Database Query Results : Magnetic Fields, , ChemoSen

MF, Magnetic Fields: Click to Expand ⟱

Features: Therapy

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

Non-Static Magnetic Fields (AC / Pulsed / Oscillating MF)

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	Reactive oxygen species (ROS)	↑ ROS (P→R); often sustained (G)	↑ ROS (P); ↔/↓ net ROS (R→G)	P, R, G	Upstream redox perturbation	MF perturbs electron/radical dynamics: normal cells often adapt (ROS setpoint ↓), cancer cells less so
2	NRF2 antioxidant response	↔ / insufficient NRF2 induction (R→G)	↑ NRF2 activation (R→G)	R, G	Adaptive redox defense	Explains mixed ROS direction in normal cells (initial ↑ then adaptive ↓)
3	Glutathione (GSH) homeostasis	↓ GSH (R→G)	↔ or transient ↓ (R) with recovery (G)	R, G	Redox buffering capacity	GSH depletion reflects sustained oxidative load; recovery indicates successful adaptation
4	Superoxide dismutase (SOD) / antioxidant enzymes	↔ or inadequate enzyme upshift (G)	↑ SOD/GPx/CAT capacity (G)	G	Longer-term antioxidant remodeling	Often the “endpoint” readout that correlates with ROS-normalization in normal tissue
5	Mitochondrial ETC / respiration	↓ ETC efficiency; ↑ electron leak (P→R)	↔ mild, reversible ETC perturbation (P→R)	P, R	Bioenergetic destabilization	ETC perturbation is a mechanistic bridge between MF exposure and ROS/ΔΨm changes
6	Mitochondrial membrane potential (ΔΨm / MMP)	↓ ΔΨm (R); may progress (G)	↔ preserved or reversible dip (R)	R, G	Mitochondrial dysfunction thresholding	ΔΨm loss typically follows ROS/ETC disruption rather than preceding it
7	Ca²⁺ signaling (VGCC / ER–mitochondria Ca²⁺ flux)	↑ dysregulated Ca²⁺ influx/transfer (P→R); overload may persist (G)	↑ transient Ca²⁺ signaling (P); homeostasis restored (R→G)	P, R, G	Stress signal amplification	Ca²⁺ dysregulation links ROS/ETC perturbation to ER stress and mitochondrial dysfunction (amplifies ΔΨm loss and UPR commitment)
8	Mitochondrial permeability transition pore (MPTP)	↑ MPTP opening propensity (R); sustained opening possible (G)	↔ transient or closed (R→G)	P, R, G	Commitment point for mitochondrial failure	MPTP opening integrates ROS, Ca²⁺ overload, and ΔΨm loss; acts as a threshold event converting reversible stress into irreversible mitochondrial dysfunction
9	ER stress / UPR	↑ ER stress (R); CHOP-commitment possible (G)	↑ adaptive UPR (R); resolves (G)	R, G	Proteostasis stress	Often downstream of ROS + Ca²⁺ handling perturbations
10	DNA damage (oxidative)	↑ damage markers (R→G)	↔ or repaired (G)	R, G	Checkpoint pressure	Generally secondary to ROS; interpret as stress consequence not “direct genotoxicity”
11	LDH / glycolytic flux	↓ glycolytic performance (R→G)	↔ flexible substrate switching (R→G)	R, G	Metabolic vulnerability	Redox imbalance can destabilize high-rate glycolysis in cancer-biased contexts
12	Thioredoxin system (Trx / TrxR)	↓ functional reserve / overload (R→G)	↔ preserved capacity (G)	R, G	Parallel antioxidant system stress	Useful when GSH-only does not explain redox phenotype

Time-Scale Flag: TSF = P / R / G
  P: 0–30 min (physical / electron / radical effects)
  R: 30 min–3 hr (redox signaling & stress response)
  G: >3 hr (gene-regulatory adaptation)

MPTP: opening represents a mitochondrial commitment event integrating ROS and Ca²⁺ stress; sustained opening indicates irreversible bioenergetic failure.

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”.

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

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.

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↓, reducing the expression and activation levels of VEGFR2
P-gp↓, 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

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.

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

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,

MCF-7

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.

501-

MF,

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

in-vitro,

BC,

MCF-7

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.

512-

MF,

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

in-vitro,

BC,

MCF-7

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.

5246-

MF,

Chemo,

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

in-vitro,

BC,

MCF-7

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

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,

MCF-7

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.

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

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

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

Functional Outcomes ⓘ

toxicity?, 1, toxicity↓, 2,
Total Targets: 7

Scientific Paper Hit Count for: ChemoSen, chemo-sensitization

12 Magnetic Fields
2 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

Database Query Results : Magnetic Fields, , ChemoSen

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Functional Outcomes ⓘ

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