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      Increased APOBEC3B Predicts Worse Outcomes in Lung Cancer: A Comprehensive Retrospective Study

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          Abstract

          Lung cancer ranks as the most common and lethal malignancy in America and worldwide. APOBEC3B is a newly identified DNA cytosine deaminase, which is supposed to function as a major source of DNA mutation in many different tumors. In this study, we combine the data of online databases and two hundred and twenty-one primary non-small-cell lung carcinoma (NSCLC) specimens from Sun Yat-sen University Cancer Center to investigate, for the first time, the clinical role of APOBEC3B in lung cancer. We found that the APOBEC3 expression was commonly elevated in NSCLC tissues and overexpression of APOBEC3B was correlated with unfavorable prognosis of the patients with NSCLC. Furthermore, APOBEC3B expression was associated with nodal status, TNM staging and adjuvant chemotherapy of the patients with NSCLC. Further research is warranted.

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          APOBEC3B upregulation and genomic mutation patterns in serous ovarian carcinoma.

          Brandon Leonard, Crystal Carpenter, S Kaufmann … (2013)
          Ovarian cancer is a clinically and molecularly heterogeneous disease. The driving forces behind this variability are unknown. Here, we report wide variation in the expression of the DNA cytosine deaminase APOBEC3B, with elevated expression in the majority of ovarian cancer cell lines (three SDs above the mean of normal ovarian surface epithelial cells) and high-grade primary ovarian cancers. APOBEC3B is active in the nucleus of several ovarian cancer cell lines and elicits a biochemical preference for deamination of cytosines in 5'-TC dinucleotides. Importantly, examination of whole-genome sequence from 16 ovarian cancers reveals that APOBEC3B expression correlates with total mutation load as well as elevated levels of transversion mutations. In particular, high APOBEC3B expression correlates with C-to-A and C-to-G transversion mutations within 5'-TC dinucleotide motifs in early-stage high-grade serous ovarian cancer genomes, suggesting that APOBEC3B-catalyzed genomic uracil lesions are further processed by downstream DNA "repair" enzymes including error-prone translesion polymerases. These data identify a potential role for APOBEC3B in serous ovarian cancer genomic instability. ©2013 AACR.
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            APOBEC3B expression in breast cancer reflects cellular proliferation, while a deletion polymorphism is associated with immune activation.

            David W. Cescon, Benjamin Haibe-Kains, Tak W Mak (2015)
            Genomic sequencing studies of breast and other cancers have identified patterns of mutations that have been attributed to the endogenous mutator activity of APOBEC3B (A3B), a member of the AID/APOBEC family of cytidine deaminases. A3B gene expression is increased in many cancers, but its upstream drivers remain undefined. Furthermore, there exists a common germ-line deletion polymorphism (A3B(del)), which has been associated with a paradoxical increase in breast cancer risk. To examine causes and consequences of A3B expression and its constitutive absence in breast cancer, we analyzed two large clinically annotated genomic datasets [The Cancer Genome Atlas (TCGA) and the Molecular Taxonomy of Breast Cancer International Consortium (METABRIC)]. We confirmed that A3B expression is associated with aggressive clinicopathologic characteristics and adverse outcomes and show that A3B expression is highly correlated with proliferative features (mitosis and cell cycle-related gene expression) in breast and 15 of 16 other solid tumor types. However, breast cancers arising in homozygous A3B(del) individuals with A3B absent did not differ in these features, indicating that A3B expression is a reflection rather than a direct cause of increased proliferation. Using gene set enrichment analysis (GSEA), we detected a pattern of immune activation in A3B(del) breast cancers, which seems to be related to hypermutation arising in A3B(del) carriers. Together, these results provide an explanation for A3B overexpression and its prognostic effect, giving context to additional study of this mutator as a cancer biomarker or putative drug target. In addition, although immune features of A3B(del) require additional study, these findings nominate the A3B(del) polymorphism as a potential predictor for cancer immunotherapy.
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              AID/APOBEC cytosine deaminase induces genome-wide kataegis

              Artem G. Lada, Alok Dhar, Robert J. Boissy … (2012)
              Clusters of localized hypermutation in human breast cancer genomes, named “kataegis” (from the Greek for thunderstorm), are hypothesized to result from multiple cytosine deaminations catalyzed by AID/APOBEC proteins. However, a direct link between APOBECs and kataegis is still lacking. We have sequenced the genomes of yeast mutants induced in diploids by expression of the gene for PmCDA1, a hypermutagenic deaminase from sea lamprey. Analysis of the distribution of 5,138 induced mutations revealed localized clusters very similar to those found in tumors. Our data provide evidence that unleashed cytosine deaminase activity is an evolutionary conserved, prominent source of genome-wide kataegis events. Reviewers This article was reviewed by: Professor Sandor Pongor, Professor Shamil R. Sunyaev, and Dr Vladimir Kuznetsov.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Cancer
                Journal ID (iso-abbrev): J Cancer
                Journal ID (publisher-id): jca
                Title: Journal of Cancer
                Publisher: Ivyspring International Publisher (Sydney )
                ISSN (Electronic): 1837-9664
                Publication date Collection: 2016
                Publication date (Electronic): 19 March 2016
                Volume: 7
                Issue: 6
                Pages: 618-625
                Affiliations
                1. State Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Guangzhou City, Guangdong Province, P.R. China;
                2. Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou City, Guangdong Province, P.R. China;
                3. Department of Molecular Oncology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA;
                4. State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou City, Guangdong Province, P.R. China;
                5. Department of Biological Sciences, University of Illinois at Chicago, Chicago, Illinois 60607, USA.
                Author notes
                ✉ Corresponding authors: Qiuliang Wu, MD, Department of Pathology, State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, No. 651 Dongfeng Road East, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, P.R. China; Tel: +86- 20-87343268, E-mail: wuql@ 123456sysucc.org.cn Or Yong Li, MD, Department of Pathology, State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, No. 651 Dongfeng Road East, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, P.R. China; Tel: +86- 20-87343268, E-mail: liyong@ 123456sysucc.org.cn .

                * These authors contributed equally to this work and share the first authorship.

                Conflicts of interest: The authors declare that there is no conflict of interest.

                Article
                Publisher ID: jcav07p0618
                DOI: 10.7150/jca.14030
                PMC ID: 4829547
                PubMed ID: 27076842
                SO-VID: ad3b7ef9-4ea3-4737-9252-115b3a936d87
                Copyright © © Ivyspring International Publisher. Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited. See http://ivyspring.com/terms for terms and conditions.
                History
                Date received : 2 October 2015
                Date accepted : 26 January 2016
                Categories
                Subject: Research Paper

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: apobec3b,non-small-cell lung cancer,immunohistochemistry,prognosis.
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: apobec3b, non-small-cell lung cancer, immunohistochemistry, prognosis.

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