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⟱
4103- MF,    Comparing the Effects of Long-term Exposure to Extremely Low-frequency Electromagnetic Fields With Different Values on Learning, Memory, Anxiety, and β-amyloid Deposition in Adult Rats
- in-vivo, Nor, NA
*Dose↝, *memory↑, *ROS↑, *MDA↑,
4102- MF,    Modulation of antioxidant enzyme gene expression by extremely low frequency electromagnetic field in post-stroke patients
- Human, Stroke, NA
*Catalase↑, *SOD1↑, *SOD2↑, *GPx1↑, *GPx4↑, *Dose↝,
4101- MF,    Benign Effect of Extremely Low-Frequency Electromagnetic Field on Brain Plasticity Assessed by Nitric Oxide Metabolism during Poststroke Rehabilitation
- Human, Stroke, NA
*motorD↑, *cognitive↑, *eff↑, *NO↑, *other↝, *neuroP↑,
4100- MF,    Neurobiological effects and mechanisms of magnetic fields: a review from 2000 to 2023
- Review, Var, NA
*memory↑, *Mood⇅,
4099- MF,    Extremely low frequency electromagnetic field reduces oxidative stress during the rehabilitation of post-acute stroke patients
- Trial, Stroke, NA
*ROS↓,
4098- MF,    Extremely low frequency electromagnetic field (ELF-EMF) reduces oxidative stress and improves functional and psychological status in ischemic stroke patients
- Trial, Stroke, NA
*antiOx↑, *cognitive↑, *Dose↝,
3739- MF,    Early intervention using long-term rhythmic pulsed magnetic stimulation alleviates cognitive decline in a 5xFAD mouse model of Alzheimer's disease
- in-vivo, AD, NA
*memory↑, *cognitive↑, *Aβ↓, *FGF↑,
4096- MF,    Extremely Low‐Frequency and Low‐Intensity Electromagnetic Field Technology (ELF‐EMF) Sculpts Microtubules
- in-vitro, AD, NA
*p‑tau↓, *neuroP↑, *Dose↝,
4095- MF,    Frequency-tuned electromagnetic field therapy improves post-stroke motor function: A pilot randomized controlled trial
- Trial, Stroke, NA
*Dose↝, *motorD↑,
3740- MF,    Gamma rhythm low field magnetic stimulation alleviates neuropathologic changes and rescues memory and cognitive impairments in a mouse model of Alzheimer's disease
- in-vivo, AD, NA
*cognitive↑, *Dose↝, *Aβ↓, *PSD95↑,
4093- MF,    Low-intensity electromagnetic fields induce human cryptochrome to modulate intracellular reactive oxygen species
- in-vivo, Nor, NA
*ROS↑, *eff↑,
3741- MF,    Promising application of Pulsed Electromagnetic Fields (PEMFs) in musculoskeletal disorders
- Review, Nor, NA
*eff↑, *BMD↑, *Inflam↓, *PGE2↓, *IL6↓, *IL8↓, *NF-kB↓, *mTOR↝,
3742- MF,    The role of magnetic fields in neurodegenerative diseases
- Review, AD, NA - Review, Park, NA
cognitive↑,
4092- MF,    Mechanisms and therapeutic effectiveness of pulsed electromagnetic field therapy in oncology
- Review, Var, NA
Apoptosis↑, selectivity↑, ROS↑, Catalase↓, TumVol↓, angioG↓, Ca+2↝, eff↝, angioG↓, Imm↝, TNF-α↑, Casp8↑,
3744- MF,    Cognitive improvement via a modulated rhythmic pulsed magnetic field in D-galactose-induced accelerated aging mice
- in-vivo, AD, NA
*cognitive↑, *memory↑,
3746- MF,    Low-Frequency Pulsed Electromagnetic Field Is Able to Modulate miRNAs in an Experimental Cell Model of Alzheimer's Disease
- in-vitro, AD, NA
*cognitive↑, *memory↑, *BACE/β-secretase↓,
3942- MF,    Chronic-Exposure Low-Frequency Magnetic Fields (Magnetotherapy and Magnetic Stimulation) Influence Serum Serotonin Concentrations in Patients with Low Back Pain-Clinical Observation Study
- Human, AD, NA
*5HT↑,
4015- MF,    Evaluation of the PTEN and circRNA-CDR1as Gene Expression Changes in Gastric Cancer and Normal Cell Lines Following the Exposure to Weak and Moderate 50 Hz Electromagnetic Fields
- in-vitro, GC, AGS - in-vitro, Nor, HU02
*PTEN↑, PTEN↓, Dose↝,
4094- MF,    EMAGINE-Study protocol of a randomized controlled trial for determining the efficacy of a frequency tuned electromagnetic field treatment in facilitating recovery within the subacute phase following ischemic stroke
- Study, Stroke, NA
*neuroP↑, *Dose↝,
3492- MFrot,  Chemo,  MF,    Synergistic Effect of Chemotherapy and Magnetomechanical Actuation of Fe-Cr-Nb-B Magnetic Particles on Cancer Cells
- in-vitro, Var, NA
eff↑, TumCD↑,
3745- MFrot,  MF,    The neurobiological foundation of effective repetitive transcranial magnetic brain stimulation in Alzheimer's disease
- Review, AD, NA
*neuroP↑, *ROS↓, *Inflam↓, *5HT↑, *cFos↑, *Aβ↓, *memory↑, *BDNF↑, *Ach↑, *AChE↓, *cognitive↑, *BDNF↑, *NGF↑, *β-catenin/ZEB1↑, *p‑Akt↓, *mTOR↓, *MMP1↓, *MMP9↓, *MMP-10↓, *TIMP1↑, *TIMP2↑,
3488- MFrot,  MF,    Rotating magnetic field improves cognitive and memory impairments in APP/PS1 mice by activating autophagy and inhibiting the PI3K/AKT/mTOR signaling pathway
- in-vivo, AD, NA
*cognitive↑, *memory↑, *neuroP↑, *Aβ↓, *PI3K↓, *Akt↓, *mTOR↓,
3489- MFrot,  MF,    Rotating magnetic field inhibits Aβ protein aggregation and alleviates cognitive impairment in Alzheimer's disease mice.
