-MFs (300 mT, 6 Hz, 24 h) also induced apoptosis by suppressing protein kinase B (Akt) signaling, activating p38 mitogen-activated protein kinase (MAPK) signaling, and caspase-9, which is the executor of the mitochondrial apoptosis pathway
MAPK↑,
Casp9↑,
VEGFR2/KDR/Flk1↓, reducing the expression and activation levels of VEGFR2
P-gp/ABCB1↓, A combination with the SMF (8.8 m T, 12 h) decreased the expression of P-glycoprotein (P-gp) in K562 cancer cells, while adriamycin itself induced an increase

3466- MF,    The effect of magnetic fields on tumor occurrence and progression: Recent advances
- Review, Var, NA
angioG↓, magnetic fields suppress tumor angiogenesis, microcirculation, and enhance the immune response.
ROS↝, magnetic fields suppress tumors by interfering with DNA synthesis, reactive oxygen species level, second messenger molecule delivery, and orientation of epidermal growth factor receptors.
EGFR↝,
TumCG↓, increasing evidence that MFs can inhibit tumor progression, the underlying mechanism is still poorly understood

2255- MF,    Pulsed Electromagnetic Fields Induce Skeletal Muscle Cell Repair by Sustaining the Expression of Proteins Involved in the Response to Cellular Damage and Oxidative Stress
- in-vitro, Nor, SkMC
*HSP70/HSPA5↑, HSP70), which can promote muscle recovery, inhibits apoptosis and decreases inflammation in skeletal muscle, together with thioredoxin, paraoxonase, and superoxide dismutase (SOD2), which can also promote skeletal muscle regeneration following injury
*Apoptosis↓,
*Inflam↓,
*Trx↓,
*PONs↓, Paraoxonase 2 (PON2, Paraoxonase 3 (PON3) (+19% vs. controls)
*SOD2↓,
*TumCG↑, PEMF treatment enhanced muscle cell proliferation by approximately 20% both in cells grown in complete medium
*Diff↑, suggest the potential role of PEMF in the induction of muscle differentiation
*HIF2a↑, hypoxia-inducible transcription factor 2a (HIF-2a) (+40% vs. controls),
*Cyt‑c↑, Cytochrome c (+39% vs. controls)
P21↑, p21/CIP1 (+27% vs. controls)

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↓, proliferation of human glioblastoma multiforme (GBM) cells (U87 and LN229) was inhibited upon exposure to AMF within a specific narrow frequency range, including around 227 kHz.
TumCG↓, daily exposure to AMF for 30 min over 21 days significantly suppressed tumor growth and prolonged overall survival
OS↑,
ROS↑, This effect was associated with heightened reactive oxygen species (ROS) production and increased manganese superoxide dismutase (MnSOD) expression.
SOD2↑,
eff↓, anti-cancer efficacy of AMF was diminished by either a mitochondrial complex IV inhibitor or a ROS scavenger.
ECAR↓, decrease in the extracellular acidification rate (ECAR) and an increase in the oxygen consumption rate (OCR).
OCR↑,
selectivity↑, This suggests that AMF-induced metabolic reprogramming occurs in GBM cells but not in normal cells. Furthermore, in cancer cells, AMF decreased ECAR and increased OCR, while there were no changes in normal cells.
*toxicity∅, did not affect non-cancerous human cells [normal human astrocyte (NHA), human cardiac fibroblast (HCF), human umbilical vein endothelial cells (HUVEC)].
TumVol↓, The results showed a significant treatment effect, as assessed by tumor volume, after conducting AMF treatment five times a week for 2 weeks
PGC-1α↑, Corresponding to the rise in ROS, there was also a time-dependent increase in PGC1α protein expression post-AMF exposure
OXPHOS↑, enhancing mitochondrial oxidative phosphorylation (OXPHOS), leading to increased ROS production
Glycolysis↓, metabolic mode of cancer cells to shift from glycolysis, characteristic of cancer cells, toward OXPHOS, which is more typical of normal cells.
PKM2↓, We extracted proteins that changed commonly in U87 and LN229 cells. Among the individual proteins related to metabolism, pyruvate kinase M2 (PKM2) was found to be inhibited in both.

