AIDing the immune system—DIAbolic in cancer

Schmitz, Kerstin-Maike; Petersen-Mahrt, Svend K.

doi:10.1016/j.smim.2012.07.001

Cited by 22 publications

(20 citation statements)

References 29 publications

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“…Recent studies showed that the mutation signature that accumulates in tumor tissues provides the clue to identifying the cause of genetic alterations during tumor development [22][23][24][25][26][27]43 . It was shown that C:G>T:A transitions at XpCpG trinucleotides were especially prominent in many cancer types 27,44 .…”

Section: Discussionmentioning

confidence: 99%

“…It was shown that C:G>T:A transitions at XpCpG trinucleotides were especially prominent in many cancer types 27,44 . Among the C:G>T:A transitions, the footprint of AID is characterized by C:G>T:A alterations that occur in GpCpX or ApCpX sequences 22,28,29,[45][46][47] . In the current study, previously established mouse models with inflammation-associated gastric carcinogenesis [50][51][52] .…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies showed that the pattern of nucleotide alterations could provide a clue to determine the molecular process underlying mutation occurrence [22][23][24][25][26][27] . We first confirmed that over half of the SNVs that accumulated in the exome sequences of gastric cancer tissues were enriched with a C:G>T:A transition (p<0.01 by ANOVA, Figure 1C).…”

Section: Mutation Profiles Of Mss and Msi Gastric Cancer Tissuesmentioning

confidence: 99%

“…These mutational signatures suggested that cytidine to uracil deamination is deeply implicated in the mutational process underlying H pylori-associated gastric carcinogenesis. Among the cytidine deaminase family proteins, AID exhibits a strong preference for deaminating C residues flanked by a 5'-purine (G or A) 22,28,29 . In contrast, APOBEC3 family enzymes and APOBEC1 favor C residues flanked by 5'-T 30,31 .…”

Section: Mutation Profiles Of Mss and Msi Gastric Cancer Tissuesmentioning

confidence: 99%

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Accumulation of Somatic Mutations in TP53 in Gastric Epithelium With Helicobacter pylori Infection

et al. 2014

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Mutation Profiles Of Mss and Msi Gastric Cancer Tissuesmentioning

confidence: 99%

Section: Mutation Profiles Of Mss and Msi Gastric Cancer Tissuesmentioning

confidence: 99%

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Accumulation of Somatic Mutations in TP53 in Gastric Epithelium With Helicobacter pylori Infection

et al. 2014

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“…First, many of the APOBEC3s have been described to defend against a diverse array of viral pathogens, including retroviruses, hepatitis viruses, papillomaviruses, and others. [20][21][22][23][24] Of note, APOBEC3D, F, G, and H have been shown to restrict HIV-1 replication by deaminating cDNA intermediates that normally occur during the HIV-1 life cycle. [25,26] Second, several APOBEC3s, including APOBEC3A, B, and F, have been shown to inhibit retrotransposition of L1 and Alu elements in human cells.…”

Section: The Apobec Familymentioning

confidence: 99%

APOBEC3B: Pathological consequences of an innate immune DNA mutator

Burns¹,

Leonard²,

Harris³

2015

Biomed J

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Cancer is a disease that results from alterations in the cellular genome. Several recent studies have identified mutational signatures that implicate a variety of mutagenic processes in cancer, a major one of which is explained by the enzymatic activity of the DNA cytosine deaminase, APOBEC3B. As a deaminase, APOBEC3B converts cytosines to uracils in single-stranded DNA. Failure to properly repair these uracil lesions can result in a diverse array of mutations. For instance, DNA uracils can template the insertion of complementary adenines leading to C-to-T transition mutations. DNA uracils can also be converted into abasic sites that, depending upon the DNA polymerase recruited to bypass this lesion in the template strand, can lead to adenine insertion and C-to-T mutations as well as cytosine insertion and C-to-G transversion mutations. Finally, DNA uracils can also be converted into DNA breaks that may precipitate some types of larger chromosomal aberrations observed in cancer. These studies cumulatively demonstrate that APOBEC3B is a major source of genetic heterogeneity in several human cancers and, as such, this enzyme may prove to be a critical diagnostic and therapeutic target. (Biomed J 2015;38:102-110)

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Activation‐Induced Deaminase

Petersen-Mahrt

Conticello²,

Munagala³

2018

Encyclopedia of Life Sciences

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Activation‐induced deaminase is a simple evolutionary tool that nature has utilised to create a very powerful immune system. Hydrolytic deamination is one of the most ancient of enzymatically catalysed reactions, and yet in the context of deoxyribonucleic acid (DNA) can lead to wanted mutations and chromosomal rearrangements in the humoral immune system, changes in the epigenome and inactivation of foreign DNA. While on the dark side, it can lead to oncogenic mutations and translocations across the whole genome and serve as a conduit for nonmutagenic compounds to become mutagenic. Key Concepts AID is the ancestor to APOBEC1, and unlike APOBEC1, AID's enzymatic activity is restricted to DNA. AID does not act on cytidine (the RNA nucleoside); hence, it should be classified as activation‐induced deoxy‐cytosine deaminase, or simply activation‐induced deaminase (AID). AID was the first enzyme discovered to actively induce DNA lesions as part of its physiological function. Nearly 70% of all cancer mutations are derived from the AID/APOBEC family. Environmental factors (e.g. oestrogen) can drive AID expression, allowing for nonmutagenic compounds to elicit oncogenic mutations. AID can be expressed in various tissues and lead to local and global DNA instability. AID's ability to deaminate 5‐methyl cytosine can lead to active DNA demethylation and epigenetic reprogramming. The physiological mutation activity of AID can be harnessed in new tools of biotechnology for in vivo genome editing.

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AIDing the immune system—DIAbolic in cancer

Cited by 22 publications

References 29 publications

Accumulation of Somatic Mutations in TP53 in Gastric Epithelium With Helicobacter pylori Infection

Accumulation of Somatic Mutations in TP53 in Gastric Epithelium With Helicobacter pylori Infection

APOBEC3B: Pathological consequences of an innate immune DNA mutator

Activation‐Induced Deaminase

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