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  1 / 3519 MEDLINE  
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[PMID]:28704770
[Au] Autor:Di Bonito P; Iaconelli M; Gheit T; Tommasino M; Della Libera S; Bonadonna L; La Rosa G
[Ad] Endereço:Department of Infectious Diseases, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy.
[Ti] Título:Detection of oncogenic viruses in water environments by a Luminex-based multiplex platform for high throughput screening of infectious agents.
[So] Source:Water Res;123:549-555, 2017 Oct 15.
[Is] ISSN:1879-2448
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Recent studies documented the detection of viruses strongly associated with human cancer in urban sewages and other water environments worldwide. The aim of this study was to estimate the occurrence of human oncogenic viruses in environmental samples (sewage, river, marine, and pool/spa water) using highly sensitive and specific multiplex bead-based assays (Luminex technology). A total of 33 samples were analysed for 140 oncogenic viral agents, including mucosal and cutaneous human papillomaviruses (HPVs), human polyomaviruses (HPyV), human herpesviruses (HHV) and mouse mammary tumour virus (MMTV). Eighty-eight percent of the samples tested positive for at least one viral pathogen and the simultaneous presence of more than one virus was frequent (mean number of positivities/sample = 3.03). A total of 30 different Alpha, Beta and Gamma HPVs were detected, including mucosal and cutaneous types. The high-risk type HPV16 was the most frequently detected virus, identified in 73% of the samples. Of the 12 HPyVs tested, only two (BKPyV and MCPyV) were detected. At least one of these two was present in 48% of the samples. MMTV was detected in 21% of the samples, while herpesviruses - HHV-6 and HHV-1 - were detected in two samples (6%). The present study is the first to provide a comprehensive picture of the occurrence of oncogenic viruses belonging to different families and species in diverse water environments, and the first to successfully use, in environmental samples, a Luminex-based multiplex platform for high throughput screening of infectious agents. Our findings, showing that oncogenic viruses are ubiquitous in water environments, pave the way for future studies on the fate of these pathogens in water environments as well as on their potential for transmission via the waterborne route.
[Mh] Termos MeSH primário: Vírus Oncogênicos
Esgotos
[Mh] Termos MeSH secundário: Animais
Monitoramento Ambiental
Seres Humanos
Papillomaviridae
Polyomavirus
Rios
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Sewage)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE


  2 / 3519 MEDLINE  
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[PMID]:28410134
[Au] Autor:Yoshida N; Kimura T
[Ad] Endereço:Laboratory of Microbiology and Cell Biology, Department of Pharmacy, College of Pharmaceutical Sciences, Ritsumeikan University, 1-1-1 Noji-Higashi, Kusatsu, Shiga 525-8577, Japan.
[Ti] Título:Pathogen-associated regulatory non-coding RNAs and oncogenesis.
[So] Source:Front Biosci (Landmark Ed);22:1599-1621, 2017 Jun 01.
[Is] ISSN:1093-4715
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Among all new cancer cases in 2012, on average, 15.4% were caused by or oncoviruses, including Epstein-Barr virus, human papillomavirus, , , Kaposi sarcoma-associated herpesvirus and human T-lymphotropic virus. These pathogens encode a variety of non-coding RNAs, which are important cofactors for oncogenesis. In this review, we focus on recent developments in the study of long and small non-protein-coding RNAs, including microRNAs, of oncogenic pathogens, and discuss their mechanisms of action in the multiple steps of oncogenesis.
[Mh] Termos MeSH primário: Carcinogênese/genética
Vírus Oncogênicos/genética
RNA não Traduzido/genética
RNA Viral/genética
[Mh] Termos MeSH secundário: Regulação Neoplásica da Expressão Gênica
Regulação Viral da Expressão Gênica
Seres Humanos
MicroRNAs/genética
Neoplasias/genética
Neoplasias/patologia
Neoplasias/virologia
Vírus Oncogênicos/classificação
RNA Mensageiro/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (MicroRNAs); 0 (RNA, Messenger); 0 (RNA, Untranslated); 0 (RNA, Viral)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE


  3 / 3519 MEDLINE  
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[PMID]:28104704
[Au] Autor:McBride AA
[Ad] Endereço:From the ‡Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, 33 North Drive, MSC3209, National Institutes of Health, Bethesda, Maryland 20892 amcbride@nih.gov.
[Ti] Título:The Promise of Proteomics in the Study of Oncogenic Viruses.
[So] Source:Mol Cell Proteomics;16(4 suppl 1):S65-S74, 2017 Apr.
[Is] ISSN:1535-9484
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oncogenic viruses are responsible for about 15% human cancers. This article explores the promise and challenges of viral proteomics in the study of the oncogenic human DNA viruses, HPV, McPyV, EBV and KSHV. These viruses have coevolved with their hosts and cause persistent infections. Each virus encodes oncoproteins that manipulate key cellular pathways to promote viral replication and evade the host immune response. Viral proteomics can identify cellular pathways perturbed by viral infection, identify cellular proteins that are crucial for viral persistence and oncogenesis, and identify important diagnostic and therapeutic targets.
[Mh] Termos MeSH primário: Neoplasias/virologia
Proteínas Oncogênicas/metabolismo
Vírus Oncogênicos/fisiologia
Proteômica/métodos
[Mh] Termos MeSH secundário: Infecções por Vírus de DNA/imunologia
Infecções por Vírus de DNA/virologia
Interações Hospedeiro-Patógeno
Seres Humanos
Vírus Oncogênicos/metabolismo
Proteínas Virais/metabolismo
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Oncogene Proteins); 0 (Viral Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170121
[St] Status:MEDLINE
[do] DOI:10.1074/mcp.O116.065201