2261- MF,    Tumor-specific inhibition with magnetic field
- in-vitro, Nor, GP-293 - in-vitro, Liver, HepG2 - in-vitro, Lung, A549
ROS↑, It enhances cell oxidative stress response and regulates apoptosis signaling pathway, changing intracellular Ca2+ concentration to induce apoptosis
Ca+2↓,
Apoptosis↑,
*selectivity↑, No signicant difference was found between the exposed 293T cell count versus the control group without magnetic exposure on the third day of exposure.
TumCG↓, Hepg2, A549 cell counts were signicantly lower than the unexposed control groups (the highest inhibition rate of Hepg2 was about 18%, and the highest inhibition rate of A549 was about 30%).
*i-Ca+2↓, Normal cells 293T showed a significant decrease in intracellular free calcium ion,
i-Ca+2↑, solid tumor cells showed no signicant change, while suspended tumor showed a slight increase in calcium ion

497- MF,    In Vitro and in Vivo Study of the Effect of Osteogenic Pulsed Electromagnetic Fields on Breast and Lung Cancer Cells
- vitro+vivo, NA, MCF7 - vitro+vivo, NA, A549
TumCG↓, growth inhibition (∼5%)
TumVol↓, 9% for PMF2
Casp3↑,
Casp7↑,
Apoptosis↑,
DNAdam↑,
TumCCA↑,
ChemoSen↑, PEMF synergistically enhances the potency of chemotherapy agents such as doxorubicin, 17 vincristine, 18 mitomycin C, 18 cisplatin, 18 and actinomycin.
EPR↑, PEMF can increase cell permeability. longer PEMF exposure may be required to increase cell membrane permeability.

507- MF,    Effects of extremely low frequency electromagnetic fields on the tumor cell inhibition and the possible mechanism
- in-vitro, Liver, HepG2 - in-vitro, Lung, A549 - in-vitro, Nor, GP-293
MMP↓,
TumCG↓,
ROS↑, key to tumor growth inhibition
*Ca+2↓, Normal 293 T cells showed a significant decrease in the intracellular free calcium ion concentration.
Ca+2↑, The solid tumor cells showed no significant change, while the suspended tumor cells showed a slight increase in the calcium ion concentration
selectivity↑,
i-pH↑, In addition, the intracellular pH of A549 cells increased under the magnetic field.

513- MF,    Exposure to a specific time-varying electromagnetic field inhibits cell proliferation via cAMP and ERK signaling in cancer cells
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468 - in-vitro, BC, MCF7 - in-vivo, Pca, HeLa
TumCG↓, but did not affect non-malignant cells. ****
p‑ERK↑,
cAMP⇅, changed the level

517- MF,  Rad,    Therapeutic Electromagnetic Field (TEMF) and gamma irradiation on human breast cancer xenograft growth, angiogenesis and metastasis
- in-vivo, NA, MDA-MB-231
TumMeta↓, IR or TEMF had significantly fewer lung metastatic sites
TumCG↓,

504- MF,    Effect of Magnetic Fields on Tumor Growth and Viability
- in-vivo, NA, NA
TumCG↓, 44x vs 500x for control (360mins only)

502- MF,    Electromagnetic field investigation on different cancer cell lines
- in-vitro, BC, MDA-MB-231 - in-vitro, Colon, SW480 - in-vitro, CRC, HCT116
TumCG↓, all 3 cell lines, but BC line more sensitive
Apoptosis↑,

