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https://www.readbyqxmd.com/read/29769532/aid-apobec-like-cytidine-deaminases-are-ancient-innate-immune-mediators-in-invertebrates
#1
Mei-Chen Liu, Wen-Yun Liao, Katherine M Buckley, Shu Yuan Yang, Jonathan P Rast, Sebastian D Fugmann
In the course of both innate and adaptive immunity, cytidine deaminases within the activation induced cytidine deaminase (AID)/apolipoprotein B editing complex (APOBEC) family modulate immune responses by mutating specific nucleic acid sequences of hosts and pathogens. The evolutionary emergence of these mediators, however, seems to coincide precisely with the emergence of adaptive immunity in vertebrates. Here, we show a family of genes in species within two divergent invertebrate phyla-the echinoderm Strongylocentrotus purpuratus and the brachiopod Lingula anatina-that encode proteins with similarities in amino acid sequence and enzymatic activities to the vertebrate AID/APOBECs...
May 16, 2018: Nature Communications
https://www.readbyqxmd.com/read/29748584/the-effects-of-mutational-processes-and-selection-on-driver-mutations-across-cancer-types
#2
Daniel Temko, Ian P M Tomlinson, Simone Severini, Benjamin Schuster-Böckler, Trevor A Graham
Epidemiological evidence has long associated environmental mutagens with increased cancer risk. However, links between specific mutation-causing processes and the acquisition of individual driver mutations have remained obscure. Here we have used public cancer sequencing data from 11,336 cancers of various types to infer the independent effects of mutation and selection on the set of driver mutations in a cancer type. First, we detect associations between a range of mutational processes, including those linked to smoking, ageing, APOBEC and DNA mismatch repair (MMR) and the presence of key driver mutations across cancer types...
May 10, 2018: Nature Communications
https://www.readbyqxmd.com/read/29746667/a-fluorescent-reporter-for-quantification-and-enrichment-of-dna-editing-by-apobec-cas9-or-cleavage-by-cas9-in-living-cells
#3
Amber St Martin, Daniel Salamango, Artur Serebrenik, Nadine Shaban, William L Brown, Francesco Donati, Uday Munagala, Silvestro G Conticello, Reuben S Harris
Base editing is an exciting new genome engineering technology. C-to-T mutations in genomic DNA have been achieved using ribonucleoprotein complexes comprised of rat APOBEC1 single-stranded DNA deaminase, Cas9 nickase (Cas9n), uracil DNA glycosylase inhibitor (UGI), and guide (g)RNA. Here, we report the first real-time reporter system for quantification of APOBEC-mediated base editing activity in living mammalian cells. The reporter expresses eGFP constitutively as a marker for transfection or transduction, and editing restores functionality of an upstream mCherry cassette through the simultaneous processing of two gRNA binding regions that each contain an APOBEC-preferred 5'TCA target site...
May 9, 2018: Nucleic Acids Research
https://www.readbyqxmd.com/read/29732392/bladder-cancer-genetic-susceptibility-a-systematic-review
#4
Evangelina López de Maturana, Marta Rava, Chiaka Anumudu, Olga Sáez, Dolores Alonso, Núria Malats
Background: The variant/gene candidate approach to explore bladder cancer (BC) genetic susceptibility has been applied in many studies with significant findings reported. However, results are not always conclusive due to the lack of replication by subsequent studies. Objectives: To identify all epidemiological investigations on the genetic associations with BC risk, to quantify the likely magnitude of the associations by applying metaanalysis methodology and to assess whether there is a potential for publication/reporting bias...
April 26, 2018: Bladder Cancer
https://www.readbyqxmd.com/read/29695832/apobec3b-and-apobec-mutational-signature-as-potential-predictive-markers-for-immunotherapy-response-in-non-small-cell-lung-cancer
#5
Shixiang Wang, Mingming Jia, Zaoke He, Xue-Song Liu
Non-small cell lung cancer (NSCLC) is known to carry heavy mutation load. Besides smoking, cytidine deaminase APOBEC3B plays a key role in the mutation process of NSCLC. APOBEC3B is also reported to be upregulated and predicts bad prognosis in NSCLC. However, targeting APOBEC3B high NSCLC is still a big challenge. Here we show that APOBEC3B upregulation is significantly associated with immune gene expression, and APOBEC3B expression positively correlates with known immunotherapy response biomarkers, including: PD-L1 expression and T-cell infiltration in NSCLC...
