Expression of <scp>AID</scp> in malignant melanoma with <scp>BRAF</scp><sup>V600E</sup> mutation

Okura, Risa; Yoshioka, Haruna; Yoshioka, Manabu; Hiromasa, Kana; Nishio, Daisuke; Nakamura, Motonobu

doi:10.1111/exd.12402

Cited by 14 publications

(9 citation statements)

References 15 publications

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“…As mentioned, both are components of ovulation. AID has been implicated in inflammation-associated malignancies [28], [29], such as Helicobacter pylori –induced gastric adenocarcinoma [30], [31], HBV-related hepatocellular carcinoma [32], [33] and cholangiocarcinoma [34], and also in breast carcinoma [35], and malignant melanoma [36]. AID is up-regulated as early as in esophageal intraepithelial squamous carcinoma, and persists in invasive carcinoma [37].…”

Section: Introductionmentioning

confidence: 99%

Activation-Induced Cytidine Deaminase Links Ovulation-Induced Inflammation and Serous Carcinogenesis

et al. 2016

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In recent years, the notion that ovarian carcinoma results from ovulation-induced inflammation of the fallopian tube epithelial cells (FTECs) has gained evidence. However, the mechanistic pathway for this process has not been revealed yet. In the current study, we propose the mutator protein activation-induced cytidine deaminase (AID) as a link between ovulation-induced inflammation in FTECs and genotoxic damage leading to ovarian carcinogenesis. We show that AID, previously shown to be functional only in B lymphocytes, is expressed in FTECs under physiological conditions, and is induced in vitro upon ovulatory-like stimulation and in vivo in carcinoma-associated FTECs. We also report that AID activity results in epigenetic, genetic and genomic damage in FTECs. Overall, our data provides new insights into the etiology of ovarian carcinogenesis and may set the ground for innovative approaches aimed at prevention and early detection.

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Section: Introductionmentioning

confidence: 99%

Activation-Induced Cytidine Deaminase Links Ovulation-Induced Inflammation and Serous Carcinogenesis

et al. 2016

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“…Furthermore, the induction of a point mutation is speculated to be closely associated with carcinogenesis. When the expression of AID was examined in malignant melanoma, it was revealed that malignant melanoma with high expression of AID frequently causes BRAF V600E mutation and has a poor prognosis [17] .…”

Section: Aid and Malignant Melanomamentioning

confidence: 99%

Pathomechanism of malignant melanoma

Nakamura

2021

Trends Immunother

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Treatment of malignant melanoma has made great strides in the last decade. On the one hand, immune checkpoint inhibitors and molecular targeted drugs improved the prognosis of patients. On the other hand, it is very important to be aware of the causes of malignant melanoma based on the latest knowledge. In this review, I will briefly review the carcinogenic mechanism of malignant melanoma from the aspects of ultraviolet rays, mechanical stress, trauma and so on.

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“…The majority of melanoma mutations are C>T transitions, and while primarily due to UV light, other processes may play a role. Okura et al ., demonstrate immunohistological evidence of deaminating enzymes, activation‐induced cytidine deaminase (AID) and apolipoprotein B mRNA‐editing enzyme catalytic polypeptide‐like 3B (APOBEC3B) in melanoma with AID expression enriched in BRAF mutant tumors . APOBEC3B is thought to play a role in innate immunity against endogenous retroelements and exogenous viruses .…”

Section: Commentarymentioning

confidence: 99%

Melanoma's high C>T mutation rate: is deamination playing a role?

Sánchez

Grichnik

2014

Experimental Dermatology

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The majority of melanoma mutations are C>T transitions, and most bear UV signatures. However, other process may contribute to the high C>T mutation rate. Okura et al., have demonstrated immunohistochemical evidence of deaminating enzymes, activation-induced cytidine deaminase (AID) and apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3B (APOBEC3B) in melanoma. Both have been implicated in cancer. While further validation is necessary, these findings warrant consideration of a role for deamination in melanomagenesis. Deamination primarily drives C>T transitions. Compared with trunk/extremity melanomas, acral melanomas display a significantly higher percentage of 'spontaneous' and 'AID' mutation signature events suggesting deamination may be particularly important in this subgroup.Key words: BRAF -deaminase -melanoma -mutagenesis Accepted for publication 8 May 2014Commentary Melanoma is a highly genomically unstable tumor with one of the highest mutation rates in cancer (1,2). The majority of melanoma mutations are C>T transitions, and while primarily due to UV light, other processes may play a role. Okura et al., demonstrate immunohistological evidence of deaminating enzymes, activationinduced cytidine deaminase (AID) and apolipoprotein B mRNAediting enzyme catalytic polypeptide-like 3B (APOBEC3B) in melanoma with AID expression enriched in BRAF mutant tumors (3). APOBEC3B is thought to play a role in innate immunity against endogenous retroelements and exogenous viruses (4). AID normally functions to create mutations and double-strand breaks to allow recombination for antibody diversification (5). Both AID (6) and APOBEC3B (4) have been implicated in cancer. Okura et al., also noted AID association with BRAF-mutated tumors, which leads to the question as to whether AID could be involved in driving the T>A V600E mutation. In mice, overexpression of AID primarily causes C>T mutations, but 1 T>A (4%) mutation was noted (6). Of note, this is also around the level reported for UV causing a T>A transversion (5% by UVB, 3% by sunlight and 1% by UVA) (7). Even though this frequency is low, it could be a causative factor. While further validation is necessary, the findings of Okura et al., warrant the consideration of a potential role for deamination in melanomagenesis.The primary mutation caused by deamination is a C>T transition. Overexpression of AID has suggested a signature sequence of 5 0 (G/A)C(A/C/T)3 0 (8) for this event. This is in contrast to a signature sequence 5 0 NCG3 0 for spontaneous deamination and 5 0 (C/ T)CN3 0 for UV (8). The signature sequence for APOPBEC3B is 5 0 (C/G)TC(A/G)3 0 (4), but it is entirely included in the UV signature, making it difficult to tease out a contribution compared with UV. However, it is possible to evaluate AID, UV and spontaneous deamination signature mutations in melanoma. Data sets of mutations in melanoma have confirmed UV signature C>T transitions solidifying UVs role in melanomagenesis. In COLO-82 melanoma, 71% of dinucleotide substitutions w...

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Expression of AID in malignant melanoma with BRAF^V600E mutation

Cited by 14 publications

References 15 publications

Activation-Induced Cytidine Deaminase Links Ovulation-Induced Inflammation and Serous Carcinogenesis

Activation-Induced Cytidine Deaminase Links Ovulation-Induced Inflammation and Serous Carcinogenesis

Pathomechanism of malignant melanoma

Melanoma's high C>T mutation rate: is deamination playing a role?

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Expression of AID in malignant melanoma with BRAFV600E mutation

Cited by 14 publications

References 15 publications

Activation-Induced Cytidine Deaminase Links Ovulation-Induced Inflammation and Serous Carcinogenesis

Activation-Induced Cytidine Deaminase Links Ovulation-Induced Inflammation and Serous Carcinogenesis

Pathomechanism of malignant melanoma

Melanoma's high C>T mutation rate: is deamination playing a role?

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Expression of AID in malignant melanoma with BRAF^V600E mutation