8489- MF,    Pulsed electromagnetic fields induce ferroptosis in osteosarcoma cells and promote osteogenic differentiation
- in-vitro, OS, U2OS - in-vitro, OS, MG63
TumCP↓, PEMF markedly suppressed the proliferation and migration of osteosarcoma cells and triggered ferroptosis, manifested by down-regulated expression of GPX4 and SLC7A11 as well as elevated malondialdehyde (MDA) levels.
TumCMig↓,
Ferroptosis↑, Pulsed electromagnetic fields induce ferroptosis in osteosarcoma cells
GPx4↓,
xCT/SLC7A11↓,
BMD↑, PEMF facilitated osteoblast differentiation and improved bone mineral density and trabecular-bone-related parameters, without obvious damage observed to normal bone tissue.
selectivity↑,
Dose↝, intermittent pulsed electromagnetic fields at a frequency of 11.4 Hz, with a pulsed width of 50 μs, an interpulse interval of 80 ms, and a peak magnetic field intensity of 1.5 mT. produced by Helmholtz coils.
TumCG↓, Pulsed electromagnetic fields suppress osteosarcoma cell growth
Dose↝, with a daily exposure time of 15 min for 3 days to observe cell proliferation
OS↑, results revealed that PEMF could effectively improve lung metastasis of osteosarcoma (Fig. 1J-K) and enhance the survival rate of tumor-bearing mice
ROS↑, results showed that the increase in ROS, MDA, and Fe2+ levels induced by pulsed electromagnetic fields treatment
MDA↑,
Iron↑,
ChemoSen↑, n breast cancer cells, PEMF exposure potentiated the cytotoxic effects of doxorubicin and etoposide by further activating ROS generation and topoisomerase II inhibition pathways
TOP2↑,
radioP↑, PEMF has been shown to specifically protect osteoblasts from radiation-induced bone loss via intracellular calcium oscillation signaling, mitigating a major dose-limiting side effect of radiotherapy

8486- MF,    Silent forces, hidden currents: the influence of static magnetic field stimulation on tumor biophysics
- Review, Var, NA
Ca+2↑, biochemical targets, including collagen fibril alignment, cell membrane potential and integrity, DNA integrity, Ca2+ dynamics, cytoskeletal organization, and redox balance
TumCG↓, figure 2
MMP↓,
CellMemb↑,
SOX2↓,
Nanog↓,
cMyc↓,
CD44↓,
CD133↓,
P53↑,
ROS↑, ROS generated from Fenton chemistry
DNAdam↑,
CDK1↓,
CycB/CCNB1↓,
TumCCA↑,
TumCP↓,
pH↓, Increased SMF also caused depolarization and pH decline (altering the electrochemical gradient).
TumCP↓, Proliferation rate decreased by 1-fold at 20 mT;
Telomerase↓, via upregulation of E2F1-indicating suppression of telomerase function.
ChemoSen↑, Synergistically enhanced capsaicin’s anticancer effect on HepG2 cells by increasing TRPV1-mediated calcium influx,
TRPV1↝,
Bax:Bcl2↑, apoptosis through elevated Bax/Bcl-2 ratio and caspase-3 activation.
Casp3↑,
Akt↓, Inhibited the Akt/mTOR pathway in CNE-2Z cells;
mTOR↓,
mitA↑, mitotic arrest, and enhanced sensitivity to chemotherapeutic agents (5-FU and Taxol), leading to reduced proliferation.
ROS↓, MNNG/HOS, U-2 OS, and MG63 human osteosarcoma cell lines Inhibited cell proliferation, Intracellular ROS levels were reduced
P-gp/ABCB1↓, Downregulation of P-glycoprotein (MDR1),
MDR1↓,
RadioS↑, The SMF 1.5 T enhanced the biological impact of X‑ray irradiation by increasing radiation‑induced apoptosis
Apoptosis↑, SMF stimulation in the 1–10 mT range can also induce apoptosis over longer durations.
GSH↓, 6 mT SMF stimulation for 2 h increased ROS concentration, as expected from the radical-pair mechanism. Additionally, a concomitant decrease in concentration of the antioxidant glutathione (GSH)
lipid-P↑, Consistent with SMF-induced ROS accumulation123, the study also reported increased concentration of the lipid peroxidation marker malondialdehyde.
Iron↑, 12,000 mT SMF stimulation for 24–48 h inhibits the proliferation of human osteosarcoma MNNG/HOS, U2OS, and MG63 cell lines via intracellular iron accumulation, leading to ROS-associated cell cycle arrest
Iron↓, On the other hand, another report mentions that MCF-7 cells exhibit a significant decrease in intracellular concentration of iron (Fe (II) and Fe (III)) in the presence of 10 mT SMF (for 24 and 48 h)
Fenton↑, 10 mT SMF stimulation for 48 h in combination with 0.1 μM doxorubicin doubled ROS production via the Fenton reaction in human breast cancer MCF-7 cell

