Abstract
A variety of genetic alterations including gene mutations and chromosomal disorders have a critical role in cancer development. Activation-induced cytidine deaminase (AID) is capable of inducing nucleotide alterations in immunoglobulin genes and contributes to somatic hypermutation and class-switch recombination in B cells under physiological conditions. Although AID expression is tightly controlled because of its mutagenic potential, various types of pathogens and inflammation accompanied with the infection induce dysregulated and ectopic AID expression through the activation of the nuclear factor κB pathway. The constitutive aberrant AID expression causes the accumulation of nucleotide alterations and chromosomal abnormalities, leading to cancer development in various organs. Studies focused on the activity of aberrantly expressed AID provide a new insight into the mutagenic mechanisms during carcinogenesis.
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