- in-vivo, AD, NA
*Aβ↓, *motorD↑, *cognitive↑, *memory↑, *ROS↓,
3491- MFrot,  MF,    Magnetically controlled cyclic microscale deformation of in vitro cancer invasion models
- in-vitro, BC, MDA-MB-231
Ca+2↑, ATF3↑, FOSB↑,
3493- MFrot,  MF,    Mechanical nanosurgery of chemoresistant glioblastoma using magnetically controlled carbon nanotubes
- in-vivo, GBM, NA
TumCD↑, MMP↓, Cyt‑c↑, Apoptosis↑, OS↑, DNAdam↑,
3494- MFrot,  MF,    Magnetically switchable mechano-chemotherapy for enhancing the death of tumour cells by overcoming drug-resistance
- in-vitro, Var, NA
eff↑, TumCD↑,
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↓,
3496- MFrot,  GoldNP,  MF,    Enhancement of chemotherapy effects by non-lethal magneto-mechanical actuation of gold-coated magnetic nanoparticles
- in-vitro, Cerv, HeLa
eff↑, tumCV↓,
3497- MFrot,  MF,    The Effect of a Rotating Magnetic Field on the Regenerative Potential of Platelets
- Human, Nor, NA
*PDGFR-BB↑, *TGF-β↑, *IGF-1↑, *FGF↑, *angioG↑, *Inflam↓, *ROS↓,
3499- MFrot,  MF,    Rotating magnetic field delays human umbilical vein endothelial cell aging and prolongs the lifespan of Caenorhabditis elegans
- in-vitro, Nor, HUVECs
*AntiAge↑, *AMPK↑, *mPGES-1↓, *Ca+2↑, *ER Stress↑, *OS↑, *ROS↓,
3567- MFrot,  MF,    The Effect of Extremely Low-Frequency Magnetic Field on Stroke Patients: A Systematic Review
- Review, Stroke, NA
*Stroke↓, *ROS↓, *Inflam↓, *cognitive↑, *Catalase↑, *SOD↑, *SOD1↑, *SOD2↑, *GPx1↑, *GPx4↑, *IL1β↑, *neuroP↑, *toxicity∅,
3535- MFrot,  MF,    Pulsed Electromagnetic Field Stimulation in Osteogenesis and Chondrogenesis: Signaling Pathways and Therapeutic Implications
- Review, Nor, NA
*eff↑, *COL2A1↑, *SOX9↑, *Ca+2↑, *FAK↑, *F-actin↑, *Inflam↓, *other↑, *Diff↑, *BMD↑,
201- MFrot,  MF,    Gradient Rotating Magnetic Fields Impairing F-Actin-Related Gene CCDC150 to Inhibit Triple-Negative Breast Cancer Metastasis by Inactivating TGF-β1/SMAD3 Signaling Pathway
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549 - in-vitro, BC, MDA-MB-468
CCDC150↓, TGF-β↓, SMAD3↓,
212- MFrot,  MF,    Rotating magnetic field inhibits Aβ protein aggregation and alleviates cognitive impairment in Alzheimer’s disease mice
- in-vivo, AD, SH-SY5Y
*β-Amyloid↓, *cognitive↑, *motorD↑, *ROS↓, *memory↑, *Aβ?,
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↓, MMPs↓, ECM/TCF↓,
203- MFrot,  MF,    Rotating Magnetic Field Induced Oscillation of Magnetic Particles for in vivo Mechanical Destruction of Malignant Glioma
- vitro+vivo, GBM, U87MG
lysoMP↓, TumVol↓, eff↑, Apoptosis↑, Ca+2↑,
204- MFrot,  MF,    Rotating magnetic field improved cognitive and memory impairments in a sporadic ad model of mice by regulating microglial polarization
- in-vivo, AD, NA
*NF-kB↓, *MAPK↓, *TLR4↓, *memory↑, *cognitive↑, *TGF-β1↑, *ARG1/2↑, *IL4↑, *IL10↑, *IL6↓, *IL1↓, *TNF-α↓, *iNOS↓, *ROS↓, *NO↓, *MyD88↓, *p‑IKKα↓, *p‑IκB↓, *p‑p65↓, *p‑JNK↓, *p‑p38↓, *ERK↓, *neuroP↑, *Aβ↓,