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↓, MF exposure induced significant cell growth inhibition and apoptosis in an intensity- and time-dependent manner, in which cell cycle arrest, cleaved Caspase-3, and reactive oxygen species (ROS) increased.
Apoptosis↑,
TumCCA↑,
cl‑Casp3↑,
ROS↑, 60-Hz sinusoidal MF hampered the growth of prostate cancer cells in vitro largely through apoptosis and cell cycle arrest and that this process essentially requires increased ROS.
eff↓, Pretreatment with a Caspase-3 inhibitor or antioxidant, N-acetyl-L-cysteine (NAC), significantly attenuated MF-induced cell growth inhibition and cell death.
Dose↝, 20 cm apart and was capable of generating a field strength of up to 2.5 mT. In each incubator the stray MF intensity was less than 0.05 mT and the temperature was regulated within 37 + 0.18C throughout the experiments.
Dose↝, Collectively, continuous 60-Hz sinusoidal MF exposure impeded the cell growth of prostate cancer cells in vitro.
H2O2↑, MF exposure activated an increase in intracellular H 2O 2

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↝, 20 mT, 50 Hz sinusoidal magnetic field
TumCG↓, Inhibition of cell growth was observed.
Na+↑, exposure also increased the Na+, K+ ion concentration and osmolarity in cell supernatant compared to the control group.
K+↑,

5532- MF,    Magnetoporation: New Method for Permeabilization of Cancerous Cells to Hydrophilic Drugs
- in-vivo, BC, NA
Dose↑, pulsed magnetic field (MF) (3.5 T, 1 Hz, 8 square-wave/160 µs)
CellMemb↑, Uptake of BLM molecules by tumoral cells in the BLM plus 3.5 T MF group versus the BLM control group was 7- folds higher
eff↝, Significant cell permeabilization to BLM requires greater MF strength or exposure time.
other↝, pulsed low electric fields (2.5-20 V/cm) can increase cell membrane permeability by up to 10-fold. induced electric field intensity caused by an alternating magnetic field at 3.5 T is 7.5 V/cm at a 1cm distance from the probes
TumCG↓, figure 1

3495- MFrot,  MF,    Synthesis of urchin-like nickel nanoparticles with enhanced rotating magnetic field-induced cell necrosis and tumor inhibition
- in-vivo, BC, NA
TumCG↓, UNNPs showed obvious suppression against tumor cell growth in a mouse model of malignant breast cancer under the induction of low-frequency RMF.

