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Tumor treating fields-mediated mitotic machinery disruption (TTFields (for the modality; no standard abbreviation for the "target" itself))

Target
TTFields (for the modality; no standard abbreviation for the "target" itself)
Molecular classification
Other
01

Overview

Tumor treating fields-mediated mitotic machinery disruption refers to the use of low-intensity, intermediate-frequency alternating electric fields—known as tumor treating fields (TTFields)—to interfere with the process of cell division in cancer cells. This is not a single molecular target but rather a biophysical intervention that exploits unique properties of dividing tumor cells. TTFields disrupt mitosis by exerting rotational forces on polar molecules such as tubulin dimers during spindle formation. This impairs microtubule assembly and function, leading to prolonged or arrested mitosis, abnormal chromosome segregation, multinucleation, and ultimately caspase-dependent apoptosis in daughter cells. The effect is most pronounced in rapidly dividing cancerous tissues due to their higher susceptibility compared to normal tissues[1][3][4]. Unlike conventional drugs that bind specific proteins or receptors, TTFields act through physical principles—dielectrophoresis and dipole alignment—to selectively disrupt cellular structures essential for proliferation.

Other names
Tumor treating fieldsAlternating electric field therapyTTFieldsElectric field-induced mitotic disruption
02

Mechanism of action

Disruption of microtubule polymerization and spindle assembly via dielectrophoresis and dipole alignment in dividing cells[1][3][4] Induction of metaphase arrest and abnormal chromosome segregation leading to apoptosis[1][3][4]

03

Biological functions

Cell cycleCell divisionMitosisCell death
04

Disease associations

Cancer
05

Safety considerations

Localized skin irritation from electrode arrays[1]Potential off-target effects on normal proliferating cells (though generally less affected than cancer cells)[1]
06

Interacting drugs

None (TTFields is a physical modality, not a drug-interacting molecular target)
07

Biomarkers

High cell division rate (as rapidly dividing tumor cells are more susceptible)[1][3]Tubulin polymerization status (experimental)

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