Kataegis

[1] Compared to other cancer-related mutations, such as chromothripsis, kataegis is more commonly seen; it is not an accumulative process but likely happens during one cycle of replication.

It was first used by scientists at the Wellcome Trust Sanger Institute to describe their observations of breast cancer cells.

When these enzymes try to mend the mutational damage, they unwind DNA into single strands and create lesion regions that do not have a purine/pyrimidine base.

Across the lesion region, the bases in the unpaired, single-stranded DNA(ssDNA) are more accessible to the modifying enzyme groups that can cause further damage in the sequence, thus forming the mutational clusters seen in kataegis.

[citation needed] APOBEC family is a group of cytidine deaminase enzymes that plays an important role in immune system.

Its major function is to induce genetic mutations in antibodies, which need a huge variety of genes in order to bind to different antigens.

[6] As shown in Figure 1, the base mutations in kataegis regions were found to be almost exclusively cytosine to thymine in the context of a TpC dinucleotide(p denotes the phosphoribose backbone).

[7] Recent evidence has linked the over-expression of the family member APOBEC3B with multiple human cancers, highlighting its possible contribution to genomic instability and kataegis.

[11] Meanwhile, activation-induced cytidine deaminase (AID) is shown to facilitate kataegis formation in human lymphomas.

[13] Pol ζ is another kind of TLS DNA polymerase that collaborates with Rev1(mostly Rev1p) in the process of forming hypermutations in eukaryotes.