Magnetic Fields / ChemoSen 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):

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.
Ca²⁺ and ion-channel modulation, particularly TRPC, voltage-gated channels, intracellular Ca²⁺ handling, and ER–mitochondrial Ca²⁺ communication.
Mitochondrial and bioenergetic modulation, including membrane potential, electron transport, ATP production, mitochondrial permeability, and metabolic reprogramming.
Cell proliferation, cell-cycle, apoptosis, and senescence signaling through pathways including EGFR/PI3K/AKT/mTOR, MAPK/ERK, caspases, PARP, Bax and survivin.
Membrane permeability and drug-uptake modulation, producing context-dependent chemosensitization to agents including doxorubicin, etoposide and methotrexate.
Inflammatory and stress-response modulation including NF-κB, cytokine signaling, HSPs, ER stress and adaptive antioxidant pathways.
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

ChemoSen, chemo-sensitization: Click to Expand ⟱

Source:

Type:

The effectiveness of chemotherapy by increasing cancer cell sensitivity to the drugs used to treat them, which is known as “chemo-sensitization”.

Possible Chemo-Sensitizers:
-Curcumin
-Resveratrol
-EGCG
-Quercetin
-Genistein
-Berberine
-Piperine: alkaloid from black pepper
-Ginsenosides: active components of ginseng
-Silymarin
-Allicin
-Lycopene
-Ellagic acid
-Caffeic acid phenethyl ester
-flavopiridol
-oleandrin
-Ursolic acid
-butein
-Betulinic acid

Scientific Papers found: Click to Expand⟱

529-

MF,

Low-frequency magnetic field therapy for glioblastoma: Current advances, mechanisms, challenges and future perspectives

Review,

GBM,

Ca+2↑, U-373MG 50 Hz, 3 mT 24 h Increased the intracellular Ca2+
ROS↑, BT115, U87, BT175 50–350 Hz, 1–58 mT 2–4 h Increased the ROS level and cell death
ChemoSen↑, A growing amount of evidence has validated that LF-MFs combined with chemotherapeutic drugs have a synergistic effect in the treatment of GBM
QoL↑, For example, researchers have discovered that LF-MFs can improve the quality of life of patients with recurrent GBM
OS↑, clinical trials have also validated the excellent therapeutic efficacy of LF-MFs in prolonging OS and improving quality of life in GBM patients

3464-

MF,

Progressive Study on the Non-thermal Effects of Magnetic Field Therapy in Oncology

Review,

Var,

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

2251-

MF,

Rad,

BEMER Electromagnetic Field Therapy Reduces Cancer Cell Radioresistance by Enhanced ROS Formation and Induced DNA Damage

in-vitro,

Lung,

A549

 0 μT to 35 μT and a mattress applicator

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,

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.

3457-

MF,

Cellular stress response to extremely low‐frequency electromagnetic fields (ELF‐EMF): An explanation for controversial effects of ELF‐EMF on apoptosis

Review,

Var,

Apoptosis↑, Ding et al., 8 it was demonstrated that 24‐h exposure to 60 Hz, 5 mT ELF‐EMF could potentiate apoptosis induced by H2O2 in HL‐60 leukaemia cell lines.
H2O2↑,
ROS↑, One of the main mechanisms proposed for defining anticancer effects of ELF‐EMF is induction of apoptosis through upregulation of reactive oxygen species (ROS) which has also been confirmed by different experimental studies.
eff↑, intermittent 100 Hz, 0.7 mT EMF significantly enhanced rate of apoptosis in human hepatoma cell lines pretreated with low‐dose X‐ray radiation.
eff↑, 50 Hz, 45 ± 5 mT pulsed EMF, significantly potentiated rate of apoptosis induced by cyclophosphamide and colchicine
Ca+2↑, Over the past few years, lots of data have shown that ELF‐EMF exposure regulates intracellular Ca2+ level
MAPK↑, Mitogen‐activated protein kinase (MAPK) cascades are among the other important signalling cascades which are stimulated upon exposure to ELF‐EMF in several types of examined cells
*Catalase↑, ELF‐EMF exposure can upregulate expression of different antioxidant target genes including CAT, SOD1, SOD2, GPx1 and GPx4.
*SOD1↑,
*GPx1↑,
*GPx4↑,
*NRF2↑, Activation and upregulation of Nrf2 expression, the master redox‐sensing transcription factor may be the most prominent example in this regard which has been confirmed in a Huntington's disease‐like rat model.
TumAuto↑, Activation of autophagy, ER stress, heat‐shock response and sirtuin 3 expression are among the other identified cellular stress responses to ELF‐EMF exposure
ER Stress↑,
HSPs↑,
SIRT3↑,
ChemoSen↑, Contrarily, when chemotherapy and ELF‐EMF exposure are performed simultaneously, this increase in ROS levels potentiates the oxidative stress induced by chemotherapeutic agents
UPR↑, In consequence of ER stress, cells begin to initiate UPR to counteract stressful condition.
other↑, Since the only proven effects of ELF‐EMF exposure on cells are cellular adaptive responses, ROS overproduction and intracellular calcium overload
PI3K↓, figure 3
JNK↑,
p38↑,
eff↓, ontrarily, when cells are exposed to ELF‐EMF, a new source of ROS production is introduced in cells which can at least partially reverse anticancer effects observed with cell's treatment with melatonin.
*toxicity?, More importantly, ELF‐EMF exposure to normal cells in most cases has shown to be safe and un‐harmful.

