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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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| Also known as CP32. Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death. As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression. Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy. Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent. On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer. Procaspase-3 is a apoptotic marker protein. Prognostic significance: • High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers. • Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers. |
| 5519- | EP, | Nanosecond Pulsed Electric Fields (nsPEFs) for Precision Intracellular Oncotherapy: Recent Advances and Emerging Directions |
| - | Review, | Var, | NA |
| 3460- | EP, | Picosecond pulsed electric fields induce apoptosis in HeLa cells via the endoplasmic reticulum stress and caspase-dependent signaling pathways |
| - | in-vitro, | Cerv, | HeLa |
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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