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

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

198- MFrot,  MF,    Biological effects of rotating magnetic field: A review from 1969 to 2021
- Review, Var, NA
AntiCan↑, RMF can inhibit the growth of various types of cancer cells in vitro and in vivo and improve clinical symptoms of patients with advanced cancer.
breath↑, 0.4T, 7Hz RMF was applied to treat 13 advanced non-small cell lung cancer patients (2 h/day, 5 days per week, for 6–10 weeks)
Pain↓, Decreased pleural effusion (2 patients, 15.4%), remission of shortness of breath (5 patients, 38.5%), relief of cancer pain (5 patients, 38.5%), increased appetite (6 patients, 46.2%), improved physical strength (9 patients, 69.2%), regular bowel mov
Appetite↑,
Strength↑,
BowelM↑,
TumMeta↓, The same RMF (2 h/day, for 43 days) can also suppress the growth and metastasis of B16-F10 cells in vivo
TumCCA↑, The up-regulated transcription of miR-34a induced cell proliferation inhibition, cell cycle arrest, and cell senescence by targeting E2F1/E2F3, two members of E2F family which are major regulators of the cell cycle,
ETC↓, 2h exposure) effectively inhibited the growth of two types of cultured brain cancer cells, glioblastoma cells and diffuse intrinsic pontine glioma cells. They found that the mitochondrial electron transport chain was significantly disturbed by RMF,
MMP↓, which caused loss of mitochondrial integrity, decreased mitochondrial carbon flux in cancer cells, and eventual cancer cell death (Sharpe et al., 2021).
TumCD↑,
selectivity↑, same group further reported that the same RMF can also selectively kill cultured human glioblastoma and non-small cell lung cancer cells, and leave normal cells unharmed
ROS↑, Mechanistic studies revealed that RMF can increase the mitochondrial ROS level, which further activated the caspase-3 and disturbed the electron fflow in the respiratory chain pathway in cancer cells. (Helekar et al., 2021).
Casp3↑,
TumCG↓, 0.4T, 7.5Hz RMF (2 h/day, for 5 days) inhibited the growth of mouse melanoma cell line B16–F10 in vitro,
TumCCA↑, and its mechanism involved cell cycle arrest and decomposition of chromatins.
ChrMod↑,
TumMeta↓, (2 h/day, for 43 days) can also suppress the growth and metastasis of B16–F10 cells in vivo,
Imm↑, benefiting from improved immune function, including decreased regulatory T cells, increased T cells, and dendritic cells
DCells↑,
Akt↓, inhibiting the activation of the AKT pathway (Tang et al., 2016). T
OS⇅, 51 women with advanced breast cancer underwent RMF treatment. The results showed that 27 patients among them achieved signicant therapeutic effects, and there were no side-effects
toxicity↓,
QoL↑, 13 advanced non-small cell lung cancer patients the quality of life was improved in different degrees. Median survival and 1-year survival rate was 50% and 100% longer
hepatoP↑, In addition, it seems that the RMF can also attenuate liver damage in mice bearing MCF7 and GIST-T1 cells (Zha et al., 2018)
Pain↓, The results showed that the RMF treatment reduced abdominal pain by 42.9% (9/21), nausea/vomiting by 19.0% (4/21), weight loss by 52.4% (11/21), ongoing blood loss by 9.5% (2/21), improved physical strength by 23.8% (5/21) and sleep quality by 19.0%
Weight↑,
Strength↑,
Sleep↑,
IL6↓, Furthermore, decreased levels of interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and keratinocyte-derived chemokine (KC) were observed
CD4+↑, it was discovered that macrophages and dendritic cells were activated, CD4+ T and CD8+ T lymphocytes increased, and the ratio of Th17/Treg was balanced.
CD8+↑,
Ca+2↑, effects of RMF were strongly associated with increased calcium tunnel activity and intracellular Ca2+ level in CNS
radioP↑, These results suggest that RMF may be helpful to alleviate the damage of hematopoietic function caused by radiotherapy and chemotherapy
chemoP↑,
*BMD↑, 0.4T, 8Hz RMF treatment (30min/day, for 30 days) along with calcium supplement, synergistically improved bone density
*AntiAge↑, In 2019, Xu et al. reported that a 4h exposure to a 0.2T, 4Hz RMF delayed the aging of human umbilical vein endothelial cells (HUVEC)
*AMPK↑, Mechanistic research revealed that RMF treatment increased the expression of AMPK while reducing the expression of p21, p53 and mTOR.
*P21↓,
*P53↓,
*mTOR↓,
*OS↑, They also discovered that the RMF (2 h/day, for 6, 10 or 14days) can prolong the health status lifespan of Caenorhabditis elegans.
*β-Endo↑, 0.1–0.8T, 0.33Hz RMF treatment signicantly increased the β-endorphin level in the blood of rabbits and humans (23 times higher than before). Moreover, it decreased serotonin (5-HT) in brains, small intestine tissue and serum of mice.
*5HT↓,

