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| Electrical Pulses (Pulsed Electric Field therapies; PEF) are a bioelectromagnetic modality in oncology that delivers brief, high-voltage (or high-field) pulses to tissue to permeabilize membranes and/or ablate tumors. Clinically relevant categories commonly discussed: -Shorter, bipolar/high-frequency µs waveforms (H-FIRE) are repeatedly shown to reduce or eliminate muscle contractions versus classic monopolar IRE, improving tolerability and potentially reducing need for paralytics. -Nanosecond pulses with fast rise times can overcome membrane charging delays and directly polarize organelles, which is why rise-time engineering becomes a first-order variable for intracellular effects (mitochondria/ER, Ca²⁺, ROS, regulated death programs). -nsPEF / Nano-Pulse Stimulation (NPS) used as irreversible tumor ablation (intracellular emphasis). With ns pulses, fast rise times and short widths can drive intracellular membrane perturbation (not just plasma membrane), shifting biological response vs classic IRE.
In nsPEF systems the main engineering challenge is not current or power, but:
-generating fast rise times
-maintaining transmission line impedance
-preventing pulse distortion at the electrodes
Other important aspects of nsPEF
-mainly an electric field effect:
-Membrane breakdown typically occurs around 0.5–1 V across the membrane,
which corresponds to ~10–50 kV/cm fields in tissue.
-ns pulses terminate before plasma channels develop.
-impedance mismatch and cable dispersion is important
-nsPEF often induces programmed cell death rather than thermal ablation
The hallmark of nsPEF is simultaneous targeting of multiple intracellular pathways, particularly:
-Calcium signaling (Ca²⁺ release)
-Mitochondrial apoptosis (ΔΨm↓, Caspase-9↑, Caspase-3↑)
-ROS stress pathways
Research might show cancer cells have some greater sensitivity to nsPEF,
but nsPEF affects both normal and cancer cells
Electrical Pulses / PEF Oncology Modality — Ranked Mechanistic Axes
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| Oxidative phosphorylation (or phosphorylation) is the fourth and final step in cellular respiration. Alterations in phosphorylation pathways result in serious outcomes in cancer. Many signalling pathways including Tyrosine kinase, MAP kinase, Cadherin-catenin complex, Cyclin-dependent kinase etc. are major players of the cell cycle and deregulation in their phosphorylation-dephosphorylation cascade has been shown to be manifested in the form of various types of cancers. Many tumors exhibit a well-known metabolic shift known as the Warburg effect, where glycolysis is favored over OxPhos even in the presence of oxygen. However, this is not universal. Many cancers, including certain subpopulations like cancer stem cells, still rely on OXPHOS for energy production, biosynthesis, and survival. – In several cancers, especially during metastasis or in tumors with high metabolic plasticity, OxPhos can remain active or even be upregulated to meet energy demands. In some cancers, high OxPhos activity correlates with aggressive features, resistance to standard therapies, and poor outcomes, particularly when tumor cells exploit mitochondrial metabolism for survival and metastasis. – Conversely, low OxPhos activity can be associated with a reliance on glycolysis, which is also linked with rapid tumor growth and certain adverse prognostic features. Inhibiting oxidative phosphorylation is not a universal strategy against all cancers. Targeting OXPHOS can potentially disrupt the metabolic flexibility of cancer cells, leading to their death or making them more susceptible to other treatments. Since normal cells also rely on OXPHOS, inhibitors must be carefully targeted to avoid significant toxicity to healthy tissues. Not all tumors are the same. Some may be more glycolytic, while others depend more on mitochondrial metabolism. Therefore, metabolic profiling of tumors is crucial before adopting this strategy. Inhibiting OXPHOS is being explored in combination with other treatments (such as chemo- or immunotherapies) to improve efficacy and overcome resistance. In cancer cells, metabolic reprogramming is a hallmark where cells often rely on glycolysis (known as the Warburg effect); however, many cancer types also depend on OXPHOS for energy production and survival. Targeting OXPHOS(using inhibitor) to increase the production of reactive oxygen species (ROS) can selectively induce oxidative stress and cell death in cancer cells. -One side effect of increased OXPHOS is the production of reactive oxygen species (ROS). -Many cancer cells therefore simultaneously upregulate antioxidant systems to mitigate the damaging effects of elevated ROS. -Increase in oxidative phosphorylation can inhibit cancer growth. |
| 933- | CUR, | EP, | Effective electrochemotherapy with curcumin in MDA-MB-231-human, triple negative breast cancer cells: A global proteomics study |
| - | in-vitro, | BC, | 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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