| 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)
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. |
| Source: |
| Type: enzymes |
| Tricarboxylic Acid (TCA) cycle, also known as the Citric Acid cycle or Krebs cycle, is a key metabolic pathway that plays a central role in cellular energy production. The TCA cycle is a series of chemical reactions that occur in the mitochondria and involve the breakdown of acetyl-CoA, a molecule produced from the breakdown of carbohydrates, fats, and proteins. The TCA cycle produces: 1. NADH and FADH2 2. ATP 3. GTP Expression of TCA cycle enzymes is often downregulated in cancer cells. Since cancer cells often exhibit rewired metabolism, including alterations in the use of the TCA cycle, researchers are exploring potential therapeutic interventions that target metabolic enzymes or pathways. TCA cycle is essential for normal cellular metabolism, its role in cancer is multifaceted. Cancer cells often reprogram their metabolism—including the TCA cycle—to support rapid growth, adapt to hypoxia, and manage oxidative stress. Mutations in key TCA cycle enzymes generate oncometabolites that further contribute to cancer progression by disrupting normal cellular regulation. Rather than saying the TCA cycle is globally over- or underexpressed in cancer, it is more accurate to say that cancer cells reprogram the cycle—with selective upregulation of parts important for biosynthesis and survival and mutations or downregulation of other parts—to best support their growth and survival in a challenging microenvironment. Oncometabolites -Some metabolites in the Krebs cycle, when accumulated to abnormal levels due to genetic mutations or enzyme deficiencies, are termed “oncometabolites” because they can promote tumorigenesis. -Mutations in succinate dehydrogenase (SDH) can lead to accumulation of succinate. -Mutations in fumarate hydratase (FH) result in an accumulation of fumarate. -Mutations in isocitrate dehydrogenase (IDH1 and IDH2) result in a neomorphic enzyme activity that converts α-ketoglutarate (α-KG) to 2-hydroxyglutarate: |
| 2247- | MF, | Effects of Pulsed Electromagnetic Field Treatment on Skeletal Muscle Tissue Recovery in a Rat Model of Collagenase-Induced Tendinopathy: Results from a Proteome Analysis |
| - | in-vivo, | Nor, | NA |
| 2259- | MFrot, | MF, | Method and apparatus for oncomagnetic treatment |
| - | in-vitro, | GBM, | 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
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