April 26, 2018: Oncogene
https://www.readbyqxmd.com/read/29642934/correlation-of-gene-expression-and-associated-mutation-profiles-of-apobec3a-apobec3b-rev1-ung-and-fhit-with-chemosensitivity-of-cancer-cell-lines-to-drug-treatment
#6
Suleyman Vural, Richard Simon, Julia Krushkal
BACKGROUND: The APOBEC gene family of cytidine deaminases plays important roles in DNA repair and mRNA editing. In many cancers, APOBEC3B increases the mutation load, generating clusters of closely spaced, single-strand-specific DNA substitutions with a characteristic hypermutation signature. Some studies also suggested a possible involvement of APOBEC3A, REV1, UNG, and FHIT in molecular processes affecting APOBEC mutagenesis. It is important to understand how mutagenic processes linked to the activity of these genes may affect sensitivity of cancer cells to treatment...
April 11, 2018: Human Genomics
https://www.readbyqxmd.com/read/29618650/siv-mac239-vif-and-human-apobec3b-interactions-resemble-those-between-hiv-1-vif-and-human-apobec3g
#7
Jiayi Wang, Nadine M Shaban, Allison M Land, William L Brown, Reuben S Harris
Several members of the APOBEC3 DNA cytosine deaminase family can potently inhibit Vif-deficient HIV-1 by catalyzing cytosine deamination in viral cDNA and impeding reverse transcription. HIV-1 counteracts restriction with the virally encoded Vif protein, which targets relevant APOBEC3 proteins for proteasomal degradation. HIV-1 Vif is optimized for degrading the restrictive human APOBEC3 repertoire and, in general, lentiviral Vif proteins specifically target the restricting APOBEC3 enzymes of each host species...
April 4, 2018: Journal of Virology
https://www.readbyqxmd.com/read/29617672/increased-rna-editing-may-provide-a-source-for-autoantigens-in-systemic-lupus-erythematosus
#8
Shalom Hillel Roth, Miri Danan-Gotthold, Meirav Ben-Izhak, Gideon Rechavi, Cyrille J Cohen, Yoram Louzoun, Erez Y Levanon
RNA-editing mechanisms, which induce nucleotide substitution in the RNA, increase transcript and protein diversities. Editing dysregulation has been shown to lead to grave outcomes, and transcriptome-wide aberrant RNA editing has been found in tumors. However, little is known about the involvement of editing in other diseases. Systemic lupus erythematosus (SLE) is a multisystemic autoimmune disease characterized by a loss of tolerance for autoantigens from various tissues and the production of multiple autoantibodies...
April 3, 2018: Cell Reports
https://www.readbyqxmd.com/read/29615459/genetic-analysis-of-779-advanced-differentiated-and-anaplastic-thyroid-cancers
#9
Nikita Pozdeyev, Laurie Gay, Ethan S Sokol, Ryan J Hartmaier, Kelsi E Deaver, Stephanie N Davis, Jena D French, Pierre Vanden Borre, Daniel V LaBarbera, Aik-Choon Tan, Rebecca E Schweppe, Lauren Fishbein, Jeffrey S Ross, Bryan R Haugen, Daniel W Bowles
PURPOSE: To define the genetic landscape of advanced differentiated and anaplastic thyroid cancer and identify genetic alterations of potential diagnostic, prognostic and therapeutic significance. EXPERIMENTAL DESIGN: The genetic profiles of 583 advanced differentiated and 196 anaplastic thyroid cancers (ATC) generated with targeted next-generation sequencing cancer-associated gene panels MSK-IMPACT and FoundationOne were analyzed. RESULTS: ATC had more genetic alterations per tumor, and pediatric papillary thyroid cancer had fewer genetic alterations per tumor when compared to other thyroid cancer types...
