Magnetic Fields / RadioS 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
RadioS, RadioSensitizer: Click to Expand ⟱
Source:
Type:
A radiosensitizer is an agent that makes cancer cells more sensitive to the damaging effects of radiation therapy. By using a radiosensitizer, clinicians aim to enhance the effectiveness of radiation treatment by either increasing the damage incurred by tumor cells or by interfering with the cancer cells’ repair mechanisms. This can potentially allow for lower doses of radiation, reduced side effects, or improved treatment outcomes.
Pathways that help Radiosensitivity: downregulating HIF-1α, increase SIRT1, Txr

List of Natural Products with radiosensitizing properties:
-Curcumin:modulate NF-κB, STAT3 and has been shown in preclinical studies to enhance the effects of radiation by inhibiting cell survival pathways.
-Resveratrol:
-EGCG:
-Quercetin:
-Genistein:
-Parthenolide:

How radiosensitizers inhibit the thioredoxin (Trx) system in cellular contexts. Notable radiosensitizers, including:
-gold nanoparticles (GNPs),
-gold triethylphosphine cyanide ([Au(SCN) (PEt3)]),
-auranofin, ceria nanoparticles (CONPs),
-curcumin and its derivatives,
-piperlongamide,
-indolequinone derivatives,
-micheliolide,
-motexafin gadolinium, and
-ethane selenide selenidazole derivatives (SeDs)
Scientific Papers found: Click to Expand⟱
3477- MF,    Electromagnetic fields regulate calcium-mediated cell fate of stem cells: osteogenesis, chondrogenesis and apoptosis
- Review, NA, NA
*Ca+2↑, When cells are subjected to external mechanical stimulation, voltage-gated ion channels in the cell membrane open and intracellular calcium ion concentration rises
*VEGF↑, BMSCs EMF combined with VEGF promote osteogenesis and angiogenesis
*angioG↑,
Ca+2↑, 1 Hz/100 mT MC4-L2 breast cancer cells EMF lead to calcium ion overload and ROS increased, resulting in necroptosis
ROS↑,
Necroptosis↑,
TumCCA↑, 50 Hz/4.5 mT 786-O cells ELF-EMF induce G0/G1 arrest and apoptosis in cells lines
Apoptosis↑,
*ATP↑, causing the ATP or ADP increases, and the purinergic signal can upregulate the expression of P2Y1 receptors
*FAK↑, Our research team [53] found that ELE-EMF can induce calcium oscillations in bone marrow stem cells, up-regulated calcium ion activates FAK pathway, cytoskeleton enhancement, and migration ability of stem cells in vitro is enhanced.
*Wnt↑, ability of EMF to activate the Wnt10b/β-catenin signaling pathway to promote osteogenic differentiation of cells depends on the functional integrity of primary cilia in osteoblasts.
*β-catenin/ZEB1↑,
*ROS↑, we hypothesize that the electromagnetic field-mediated calcium ion oscillations, which causes a small amount of ROS production in mitochondria, regulates the chondrogenic differentiation of cells, but further studies are needed
p38↑, RF-EMF was able to suppress tumor stem cells by activating the CAMKII/p38 MAPK signaling pathway after inducing calcium ion oscillation and by inhibiting the β-catenin/HMGA2 signaling pathway
MAPK↑,
β-catenin/ZEB1↓,
CSCs↓, Interestingly, the effect of electromagnetic fields is not limited to tumor stem cells, but also inhibits the proliferation and development of tumor cells
TumCP↓,
ROS↑, breast cancer cell lines exposed to ELE-EMF for 24 h showed a significant increase in intracellular ROS expression and an increased sensitivity to further radiotherapy
RadioS↑,
Ca+2↑, after exposure to higher intensity EMF radiation, showed a significant increase in intracellular calcium ion and reactive oxygen species, which eventually led to necroptosis
eff↓, while this programmed necrosis of tumor cells was able to be antagonized by the calcium blocker verapamil or the free radical scavenger n -acetylcysteine
NO↑, EMF can regulate multiple ions in cells, and calcium ion play a key role [92, 130], calcium ion acts as a second messenger that can activate downstream molecules such as NO, ROS

2251- MF,  Rad,    BEMER Electromagnetic Field Therapy Reduces Cancer Cell Radioresistance by Enhanced ROS Formation and Induced DNA Damage
- in-vitro, Lung, A549 - in-vitro, HNSCC, UTSCC15 - in-vitro, CRC, DLD1 - in-vitro, PC, MIA PaCa-2
RadioS↑, enhanced cancer cell radiosensitization associated with increased DNA double strand break numbers and higher levels of reactive oxygen species upon BEMER treatment relative to controls
DNAdam↑,
ROS↑,
ChemoSen∅, Intriguingly, exposure of cells to the BEMER EMF pattern failed to result in sensitization to chemotherapy and Cetuximab
Pyruv↓, levels of pyruvate, succinate, aspartate and adenosindiphosphate (ADP) were significantly downregulated after BEMER therapy whereas serine showed significant upregulation
ADP:ATP↓,
ROS↑, BEMER therapy increases ROS levels leading to radiosensitization via increased induction of DSBs

2244- MF,    Little strokes fell big oaks: The use of weak magnetic fields and reactive oxygen species to fight cancer
- Review, Var, NA
RPM↑, WEMFs affect multiple cellular processes through mechanisms such as the radical pair mechanism (RPM), which alters reactive oxygen species (ROS) levels, mitochondrial function, and glycolysis
Glycolysis∅, WEMF parallel to the magnetic field (does not enchance glycolysis)
ROS↑, WEMF can augment this effect by enhancing mitochondrial respiration, which increases ROS levels within cancer cells. This augmentation makes cancer cells more susceptible to treatment by promoting oxidative stress that can lead to apoptosis
ChemoSen↑, Chemotherapeutic agents, such as doxorubicin, primarily exert their effects by generating ROS to induce cell death. WEMF can augment this effect by enhancing mitochondrial respiration, which increases ROS levels
RadioS↑, Similarly, WEMF can enhance the efficacy of radiation therapy by increasing ROS production and sensitizing cancer cells to radiation-induced DNA damage
selectivity↑, primary advantage of WEMF is its non-invasive, non-ionizing nature, which minimizes collateral damage to healthy tissue.

