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Mitotic catastrophe (None (no widely accepted abbreviation))

Target
None (no widely accepted abbreviation)
Molecular classification
Other (cellular process), Not an enzyme, receptor, ion channel, transporter, or transcription factor
01

Overview

Mitotic catastrophe is not a molecule or protein, but rather refers to a form of cell death resulting from aberrant progression through mitosis. It occurs when cells enter or proceed through mitosis with unrepaired DNA damage or spindle defects—often due to failed checkpoints such as the G2-M transition—and leads either directly to cellular demise during division ("mitotic death") or triggers delayed apoptosis/necrosis after division. Morphologically, it is characterized by multinucleated giant cells containing uncondensed chromosomes and micronuclei. This mechanism acts both as an oncosuppressive barrier against cancer development—by eliminating genomically unstable cells—and as one mode by which certain anti-cancer therapies exert their effects. However, because it describes a cellular fate rather than any specific gene product/protein/receptor/enzyme/transporter/etc., "mitotic catastrophe" should not be considered nor structured as a canonical drug target.

Other names
Mitotic cell deathCatastrophic mitosis
02

Mechanism of action

Drugs that induce mitotic catastrophe generally act via: Disruption of microtubule dynamics/spindle assembly checkpoint activation/inhibition; Induction of DNA damage leading to failed checkpoint arrest and aberrant chromosome segregation. This results in abnormal mitosis and subsequent cell death through apoptosis or necrosis.

03

Biological functions

Cell cycle regulationCell death (specifically following abnormal mitosis)Oncosuppression (prevention of tumorigenesis by eliminating cells with genomic instability)
04

Disease associations

Cancer (both as a barrier to cancer development and as an outcome induced by some anti-cancer therapies)Other roles are less well defined outside oncology
05

Safety considerations

Off-target toxicity in normal proliferating tissues due to non-specific action on dividing cells.Incomplete execution leading to genomic instability if apoptotic pathways are defective—potentially promoting tumor progression instead of suppression if the process fails completely.
06

Interacting drugs

Radiation therapy

6 more in the full profile.

07

Biomarkers

Multinucleation/giant cells with uncondensed chromosomes/micronuclei formation in histology/cytology assaysPersistent cyclin B1 expression (may indicate failure to exit mitosis properly)Caspase activation profilesMarkers like γH2AX (for associated DNA damage response)

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