April 3, 2018: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/29593040/within-host-variations-of-human-papillomavirus-reveal-apobec-signature-mutagenesis-in-the-viral-genome
#10
Yusuke Hirose, Mamiko Onuki, Yuri Tenjimbayashi, Seiichiro Mori, Yoshiyuki Ishii, Takamasa Takeuchi, Nobutaka Tasaka, Toyomi Satoh, Tohru Morisada, Takashi Iwata, Shingo Miyamoto, Koji Matsumoto, Akihiko Sekizawa, Iwao Kukimoto
Persistent infection with oncogenic human papillomaviruses (HPVs) causes cervical cancer, accompanied with the accumulation of somatic mutations into the host genome. There are concomitant genetic changes in the HPV genome during viral infection; however, their relevance to cervical carcinogenesis is poorly understood. Here we explored within-host genetic diversity of HPV by performing deep sequencing analyses of viral whole-genome sequences in clinical specimens. The whole genomes of HPV types 16, 52 and 58 were amplified by type-specific PCR from total cellular DNA of cervical exfoliated cells collected from patients with cervical intraepithelial neoplasia (CIN) and invasive cervical cancer (ICC), and were deep-sequenced...
March 28, 2018: Journal of Virology
https://www.readbyqxmd.com/read/29584723/transmission-of-hiv-1-drug-resistance-mutations-within-partner-pairs-a-cross-sectional-study-of-a-primary-hiv-infection-cohort
#11
Joanne D Stekler, Ross Milne, Rachel Payant, Ingrid Beck, Joshua Herbeck, Brandon Maust, Wenjie Deng, Kenneth Tapia, Sarah Holte, Janine Maenza, Claire E Stevens, James I Mullins, Ann C Collier, Lisa M Frenkel
BACKGROUND: Transmission of human immunodeficiency virus type 1 (HIV-1) drug resistance mutations, particularly that of minority drug-resistant variants, remains poorly understood. Population-based studies suggest that drug-resistant HIV-1 is less transmissible than drug-susceptible viruses. We compared HIV-1 drug-resistant genotypes among partner-pairs in order to assess the likelihood of transmission of drug resistance mutations and investigate the role of minority variants in HIV transmission...
March 2018: PLoS Medicine
https://www.readbyqxmd.com/read/29581109/b-cell-tumor-development-in-tet2-deficient-mice
#12
Enguerran Mouly, Hussein Ghamlouch, Veronique Della-Valle, Laurianne Scourzic, Cyril Quivoron, Damien Roos-Weil, Patrycja Pawlikowska, Véronique Saada, M'Boyba K Diop, Cécile K Lopez, Michaela Fontenay, Philippe Dessen, Ivo P Touw, Thomas Mercher, Said Aoufouchi, Olivier A Bernard
The TET2 gene encodes an α-ketoglutarate-dependent dioxygenase able to oxidize 5-methylcytosine into 5-hydroxymethylcytosine, which is a step toward active DNA demethylation. TET2 is frequently mutated in myeloid malignancies but also in B- and T-cell malignancies. TET2 somatic mutations are also identified in healthy elderly individuals with clonal hematopoiesis. Tet2 -deficient mouse models showed widespread hematological differentiation abnormalities, including myeloid, T-cell, and B-cell malignancies. We show here that, similar to what is observed with constitutive Tet2 -deficient mice, B-cell-specific Tet2 knockout leads to abnormalities in the B1-cell subset and a development of B-cell malignancies after long latency...