2311- MFrot,  MF,    Magnetic fields as a potential therapy for diabetic wounds based on animal experiments and clinical trials
- in-vivo, Nor, HaCaT
*COX2/PTGS2↓, *Inflam↓, *MMP9↑, *GPx↑, *Diff↑,
2262- MFrot,  MF,    Effects of 0.4 T Rotating Magnetic Field Exposure on Density, Strength, Calcium and Metabolism of Rat Thigh Bones
- in-vivo, ostP, NA
*BMD↑, *eff↓, *ALP↑, *other↑,
205- MFrot,  MF,    Intermittent F-actin Perturbations by Magnetic Fields Inhibit Breast Cancer Metastasis
- vitro+vivo, BC, MDA-MB-231
OS↑, F-actin↓, TumCI↓, TumCMig↓, Rho↓, selectivity↑, TumMeta↓,
209- MFrot,  MF,    The effect of a rotating magnetic field on the antioxidant system in healthy volunteers - preliminary study
- Human, Nor, NA
*SOD↑, *Catalase↑, *ROMO1↑, *MDA↓, *TAC↑, *ROS↓,
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↑, ChemoSen↑, MMP↓, selectivity↑, TCA?, H2O2↑, eff↑, *antiOx↑, H2O2↑, eff↓, GSH/GSSG↓, *toxicity∅, OS↑,
2258- MFrot,  MF,    EXTH-68. ONCOMAGNETIC TREATMENT SELECTIVELY KILLS GLIOMA CANCER CELLS BY INDUCING OXIDATIVE STRESS AND DNA DAMAGE
- in-vitro, GBM, GBM - in-vitro, Nor, SVGp12
TumVol↓, OS↑, γH2AX↑, DNAdam↑, selectivity↑, ROS↑, TumCD↑, eff↑, eff↓,
191- MFrot,  MF,    Early exposure of rotating magnetic fields promotes central nervous regeneration in planarian Girardia sinensis
- in-vivo, Nor, NA
*EGR4↑, *Netrins↑, *NSE↑, *NPY↑,
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↓, TumCCA↑, TumCG↓, TumMeta↓, Imm↑, P53↑, ALAT↓, AST↓,
199- MFrot,  MF,    Modulation of Cellular Response to Different Parameters of the Rotating Magnetic Field (RMF)—An In Vitro Wound Healing Study
- in-vivo, Wounds, L929 - NA, NA, HaCaT
*ROS↑, *Ca+2↓, *other↝, *other↝, *other↝, *other↝, *other↝, *other?,
198- MFrot,  MF,    Biological effects of rotating magnetic field: A review from 1969 to 2021
- Review, Var, NA
AntiCan↑, breath↑, Pain↓, Appetite↑, Strength↑, BowelM↑, TumMeta↓, TumCCA↑, ETC↓, MMP↓, TumCD↑, selectivity↑, ROS↑, Casp3↑, TumCG↓, TumCCA↑, ChrMod↑, TumMeta↓, Imm↑, DCells↑, Akt↓, OS⇅, toxicity↓, QoL↑, hepatoP↑, Pain↓, Weight↑, Strength↑, Sleep↑, IL6↓, CD4+↑, CD8+↑, Ca+2↑, radioP↑, chemoP↑, *BMD↑, *AntiAge↑, *AMPK↑, *P21↓, *P53↓, *mTOR↓, *OS↑, *β-Endo↑, *5HT↓,
185- MFrot,  MF,    Case Report: End-Stage Recurrent Glioblastoma Treated With a New Noninvasive Non-Contact Oncomagnetic Device
- Human, GBM, NA
TumVol↓, Dose↝, cognitive↑,
195- MFrot,  MF,    Application of Rotating Magnetic Fields Increase the Activity of Antimicrobials Against Wound Biofilm Pathogens
- Human, Wounds, NA
Bacteria↓,
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↝,

Showing Research Papers: 201 to 250 of 282
Prev Page 5 of 6 Next

* 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

 

Home Page