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

227- MFrot,  MF,    Low Frequency Magnetic Fields Induce Autophagy-associated Cell Death in Lung Cancer through miR-486-mediated Inhibition of Akt/mTOR Signaling Pathway
- in-vivo, Lung, A549 - in-vitro, Lung, A549
TumCG↓,
miR-486↑, decreased expression of miR-486 and an increased expression of BCAP were found in tumor tissues of lung cancer patients
BCAP↓,
Apoptosis↑,
ROS↑,
TumAuto↑, miR-486 is required for LF-MFs triggered autophagy
LC3II↑,
ATG5↑,
Beclin-1/ATG6↑,
p62↑, blocked p62 degradation
TumCP↓,

223- MFrot,  MF,    The effect of rotating magnetic fields on the growth of Deal's guinea pig sarcoma transplanted subcutaneously in guinea pigs
- in-vivo, NA, NA
TumCG↓,

222- MFrot,  MF,    LF-MF inhibits iron metabolism and suppresses lung cancer through activation of P53-miR-34a-E2F1/E2F3 pathway
- in-vitro, Lung, A549
TumCG↓,
OS↑,
miR-34a↑, enhanced miR-34a transcription
E2Fs↓, E2F1/E2F3
P53↑,
TfR1/CD71↓, TfR1 protein levels
Ferritin↓, inhibits iron metabolism

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

220- MFrot,  MF,    Effect of low frequency magnetic fields on melanoma: tumor inhibition and immune modulation
- in-vitro, Melanoma, B16-F10
OS↑, prolonged the mouse survival rate
DCells↑,
T-Cell↑,
Apoptosis↑,
IL1↑,
IFN-γ↓, most of cytokines were decreased
IL10↑,
TumCG↓, grow slowed
ROS↑, Phagocyte activity, ROS release and interleukin-1β (IL-1β) production were significantly promoted after continuous exposure to 50 Hz LF-MF (1mT)
TumCP↓, LF-MF inhibits the proliferation of B16-F10 cells
TumCCA↑, the S-phase rate was significantly decreased from 40.76% to 37.24% and the G2/M-phase rate was significantly increased from 8.9% to 11.6%
ChrMod↑, Compared with control cells, the treated cells were characterized by the breaking down of chromatin (white arrow) and black granule accumulation (black arrow).
CXCL9↓, in tumor-bearing mice groups, most of cytokines were decreased after LF-MF exposure, including KC, CCL1, IFN-γ, CXCL9, CXCL12, TREM-1, CCL12, IL-1rα and IL-16.
CXCL12↓,
CD4+↑, After LF-MF exposure, the proportions of CD3+, CD3 + CD4+ and CD3 + CD8+ T cells in tumor-bearing mice were increased to 24.0%, 13.28% and 7.46%, respectively
CD8+↑,