March 27, 2018: Blood Advances
https://www.readbyqxmd.com/read/29567676/cancer-associated-rs6983267-snp-and-its-accompanying-long-noncoding-rna-ccat2-induce-myeloid-malignancies-via-unique-snp-specific-rna-mutations
#13
Maitri Y Shah, Manuela Ferracin, Valentina Pileczki, Baoqing Chen, Roxana Redis, Linda Fabris, Xinna Zhang, Cristina Ivan, Masayoshi Shimizu, Cristian Rodriguez-Aguayo, Mihnea Dragomir, Katrien Van Roosbroeck, Maria Ines Almeida, Maria Ciccone, Daniela Nedelcu, Maria Angelica Cortez, Taghi Manshouri, Steliana Calin, Muharrem Muftuoglu, Pinaki P Banerjee, Mustafa H Badiwi, Jan Parker-Thornburg, Asha Multani, James William Welsh, Marcos Roberto Estecio, Hui Ling, Ciprian Tomuleasa, Delia Dima, Hui Yang, Hector Alvarez, M James You, Milan Radovich, Elizabeth Shpall, Muller Fabbri, Katy Rezvani, Leonard Girnita, Ioana Berindan-Neagoe, Anirban Maitra, Srdan Verstovsek, Riccardo Fodde, Carlos Bueso-Ramos, Mihai Gagea, Guillermo Garcia Manero, George A Calin
The cancer-risk-associated rs6983267 single nucleotide polymorphism (SNP) and the accompanying long noncoding RNA CCAT2 in the highly amplified 8q24.21 region have been implicated in cancer predisposition, although causality has not been established. Here, using allele-specific CCAT2 transgenic mice, we demonstrate that CCAT2 overexpression leads to spontaneous myeloid malignancies. We further identified that CCAT2 is overexpressed in bone marrow and peripheral blood of myelodysplastic/myeloproliferative neoplasms (MDS/MPN) patients...
March 22, 2018: Genome Research
https://www.readbyqxmd.com/read/29555777/expansions-diversification-and-interindividual-copy-number-variations-of-aid-apobec-family-cytidine-deaminase-genes-in-lampreys
#14
Stephen J Holland, Lesley M Berghuis, Justin J King, Lakshminarayan M Iyer, Katarzyna Sikora, Heather Fifield, Sarah Peter, Emma M Quinlan, Fumiaki Sugahara, Prashant Shingate, Inês Trancoso, Norimasa Iwanami, Elena Temereva, Christine Strohmeier, Shigeru Kuratani, Byrappa Venkatesh, Guillaume Evanno, L Aravind, Michael Schorpp, Mani Larijani, Thomas Boehm
Cytidine deaminases of the AID/APOBEC family catalyze C-to-U nucleotide transitions in mRNA or DNA. Members of the APOBEC3 branch are involved in antiviral defense, whereas AID contributes to diversification of antibody repertoires in jawed vertebrates via somatic hypermutation, gene conversion, and class switch recombination. In the extant jawless vertebrate, the lamprey, two members of the AID/APOBEC family are implicated in the generation of somatic diversity of the variable lymphocyte receptors (VLRs). Expression studies linked CDA1 and CDA2 genes to the assembly of VLRA /C genes in T-like cells and the VLRB genes in B-like cells, respectively...
March 19, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29555751/diversification-of-aid-apobec-like-deaminases-in-metazoa-multiplicity-of-clades-and-widespread-roles-in-immunity
#15
Arunkumar Krishnan, Lakshminarayan M Iyer, Stephen J Holland, Thomas Boehm, L Aravind
AID/APOBEC deaminases (AADs) convert cytidine to uridine in single-stranded nucleic acids. They are involved in numerous mutagenic processes, including those underpinning vertebrate innate and adaptive immunity. Using a multipronged sequence analysis strategy, we uncover several AADs across metazoa, dictyosteliida, and algae, including multiple previously unreported vertebrate clades, and versions from urochordates, nematodes, echinoderms, arthropods, lophotrochozoans, cnidarians, and porifera. Evolutionary analysis suggests a fundamental division of AADs early in metazoan evolution into secreted deaminases (SNADs) and classical AADs, followed by diversification into several clades driven by rapid-sequence evolution, gene loss, lineage-specific expansions, and lateral transfer to various algae...
March 19, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29555573/whole-exome-sequencing-identified-mutational-profiles-of-squamous-cell-carcinomas-of-anus
#16
Sun Shin, Hyeon-Chun Park, Min Sung Kim, Mi-Ryung Han, Sung Hak Lee, Seung Hyun Jung, Sug Hyung Lee, Yeun-Jun Chung
Anal squamous cell carcinoma (ASCC), either with human papillomavirus (HPV) (+) or (-), is a neoplastic disease with frequent recurrence and metastasis. To characterize ASCC genomes, we attempted to disclose novel alterations of ASCC genomes as well as other genetic features including mutation signatures. We performed whole-exome sequencing and copy number alteration (CNA) profiling for 8 ASCC samples from 6 patients (2 cases with primary and recurrent/metastatic tumors). We found known ASCC mutations (TP53, CDKN2A and PIK3CA) and CNAs (gains on 3q and 19q and losses on 11q and 13q)...
