What Is Electrochemotherapy (ECT)?
Electrochemotherapy is a local tumour treatment based on rendering the cell membrane transiently permeable with electric pulses and delivering a cytotoxic drug into the cell within that window. The electric field alone is not ablative: the cytotoxic effect comes from the drug, while the field gets the drug to its target.
How Does Membrane Permeability Change?
What separates the reversible and irreversible regimes is the intensity of the same physical phenomenon
At rest the cell membrane carries a potential difference of roughly −70 mV between its inside and outside. When an external electric field is applied, an additional induced transmembrane potential develops across the membrane. Once this potential exceeds a critical threshold (roughly 0.2–1 V depending on cell type), water-filled permeable structures appear in the lipid bilayer.
At field strengths just above the threshold these structures reseal within seconds to minutes after the pulse and the cell stays viable: reversible electroporation. As field strength and total energy rise, repair capacity is exceeded, homeostasis is permanently lost and the cell dies: irreversible electroporation. The boundary between the two regimes is not a sharp line but a transition zone that depends on tissue type and pulse parameters.
Why Bleomycin and Cisplatin?
Bleomycin
A hydrophilic, relatively large molecule that barely crosses an intact membrane and enters the cell only through a slow, saturable carrier. Once inside it produces single- and double-strand DNA breaks; a few hundred molecules suffice to kill the cell. Because electroporation removes this access bottleneck, intracellular accumulation rises by several hundred fold in the literature.
Cisplatin
Crosses the membrane more readily than bleomycin, so the gain from electroporation is more modest (single-digit fold increases are typically reported). In return it lends itself to intratumoural administration and offers an alternative where bleomycin is contraindicated.
Both agents suit electrochemotherapy because they are strongly cytotoxic once inside the cell. No meaningful gain is expected from electroporation for drugs that already cross the membrane freely; this principle directly governs agent selection.
Vascular Lock and Tissue-Level Effects
After the pulses a transient, pronounced reduction in tumour blood flow is observed. Known in the literature as the vascular lock, this phenomenon helps the drug that has entered the cells stay in the region longer and explains the haemostatic effect of electrochemotherapy in bleeding superficial lesions.
That tumour vascular endothelium is more sensitive to electroporation than normal tissue is one component of the observed antivascular effect. In addition, damage-associated molecular patterns released from dying tumour cells can trigger a systemic immune response in some studies. That observation started the current research line combining ECT with immune checkpoint inhibitors departs.
Historical Milestones
| Year | Development |
|---|---|
| 1982 | Neumann et al. demonstrated DNA transfer into cells by electric pulses, establishing the molecular basis of electroporation. |
| 1991 | Mir et al. reported that the antitumour effect of bleomycin can be potentiated by local electric pulses, the birth of electrochemotherapy. |
| 1993 | Belehradek et al. published the first clinical phase I–II trial. |
| 2006 | The ESOPE project defined standard operating procedures for cutaneous tumours and the Cliniporator system. |
| 2013–2014 | NICE issued interventional procedure guidance for cutaneous metastases (IPG446) and primary basal/squamous cell carcinoma (IPG478). |
| 2018 | The ESOPE procedures were updated to cover deep-seated tumours and new electrode geometries. |
| 2010s–present | Calcium electroporation, gene electrotransfer and immunotherapy combinations entered clinical trials. |
Which Literature Is This Page Based On?
The account above is an editorial synthesis based on the 774 publications in the corpus’s General Principles & Biophysics area.
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