Showing Research Papers: 1 to 28 of 28

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 28

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

K+↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Fenton↑, 1,   Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 1,   H2O2↑, 1,   Iron↓, 1,   Iron↑, 2,   lipid-P↑, 1,   MDA↑, 1,   OXPHOS↑, 2,   ROS↓, 1,   ROS↑, 12,   ROS↝, 1,   SOD2↑, 1,   xCT/SLC7A11↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↓, 1,   TfR1/CD71↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,   ETC↓, 1,   mitResp↑, 1,   MMP↓, 3,   MMP↑, 1,   OCR↑, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 2,   BCAP↓, 1,   cAMP⇅, 1,   cMyc↓, 1,   ECAR↓, 1,   Glycolysis↓, 1,   PKM2↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 3,   Apoptosis↑, 8,   Bax:Bcl2↑, 1,   Casp3↑, 3,   cl‑Casp3↑, 1,   Casp7↑, 1,   Casp9↑, 1,   Ferroptosis↑, 1,   MAPK↑, 1,   Telomerase↓, 1,   TRPV1↝, 1,   TumCD↑, 2,  

Transcription & Epigenetics(tgid=7) ⓘ

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

Protein Folding & ER Stress(tgid=8) ⓘ

HSP70/HSPA5↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1/ATG6↑, 1,   LC3II↑, 1,   p62↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 3,   P53↑, 4,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CycB/CCNB1↓, 1,   E2Fs↓, 1,   mitA↑, 1,   P21↑, 1,   TumCCA↑, 8,  

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

CD133↓, 1,   CD44↓, 1,   Diff↑, 1,   p‑ERK↑, 1,   miR-34a↑, 1,   mTOR↓, 1,   Nanog↓, 1,   SOX2↓, 1,   TOP2↑, 1,   TumCG↓, 26,  

Migration(tgid=13) ⓘ

Ca+2↓, 1,   Ca+2↑, 5,   i-Ca+2↑, 1,   CXCL12↓, 1,   miR-486↑, 1,   MMPs↓, 1,   Na+↑, 1,   TumCMig↓, 1,   TumCP↓, 6,   TumMeta↓, 5,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 2,   ECM/TCF↓, 1,   EGFR↝, 1,   EPR↑, 2,   VEGFR2/KDR/Flk1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

CellMemb↑, 2,   Na+↑, 1,   P-gp/ABCB1↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 3,   COX2/PTGS2↓, 1,   CXCc↓, 1,   CXCL9↓, 1,   DCells↑, 3,   GM-CSF↓, 1,   IFN-γ↓, 1,   IL1↑, 1,   IL10↑, 1,   IL12↑, 1,   IL6↓, 2,   Imm↑, 2,   Macrophages↑, 1,   T-Cell↑, 1,  

Cellular Microenvironment(tgid=17) ⓘ

pH↓, 1,   i-pH↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 4,   Dose↑, 1,   Dose↝, 5,   eff↓, 2,   eff↑, 1,   eff↝, 1,   MDR1↓, 1,   RadioS↑, 1,   selectivity↑, 5,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 2,   AST↓, 1,   BMD↑, 1,   EGFR↝, 1,   Ferritin↓, 1,   IL6↓, 2,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   AntiTum↑, 1,   Appetite↑, 1,   breath↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   OS↑, 5,   OS⇅, 1,   Pain↓, 2,   QoL↑, 1,   radioP↑, 2,   Sleep↑, 1,   Strength↑, 2,   toxicity↓, 1,   TumVol↓, 3,   Weight↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 3,  
Total Targets: 137

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

SOD2↓, 1,   Trx↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,   PONs↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,   Cyt‑c↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

HSP70/HSPA5↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↓, 1,  

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

Diff↑, 1,   mTOR↓, 1,   TumCG↑, 1,   TumCG∅, 1,  

Migration(tgid=13) ⓘ

Ca+2↓, 1,   Ca+2∅, 1,   i-Ca+2↓, 1,   β-Endo↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

HIF2a↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BMD↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,   OS↑, 1,   toxicity∅, 1,  
Total Targets: 25

Scientific Paper Hit Count for: TumCG, Tumor cell growth
28 Magnetic Fields
10 Magnetic Field Rotating
1 Radiotherapy/Radiation
1 Vitamin C (Ascorbic Acid)
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:172  Target#:323  State#:%  Dir#:%
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