March 16, 2018: Human Pathology
https://www.readbyqxmd.com/read/29545328/genetic-landscape-of-hepatitis-b-virus-associated-diffuse-large-b-cell-lymphoma
#17
Weicheng Ren, Xiaofei Ye, Hong Su, Wei Li, Dongbing Liu, Mohammad Pirmoradian, Xianhuo Wang, Bo Zhang, Qiang Zhang, Longyun Chen, Man Nie, Yao Liu, Bin Meng, Huiqiang Huang, Wenqi Jiang, Yixin Zeng, Wenyu Li, Kui Wu, Yong Hou, Klas G Wiman, Zhiming Li, Huilai Zhang, Roujun Peng, Shida Zhu, Qiang Pan-Hammarström
Hepatitis B virus (HBV) infection is endemic in some parts of Asia, Africa and South America and remains to be a significant public health problem in these areas. It is known as a leading risk factor for the development of hepatocellular carcinoma, but epidemiological studies have also shown that the infection may increase the incidence of several types B-cell lymphoma. Here, by characterizing altogether 275 Chinese diffuse large B-cell lymphoma (DLBCL) patients, we showed that patients with concomitant HBV infection (surface antigen positive, HBsAg+ ) are characterized by a younger age, a more advanced disease stage at diagnosis and a reduced overall survival...
March 15, 2018: Blood
https://www.readbyqxmd.com/read/29535424/comprehensive-genomic-profiling-of-neuroendocrine-bladder-cancer-pinpoints-molecular-origin-and-potential-therapeutics
#18
Peiye Shen, Ying Jing, Ruiyun Zhang, Mei-Chun Cai, Pengfei Ma, Haige Chen, Guanglei Zhuang
Neuroendocrine bladder cancer is a relatively rare but often lethal malignancy, with cell of origin, oncogenomic architecture and standard treatment poorly defined. Here we performed comprehensive whole-genome and transcriptome sequencing on a unique cohort of genitourinary neuroendocrine neoplasms, mainly small cell carcinomas of the urinary bladder. The mutational landscape and signatures of neuroendocrine bladder cancer strikingly resembled those in conventional urothelial carcinoma, along with typically mixed histologies, supporting a common cellular origin...
March 14, 2018: Oncogene
https://www.readbyqxmd.com/read/29492964/interaction-analysis-between-germline-susceptibility-loci-and-somatic-alterations-in-lung-cancer
#19
Yuzhuo Wang, Cheng Wang, Jiahui Zhang, Meng Zhu, Xu Zhang, Zhihua Li, Juncheng Dai, Hongxia Ma, Zhibin Hu, Guangfu Jin, Hongbing Shen
Emerging evidence indicates that germline variations may interact with somatic events in carcinogenesis. However, the germline-somatic interaction in lung cancer remains largely unknown. We investigated whether lung cancer driver genes (CDGs) were more likely to locate within cancer susceptibility regions. Pathway analysis was performed to identify common pathways underlying CDGs and cancer susceptibility genes (CSGs). Next, we analyzed the associations between lung cancer risk SNPs and somatic alterations, including mutations and copy number alterations, in the level of genes, pathways, and overall burden of alterations...
March 1, 2018: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/29491156/asymmetric-modification-of-hepatitis-b-virus-hbv-genomes-by-an-endogenous-cytidine-deaminase-inside-hbv-cores-informs-a-model-of-reverse-transcription
#20
Smita Nair, Adam Zlotnick
Cytidine deaminases inhibit replication of a broad range of DNA viruses by deaminating cytidines on single-stranded DNA (ssDNA) to generate uracil. While several lines of evidence have revealed hepatitis B virus (HBV) genome editing by deamination, it is still unclear which nucleic acid intermediate of HBV is modified. Hepatitis B virus has a relaxed circular double-stranded DNA (rcDNA) genome that is reverse transcribed within virus cores from a RNA template. The HBV genome also persists as covalently closed circular DNA (cccDNA) in the nucleus of an infected cell...
May 15, 2018: Journal of Virology
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