Activation-induced Cytidine Deaminase in B Cell Immunity and Cancers

Park, Seok‐Rae

doi:10.4110/in.2012.12.6.230

Cited by 37 publications

(27 citation statements)

References 117 publications

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“…54 It is also considered as an important signals to stimulate tumor initiation by producing the mutator enzyme activation-induced cytidine deaminase. 116 In fact, the major effect of NF-κB on tumorigenic is to promote cancer cells proliferation and inhibit apoptosis. 117,118 Jak-STAT3 signaling pathway…”

Section: Cytokine-involved Signaling Pathways In Tumormentioning

confidence: 99%

Crosstalk between cancer and immune cells: Role of tumor‐associated macrophages in the tumor microenvironment

et al. 2019

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Tumor microenvironment is a complex system that contains multiple cells and cytokines. Among the multiple immune cells, macrophage is particularly abundant and plays an important role throughout the tumor progression process, namely, tumor‐associated macrophage (TAM) in this special tumor microenvironment. Many kinds of cytokines from TAMs and other immune cells in tumor niche are involved in the linkage of inflammation, immunity and tumorigenesis. Inflammatory responses induced by TAMs are crucial to tumor development of different stages. This review highlights the critical role of TAMs in the linkage of inflammation, immunity, and cancer. It outlines the molecules of inflammatory cytokines, chemokines, and growth factors mainly from TAMs in tumor microenvironment and their functions in tumor development during the major issues of angiogenesis, chronic inflammation, and immune suppression. Additionally, the signaling pathways involved in tumor progression and the crosstalk between them are also summarized.

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Section: Cytokine-involved Signaling Pathways In Tumormentioning

confidence: 99%

Crosstalk between cancer and immune cells: Role of tumor‐associated macrophages in the tumor microenvironment

et al. 2019

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“…A recent study from Shimizu and colleagues on human and murine gastric tumors and tissues shows that somatic mutations are enriched in multiple genes in gastric mucosal tissues upon Helicobacter pylori infection and that increased AID activity in these tissues leads to the accumulation of these mutations, which may promote carcinogenesis in Helicobacter pylori infected patients [121]. Dysregulated AID expression can also be induced by inflammation and microbial infections, which then acts as a genotoxic factor in various human cancers [122]. Inflammatory signals that induce epithelial to mesenchymal transition are capable of inducing AID expression [123].…”

Section: Introductionmentioning

confidence: 99%

AID/APOBEC deaminases and cancer

et al. 2015

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Mutations are the basis for evolution and the development of genetic diseases. Especially in cancer, somatic mutations in oncogenes and tumor suppressor genes alongside the occurrence of passenger mutations have been observed by recent deep-sequencing approaches. While mutations have long been considered random events induced by DNA-replication errors or by DNA damaging agents, genome sequencing led to the discovery of non-random mutation signatures in many human cancer. Common non-random mutations comprise DNA strand-biased mutation showers and mutations restricted to certain DNA motifs, which recently have become attributed to the activity of the AID/APOBEC family of DNA deaminases. Hence, APOBEC enzymes, which have evolved as key players in natural and adaptive immunity, have been proposed to contribute to cancer development and clonal evolution of cancer by inducing collateral genomic damage due to their DNA deaminating activity. This review focuses on how mutagenic events through AID/APOBEC deaminases may contribute to cancer development.

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“…These two genetic processes result in the antibodies that protect against numerous pathogens. On the other hand, aberrant expression of AID can be a risk factor for cell leukemias and lymphomas, including the c‐myc translocation characteristic of BL …”

Section: Malaria Ebv and Bl—recent Findingsmentioning

confidence: 99%

Malaria, Epstein–Barr virus infection and the pathogenesis of Burkitt's lymphoma

Mawson

Majumdar

2017

Intl Journal of Cancer

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A geographical and causal connection has long been recognized between malaria, Epstein-Barr virus (EBV) infection and Burkitt's lymphoma (BL), but the underlying mechanisms remain obscure. Potential clues are that the malaria parasite Plasmodium falciparum selectively absorbs vitamin A from the host and depends on it for its biological activities; secondly, alterations in vitamin A (retinoid) metabolism have been implicated in many forms of cancer, including BL. The first author has proposed that the merozoite-stage malaria parasite, emerging from the liver, uses its absorbed vitamin A as a cell membrane destabilizer to invade the red blood cells, causing anemia and other signs and symptoms of the disease as manifestations of an endogenous form of hypervitaminosis A (Mawson AR, Path Global Health 2013;107(3):122-9). Repeated episodes of malaria would therefore be expected to expose the tissues of affected individuals to potentially toxic doses of vitamin A. It is proposed that such episodes activate latent EBV infection, which in turn activates retinoid-responsive genes. Expression of these genes enhances viral replication and induces germinal center (GC) B cell expansion, activation-induced cytidine deaminase (AID) expression, and c-myc translocation, which in turn predisposes to BL. Thus, an endogenous form of retinoid toxicity related to malaria infection may be the common factor linking frequent malaria, EBV infection and BL, whereby prolonged exposure of lymphatic tissues to high concentrations of retinoids may combine to induce B-cell translocation and increase the risk of Burkitt's lymphoma.

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Activation-induced Cytidine Deaminase in B Cell Immunity and Cancers

Cited by 37 publications

References 117 publications

Crosstalk between cancer and immune cells: Role of tumor‐associated macrophages in the tumor microenvironment

Crosstalk between cancer and immune cells: Role of tumor‐associated macrophages in the tumor microenvironment

AID/APOBEC deaminases and cancer

Malaria, Epstein–Barr virus infection and the pathogenesis of Burkitt's lymphoma

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