One of the main characteristic features of<unk>  is large numbers of complex rearrangements occurring in localised regions of single chromosomes. The ability to cause such confined damage suggests that chromosomes need to be condensed e.g. in mitosis, for<unk>  and chromosome rearrangements to be initiated. The mechanisms of<unk>  are not well understood. There are multiple ideas of how<unk>  occurs. Micronuclei model Schematic of Micronucleus model of<unk>  The Micronuclei model is the most accepted model as to how and when the breakage and repair in<unk>  occurs. In cancer cells, fragmentation of chromosomes has been correlated with the presence of micronuclei. Micronuclei are structures formed by mitotic errors in the transition from metaphase to anaphase. Cells with defective chromosome segregation will form micronuclei which contain whole chromosomes or fragments of chromosomes. The segregation of single chromosomes into individual micronuclei explains why DNA fragmentation is isolated to single chromosomes in<unk> . These micronuclei undergo defective DNA replication, which is slower than DNA replication in the main nucleus and causes a proximal DNA damage response (DDR) to be initiated. However, DNA repair and cell cycle checkpoint activation fail to follow. Consequently, chromosomes that are not correctly replicated in micronuclei become fragmented. The mechanism by which the pulverization of these chromosomes occurs is not fully understood, but it is thought to be caused either by aberrant DNA replication or by premature chromosome condensation, which entails semi-replicated chromosomes being compacted by cyclin-dependent kinase activity. The resulting fragmented chromosome segments can be joined together to give rise to a rearranged chromosome, which can subsequently be reincorporated into the main nucleus of a daughter cell. The new chromosome can persist for several generations of cell cycle divisions and contribute to the development of a cancer cell. Although the micronucleus model is appropriate, other factors are likely to contribute towards<unk>  for various cancer genomes. Ionising radiation during mitosis Chromosome shattering is triggered and reassembly of chromosome fragments in close proximity is caused by environmental stimuli such as high energy ionising radiation encountered during mitosis. Aborted apoptosis Stress stimuli such as radiation, nutrient deprivation or oxygen deprivation which causes apoptosis will lead to fragmentation of chromatin and cause most cells to apoptose. However a small subset of cells will survive apoptosis. This cleaved DNA will require repair, and when this is done incorrectly, rearrangements will be introduced into the chromosome. There is currently speculation that<unk>  might be driven by viruses such as γ-herpes viruses which cause cancer, possibly by the inhibition of apoptosis. However this speculation requires further investigation. Telomeric dysfunction Telomeric double stranded breaks or telomeric dysfunction is generated by exogenous agents or replicative stress. Telomeric dysfunctions are known to promote chromosomal abnormalities associated with cancer cells. For example, Telomeric double stranded breaks/ telomeric dysfunctions can cause sister chromatid/ end to end fusion and the formation of anaphase bridges resulting in dicentric chromosomes that can result in further rearrangements. This is a more plausible explanation as<unk>  has been seen to mostly involve telomeric regions.
Chromothripsis
Envenomation
Hospital-acquired infection
Infantilism 
Microchimerism
Female infanticide
Toxic injury
Superinfection