| 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↑">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)
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. |
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| Caspases are a cysteine protease that speed up a chemical reaction via pointing their target substrates following an aspartic acid residue.1 They are grouped into apoptotic (caspase-2, 3, 6, 7, 8, 9 and 10) and inflammatory (caspase-1, 4, 5, 11 and 12) mediated caspases. Caspase-1 may have both tumorigenic or antitumorigenic effects on cancer development and progression, but it depends on the type of inflammasome, methodology, and cancer. Catalase is an enzyme found in nearly all living cells exposed to oxygen. Its primary role is to protect cells from oxidative damage by catalyzing the conversion of hydrogen peroxide (H₂O₂), a potentially damaging byproduct of metabolism, into water (H₂O) and oxygen (O₂). This detoxification process is crucial because excess H₂O₂ can lead to the formation of reactive oxygen species (ROS) that damage proteins, lipids, and DNA. Catalase and Cancer Oxidative Stress and Cancer: Cancer cells often experience increased levels of oxidative stress due to rapid proliferation and metabolic changes. This stress can lead to DNA damage, promoting tumorigenesis. Catalase helps mitigate oxidative stress, and its expression can influence the survival and proliferation of cancer cells. Expression Levels in Different Cancers: Overexpression: In some cancers, such as breast cancer and certain types of leukemia, catalase may be overexpressed. This overexpression can help cancer cells survive in oxidative environments, potentially leading to more aggressive tumor behavior. Downregulation: Conversely, in other cancers, such as colorectal cancer, reduced catalase expression has been observed. This downregulation can lead to increased oxidative stress, contributing to tumor progression and metastasis. Prognostic Implications: Survival Rates: Studies have shown that high levels of catalase expression can be associated with poor prognosis in certain cancers, as it may enable cancer cells to resist apoptosis (programmed cell death) induced by oxidative stress. Some types of cancer cells have been reported to exhibit lower catalase activity, possibly increasing their vulnerability to oxidative damage under certain conditions. This vulnerability has even been exploited in some therapeutic strategies (for example, approaches that generate excess H₂O₂ or other ROS specifically targeting cancer cells have been researched). |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | Bladder, | HTB-22 |
| 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, | NA |
| 2253- | MF, | Low-frequency pulsed electromagnetic field promotes functional recovery, reduces inflammation and oxidative stress, and enhances HSP70 expression following spinal cord injury |
| - | in-vivo, | Nor, | NA |
| 4116- | MF, | Low‑frequency pulsed electromagnetic field promotes functional recovery, reduces inflammation and oxidative stress, and enhances HSP70 expression following spinal cord injury |
| - | in-vivo, | NA, | NA |
| 4111- | MF, | Coupling of pulsed electromagnetic fields (PEMF) therapy to molecular grounds of the cell |
| - | Review, | Arthritis, | NA |
| 4102- | MF, | Modulation of antioxidant enzyme gene expression by extremely low frequency electromagnetic field in post-stroke patients |
| - | Human, | Stroke, | NA |
| 5241- | MF, | A review on the use of magnetic fields and ultrasound for non-invasive cancer treatment |
| - | Review, | Var, | NA |
| 4147- | MF, | PEMFs Restore Mitochondrial and CREB/BDNF Signaling in Oxidatively Stressed PC12 Cells Targeting Neurodegeneration |
| - | in-vitro, | AD, | PC12 |
| 3498- | MF, | Effect of Static Magnetic Field on Oxidant/Antioxidant Parameters in Cancerous and Noncancerous Human Gastric Tissues |
| - | in-vitro, | GC, | NA |
| 3484- | MF, | Extremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of •O2 − and H2O2 |
| - | in-vitro, | Nor, | NA |
| 3567- | MFrot, | MF, | The Effect of Extremely Low-Frequency Magnetic Field on Stroke Patients: A Systematic Review |
| - | Review, | Stroke, | NA |
| 209- | MFrot, | MF, | The effect of a rotating magnetic field on the antioxidant system in healthy volunteers - preliminary study |
| - | Human, | NA, | NA |
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#:46 State#:% Dir#:2
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