| Features: | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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
|
| Source: |
| Type: |
| MOMP is the point-of-no-return decision step of intrinsic apoptosis. It is the event in which the mitochondrial outer membrane becomes permeable, allowing release of pro-death factors that irreversibly commit a cell to die. Cancer progression is characterized by systematic suppression, buffering, or decoupling of MOMP from lethal execution. MOMP occurs when BAX and/or BAK oligomerize in the mitochondrial outer membrane, forming pores that release: -Cytochrome c → apoptosome → caspase-9 -Smac/DIABLO → IAP neutralization -Other apoptogenic factors (e.g., Omi/HtrA2) Once sufficient mitochondria undergo MOMP, cell death is inevitable (even if caspases are later inhibited). Redox, Metabolism, and MOMP (Critical) -High xCT / GSH → suppress mitochondrial ROS → MOMP ↓ -Autophagic flux → removes damaged mitochondria → MOMP ↓ -Pro-oxidant overload → mitochondrial dysfunction → MOMP ↑ |
| 5519- | EP, | Nanosecond Pulsed Electric Fields (nsPEFs) for Precision Intracellular Oncotherapy: Recent Advances and Emerging Directions |
| - | Review, | Var, | 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#:248 Target#:1434 State#:% Dir#:%
wNotes=0 sortOrder:rid,rpid