512- MF,    Pulsed Electromagnetic Fields (PEMFs) Trigger Cell Death and Senescence in Cancer Cells
- in-vitro, BC, MCF7 - in-vitro, BC, MDA-MB-231 - in-vitro, Nor, FF95
TumCP↓,
*toxicity↓, PEMF application decreases the proliferation rate and viability of breast cancer cells while having the opposite effect on normal fibroblasts.
ChemoSen↑, ELF-PEMFs, as a pathology treatment approach, they have mainly been used as a complementary type of therapy, coupled with chemo-/radiotherapy,
RadioS↑,
selectivity↑, Collectively, these data indicate that PEMF irradiation exhibited not only anti-cancer properties but also beneficial effects for the normal cells.
Ca+2↑, The Thomas EMF was able to inhibit the growth of cancer cell lines including B16-BL6, MCF-7, MDA-MB-231 and HeLa via increased Ca2+ uptake through T-type Ca2+ channels but did not affect the growth of normal cells

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

8483- MF,    Magnetic Fields in Cancer Therapy: Mechanistic Insights, Signaling Pathways, and Evidence from Clinical and In Vitro Studies
- Review, Var, NA
Apoptosis↑, demonstrated the capacity to modulate proliferation, apoptosis, ferroptosis, migration, and epithelial-to-mesenchymal transition (EMT) in tumor cells, often through reactive oxygen species (ROS) modulation, ion channel regulation,
TumCP↓,
Ferroptosis↑,
TumCMig↓,
EMT↓,
ROS↝,
ChemoSen↑, The mechanistic diversity of MFs allows synergistic combination with chemotherapy, radiotherapy, and immunotherapy.
RadioS↑,
Telomerase↓, exposure to ~150 mT SMF in 4T1 breast cancer cells accelerated proliferation but inhibited migration and telomerase activity, implicating biomechanical orientation effects and transcriptional regulation
selectivity↑, 8 Hz PEMFs at ~0.011 T reduced proliferation and induced senescence selectively in cancer cells while sparing normal fibroblasts, illustrating a non-thermal, selective cytotoxic effect
ROS↑, PEMFs (2.5 mT at 70 Hz for repeated exposures) heightened etoposide-induced cell death via increased ROS generation, DNA damage response, and caspase-dependent apoptosis
DNAdam↑,
Casp↑,
Ca+2↑, Recent studies show that MF-induced calcium influx via voltage-gated and mechanosensitive channels exacerbates mitochondrial depolarization, thereby accelerating ROS generation
MMP↓,
lysoMP↑, ROS can directly trigger lysosomal membrane permeabilization (LMP) through lipid peroxidation, linking calcium signalling, oxidative stress, and lysosomal instability into a single interconnected cascade
lipid-P↑,
NA↑, MFs, particularly when combined with iron or magnetic nanoparticles (MNPs), can enhance ROS production, leading to oxidative damage of DNA and proteins.
other↑, some studies report substantial heat generation in Fe3O4 nanoparticle suspensions when exposed to 100 kHz fields, especially at field amplitudes of a few millitesla
ChemoSen↑, PEMFs can reduce cancer cell proliferation, promote apoptosis, and sensitize tumor cells to chemotherapeutic agents such as doxorubicin and cisplatin
P53↑, These effects are thought to be mediated through modulation of reactive oxygen species (ROS), intracellular calcium signaling, and p53 activation


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

NA↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Fenton↑, 1,   Ferroptosis↑, 1,   GSH↓, 1,   Iron↓, 1,   Iron↑, 1,   lipid-P↑, 2,   ROS↓, 1,   ROS↑, 7,   ROS↝, 1,   RPM↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ADP:ATP↓, 1,   MMP↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,   Glycolysis∅, 1,   Pyruv↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 3,   Bax:Bcl2↑, 1,   Casp↑, 1,   Casp3↑, 1,   Ferroptosis↑, 1,   lysoMP↑, 1,   MAPK↑, 1,   Necroptosis↑, 1,   p38↑, 1,   Telomerase↓, 2,   TRPV1↝, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 3,   P53↑, 2,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CycB/CCNB1↓, 1,   mitA↑, 1,   TumCCA↑, 2,  

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

CD133↓, 1,   CD44↓, 1,   CSCs↓, 1,   EMT↓, 1,   mTOR↓, 1,   Nanog↓, 1,   SOX2↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 5,   TumCMig↓, 1,   TumCP↓, 5,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↑, 1,  

Barriers & Transport(tgid=15) ⓘ

CellMemb↑, 1,   P-gp/ABCB1↓, 1,  

Cellular Microenvironment(tgid=17) ⓘ

pH↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 5,   ChemoSen∅, 1,   eff↓, 1,   MDR1↓, 1,   RadioS↑, 6,   selectivity↑, 3,  
Total Targets: 57

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,  

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

Wnt↑, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   FAK↑, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 1,   VEGF↑, 1,  

Functional Outcomes(tgid=23) ⓘ

toxicity↓, 1,  
Total Targets: 9

Scientific Paper Hit Count for: RadioS, RadioSensitizer
6 Magnetic Fields
1 Radiotherapy/Radiation
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#:1107  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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