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      Erratum: The RNA editing enzyme APOBEC1 induces somatic mutations and a compatible mutational signature is present in esophageal adenocarcinomas

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          Abstract

          Erratum During the typesetting of the final version of the article [1] some data in Table 1 have been accidentally changed. These data were correct in the provisional version of the article. A correct Table 1 is as follows: Table 1 List of the non-clonal mutations identified in the BCR-ABL1 fusion gene from imatinib-resistant K562 clones Samples Position AA change Codon change Sequence context Control 1409 E495G GAA > GGA 1472 R491Q CGG > CAG GCCGG 1503 Silent TTT > TTC AID 298 G100C GGC > TGC GCCTA 395 Silent AAA > AAG 568 G190D GGC > GAC TGCCA 633 T212A ACG > GCG Rat APOBEC1 344 G155D GGC > GAC GGCCA 607 L203M CTG > ATG CCCTG 613 E205K GAG > AAG CTCGG 764 K255T AAG > ACG 987 Silent GGG > GGT TTCCC Human APOBEC1 669 Silent AGC > AGT AGCCG 758 R253H CGC > CAC TGCGC 841* Silent CTG > TTG AGCTG 697 H233D CAT > GAT TTCAT 699 H233D CAT > GAC 1149* Silent GCC > GCA GCCAT 1245* F415L TTT > TTG The region analyzed (encompassing exon 13 of BCR and exon 9 of ABL1) includes the imatinib-binding region of the fusion gene. The asterisk indicates mutations found in the same clone. The local sequence context for the mutations at cytosines is shown. Compared to the AID-induced mutations found in previous reports (mutations in approximately 30% of the sequences) [41], [42], we found approximately one mutation in each of the clones analyzed. This is explained by the different procedures we used to select resistant clones: whereas the other studies focused on competing bulk populations of AID-transfected GFP(+) cells and control GFP(−) cells, we analyzed individual clones arising from the same number of cells plated in the presence of imatinib. Please note that references 41 and 42 in the table legend correspond to the reference order in the original article [1].

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          The RNA editing enzyme APOBEC1 induces somatic mutations and a compatible mutational signature is present in esophageal adenocarcinomas

          Background The AID/APOBECs are deaminases that act on cytosines in a diverse set of pathways and some of them have been linked to the onset of genetic alterations in cancer. Among them, APOBEC1 is the only family member to physiologically target RNA, as the catalytic subunit in the Apolipoprotein B mRNA editing complex. APOBEC1 has been linked to cancer development in mice but its oncogenic mechanisms are not yet well understood. Results We analyze whether expression of APOBEC1 induces a mutator phenotype in vertebrate cells, likely through direct targeting of genomic DNA. We show its ability to increase the inactivation of a stably inserted reporter gene in a chicken cell line that lacks any other AID/APOBEC proteins, and to increase the number of imatinib-resistant clones in a human cellular model for chronic myeloid leukemia through induction of mutations in the BCR-ABL1 fusion gene. Moreover, we find the presence of an AID/APOBEC mutational signature in esophageal adenocarcinomas, a type of tumor where APOBEC1 is expressed, that mimics the one preferred by APOBEC1 in vitro. Conclusions Our findings suggest that the ability of APOBEC1 to trigger genetic alterations represents a major layer in its oncogenic potential. Such APOBEC1-induced mutator phenotypes could play a role in the onset of esophageal adenocarcinomas. APOBEC1 could be involved in cancer promotion at the very early stages of carcinogenesis, as it is highly expressed in Barrett's esophagus, a condition often associated with esophageal adenocarcinoma. Electronic supplementary material The online version of this article (doi:10.1186/s13059-014-0417-z) contains supplementary material, which is available to authorized users.
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            Author and article information

            Contributors
            giulia.saraconi@ittumori.it
            francesco.severi@ittumori.it
            cesare.sala@ittumori.it
            giorgio.mattiuz@ittumori.it
            silvo.conticello@ittumori.it
            Journal
            Genome Biol
            Genome Biology
            BioMed Central (London )
            1465-6906
            1465-6914
            8 November 2014
            8 November 2014
            2014
            : 15
            : 11
            : 497
            Affiliations
            Core Research Laboratory, Istituto Toscano Tumori, viale Pieraccini 6, Firenze, 50139 Italy
            Article
            497
            10.1186/s13059-014-0497-9
            4224699
            9c0702b4-ff95-4f5b-85e8-39d85525f350
            © Saraconi et al; licensee BioMed Central Ltd. 2014

            The licensee has exclusive rights to distribute this article, in any medium, for 12 months following its publication. After this time, the article is available under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

            History
            : 15 September 2014
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            © The Author(s) 2014

            Genetics
            Genetics

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