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.

512-

MF,

Pulsed Electromagnetic Fields (PEMFs) Trigger Cell Death and Senescence in Cancer Cells

in-vitro,

BC,

MCF7

11mT, 8Hz, square wave, 2x/d 30mins, 5 d

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

506-

MF,

doxoR,

Pulsed Electromagnetic Field Stimulation Promotes Anti-cell Proliferative Activity in Doxorubicin-treated Mouse Osteosarcoma Cells

in-vitro,

OS,

LM8

5 mT, 200 Hz

x2 fold improved

The IC50 for combined PEMF and doxorubicin was about 2-fold lower than that of doxorubicin alone, suggesting that PEMF enhanced the antiproliferative activity of doxorubicin.

TumCP↓,
p‑CHK1↓, reducing the increased expression of total IĸB and phosphorylated-CHK1 induced by doxorubicin
Ca+2↑, caused by PEMF alone
Casp3↓, PEMF stimulation significantly reduced the enhancement of caspase 3/7 activity by doxorubicin at 24 h
Casp7↓, PEMF stimulation significantly reduced the enhancement of caspase 3/7 activity by doxorubicin at 24 h
p‑BAD↓,
ChemoSen↑, Our results indicate that combination of PEMF and doxorubicin could be a novel chemotherapeutic strategy.

501-

MF,

Low Intensity and Frequency Pulsed Electromagnetic Fields Selectively Impair Breast Cancer Cell Viability

in-vitro,

BC,

MCF7

2-5mT, 10-50Hz, 30-90min/d

harmless to non-malignant cell types

in-vitro,

Nor,

MCF10

Apoptosis↑, MCF10 cells were slightly benefitted by these same PEMF parameters ****
*toxicity↓, harmless to non-malignant cell types
ChemoSen↑, adjuvant treatment to more traditional chemo- and radiotherapies with the aim of reducing their dosage, mitigating any harmful secondary side effects and enhancing patient prognosis.
chemoP↑,
selectivity↑, killing of MCF7 cells : 3 mT peak-to-peak magnitude, at a pulse frequency of 20 Hz and duration of exposure of only 60 minutes per day. By stark contrast, this same pulsing paradigm (cytotoxic to MCF-7s) was innocuous to normal MCF-10 breast cells
DNAdam↑, Once again, 60 minutes of 3 mT PEMFs for three consecutive days gave the greatest DNA damage in MCF7 cancer cells.

4425-

MF,

doxoR,

Brief Magnetic Field Exposure Stimulates Doxorubicin Uptake into Breast Cancer Cells in Association with TRPC1 Expression: A Precision Oncology Methodology to Enhance Chemotherapeutic Outcome

in-vitro,

BC,

4T1

in-vitro,

BC,

MCF7

ChemoSen↑, PEMF therapy may enhance DOX cytotoxicity in breast cancer cells,
TRPC1↑, increased by TRPC1 overexpression,
Dose↓, PEMF exposure enhances DOX-mediated killing of breast cancer cells, reducing the IC50 value of DOX by half, whereas muscle cells, representative of collateral tissues, were less sensitive to PEMF-enhanced DOX-mediated cytotoxicity
selectivity↑, whereas muscle cells, representative of collateral tissues, were less sensitive to PEMF-enhanced DOX-mediated cytotoxicity.

5246-

MF,

Chemo,

Non-ionizing Electromagnetic Radiation: A Study of Carcinogenic and Cancer Treatment Potential

in-vitro,

BC,

MCF7

ChemoSen↑, improvement in the neoplastic cell kill by antineoplastic chemotherapy when coupled with a low frequency magnetic field.

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,

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

8485-

MF,

doxoR,

Static magnetic field promotes the doxorubicin toxicity effects on osteosarcoma cells

in-vitro,

OS,

G292

tumCV↓, Results demonstrated that the combination of SMF and DOX significantly reduced G292 cell viability compared to DOX alone,
Dose↝, IC50 values decreased from 3.2 µM (at 3 mT, p < 0.01) to 0.8 µM (at 24 mT, p < 0.001) at 24 h
Apoptosis↑, Apoptosis rates increased from 8.12% with DOX alone to 16% with SMF + DOX.
ROS↑, SMF further amplified apoptosis by enhancing ROS generation and disrupting iron and calcium homeostasis.
i-Iron↓, total intracellular iron concentration in G292 cancer cells significantly decreased under all treatment conditions compared to untreated controls. G292 cells may decrease intracellular iron as a protective mechanism, potentially to modulate the activ
*Ca+2↓, notable decline in total calcium ion content was observed in HFF cells following treatment, whereas calcium levels in G292 cells remained stable.
*Iron↑, Conversely, the increased iron content in HFF cells upon exposure to SMF and combined treatments suggests that SMF may promote iron retention or uptake in normal cells
*chemoP↑, The increased iron content in normal cells following SMF and combined treatments may reflect a lower cytotoxic impact of SMF on these cells.
ROS↓, Our findings reveal a complex interaction between SMF, DOX, and ROS dynamics, where SMF increases ROS production in normal cells but decreases ROS levels in cancer cells, likely due to enhanced antioxidant defenses
ChemoSen↑, The results support the hypothesis that SMF can enhance the efficacy of chemotherapeutic agents such as DOX.
selectivity↑, This study demonstrates the significant potential of combining a SMF with DOX to enhance cytotoxic effects on osteosarcoma cells while sparing non-cancerous cells.

8484-

MF,

doxoR,

Pulsed Electromagnetic Field Increases Doxorubicin-induced Mitotic Slippage in MDA-MB-231 Breast Cancer Cells

in-vitro,

BC,

MDA-MB-231

ChemoSen↑, Pulsed electromagnetic fields (PEMF) can be used to improve the efficacy of chemotherapeutic agents, such as doxorubicin (DOX).
Dose↝, DOX-treated MDA-MB-231 breast cancer cells were stimulated with a 60 min PEMF session three times daily.
eff↑, DOX treatment for three days induced mitotic slippage including cell enlargement, polyploidy, and multinucleation, which was further enhanced by PEMF exposure.
CDK1?, DOX treatment also induced CDK1 activation, histone H3 dephosphorylation, and survivin and PLK1 downregulation, which were further increased by PEMF exposure.
p‑H3↓,
survivin↓,
PLK1↓,

8483-

MF,

Magnetic Fields in Cancer Therapy: Mechanistic Insights, Signaling Pathways, and Evidence from Clinical and In Vitro Studies

Review,

Var,

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

3486-

MF,

Pulsed electromagnetic field potentiates etoposide-induced MCF-7 cell death

in-vitro,

NA,

ChemoSen↑, It is established that pulsed electromagnetic field (PEMF) therapy can enhance the effects of anti-cancer chemotherapeutic agents
tumCV↓, co-treatment with etoposide and PEMFs led to a decrease in viable cells compared with cells solely treated with etoposide.
cl‑PARP↑, PEMFs elevated the etoposide-induced PARP cleavage and caspase-7/9 activation and enhanced the etoposide-induced down-regulation of survivin and up-regulation of Bax.
Casp7↑,
Casp9↑,
survivin↓,
BAX↑,
DNAdam↑, PEMF also increased the etoposide-induced activation of DNA damage-related molecules
ROS↑, the reactive oxygen species (ROS) level was slightly elevated during etoposide treatment and significantly increased during co-treatment with etoposide and PEMF.
eff↓, Moreover, treatment with ROS scavenger restored the PEMF-induced decrease in cell viability in etoposide-treated MCF-7 cells

Showing Research Papers: 1 to 17 of 17

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 17

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↑, 1, GPx1↑, 1, GPx4↑, 1, Iron↑, 1, NRF2↑, 1, SOD1↑, 1,

Migration(tgid=13) ⓘ

Ca+2↓, 1,

Functional Outcomes(tgid=23) ⓘ

chemoP↑, 1, toxicity?, 1, toxicity↓, 2,
Total Targets: 10

Scientific Paper Hit Count for: ChemoSen, chemo-sensitization

17 Magnetic Fields
4 doxorubicin
1 Radiotherapy/Radiation
1 Chemotherapy

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#:1106  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

Magnetic Fields / ChemoSen Cancer Research Results

Magnetic Field Mechanisms in Cancer

Magnetic Stimulation in Alzheimer’s Disease

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Cellular Microenvironment(tgid=17) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Migration(tgid=13) ⓘ

Functional Outcomes(tgid=23) ⓘ

Home Page