  4 / 3519 MEDLINE  
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[PMID]:27859242
[Au] Autor:Reale A; Messa L; Vitiello A; Loregian A; Palù G
[Ad] Endereço:Department of Molecular Medicine, University of Padua, Padua, Italy.
[Ti] Título:4th European Seminars in Virology on Oncogenic and Oncolytic Viruses, in Bertinoro (Bologna), Italy.
[So] Source:J Cell Physiol;232(10):2641-2648, 2017 Oct.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The 4th European Seminars in Virology (EuSeV), which was focused on oncogenic and oncolytic viruses, was held in Bertinoro (Bologna), Italy, from June 10 to 12, 2016. This article summarizes the plenary lectures and aims to illustrate the main topics discussed at 4th EuSeV, which brought together knowledge and expertise in the field of oncogenic and oncolytic viruses from all over the world. The meeting was divided in two parts, "Mechanisms of Viral Oncogenesis" and "Viral Oncolysis and Immunotherapy," which were both focused on dissecting the complex and multi-factorial interplay between cancer and human viruses and on exploring new anti-cancer strategies. J. Cell. Physiol. 232: 2641-2648, 2017. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Pesquisa Biomédica
Transformação Celular Viral
Neoplasias/terapia
Vírus Oncogênicos/genética
Terapia Viral Oncolítica
Vírus Oncolíticos/genética
Infecções Tumorais por Vírus/virologia
Virologia
[Mh] Termos MeSH secundário: Animais
Terapia Combinada
Seres Humanos
Imunoterapia/métodos
Neoplasias/imunologia
Neoplasias/virologia
Vírus Oncogênicos/imunologia
Vírus Oncolíticos/imunologia
Infecções Tumorais por Vírus/imunologia
[Pt] Tipo de publicação:CONGRESSES
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161119
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25692


  5 / 3519 MEDLINE  
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[PMID]:27812682
[Au] Autor:Santana-Davila R; Bhatia S; Chow LQ
[Ad] Endereço:Division of Medical Oncology, Department of Medicine, University of Washington, Seattle.
[Ti] Título:Harnessing the Immune System as a Therapeutic Tool in Virus-Associated Cancers.
[So] Source:JAMA Oncol;3(1):106-112, 2017 Jan 01.
[Is] ISSN:2374-2445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: There are at least 7 viruses implicated in the pathogenesis of 10% to 15% of all human cancers worldwide. Despite a high prevalence of infection with these viruses, only a minority of infected individuals develop a subsequent malignant tumor, underscoring the important role that host and environmental factors have in cancer development. This article reviews the mechanisms of viral carcinogenesis, with an emphasis on the viral evasion of the host immune system, and discusses how to harness the immune system effectively as a therapeutic tool in select cancers. Observations: Immune evasion mechanisms of these viral infections have an important role in carcinogenesis. Increased understanding of these mechanisms has paved the way for using immunotherapy to treat virus-associated cancers. This study summarizes the use of adoptive cell therapy, tumor vaccines, immune checkpoint inhibitors, and combination immunotherapies in the treatment of select virus-associated cancers. Conclusions and Relevance: Immunotherapy is proving to be a useful strategy in the treatment of virus-associated cancers. A greater understanding of the processes of immune evasion in chronic infections and malignant tumors will continue to help in the goal of optimizing immunotherapy, which will in turn translate into remission and long-term survival in this patient population.
[Mh] Termos MeSH primário: Imunoterapia
Neoplasias/terapia
Neoplasias/virologia
Vírus Oncogênicos/patogenicidade
[Mh] Termos MeSH secundário: Carcinogênese/genética
Carcinogênese/imunologia
Terapia Baseada em Transplante de Células e Tecidos
Seres Humanos
Neoplasias/imunologia
Vírus Oncogênicos/imunologia
Linfócitos T/imunologia
Linfócitos T/patologia
Linfócitos T/virologia
Evasão Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE
[do] DOI:10.1001/jamaoncol.2016.4574


  6 / 3519 MEDLINE  
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[PMID]:27686071
[Au] Autor:Hu X; Zhu W; Chen S; Liu Y; Sun Z; Geng T; Song C; Gao B; Wang X; Qin A; Cui H
[Ad] Endereço:Institute of Epigenetics and Epigenomics and College of Animal Science and Technology, Yangzhou University, No. 48 East Wenhui Road, Yangzhou, Jiangsu, 225009, People's Republic of China.
[Ti] Título:Expression patterns of endogenous avian retrovirus ALVE1 and its response to infection with exogenous avian tumour viruses.
[So] Source:Arch Virol;162(1):89-101, 2017 Jan.
[Is] ISSN:1432-8798
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:Endogenous retroviruses (ERVs) are genomic elements that are present in a wide range of vertebrates and have been implicated in a variety of human diseases, including cancer. However, the characteristic expression patterns of ERVs, particularly in virus-induced tumours, is not fully clear. DNA methylation was analysed by bisulfite pyrosequencing, and gene expression was analysed by RT-qPCR. In this study, we first found that the endogenous avian retrovirus ALVE1 was highly expressed in some chicken tissues (including the heart, bursa, thymus, and spleen) at 2 days of age, but its expression was markedly decreased at 35 days of age. In contrast, the CpG methylation level of ALVE1 was significantly lower in heart and bursa at 2 days than at 35 days of age. Moreover, we found that the expression of ALVE1 was significantly inhibited in chicken embryo fibroblast cells (CEFs) and MSB1 cells infected with avian leukosis virus subgroup J (ALVJ) and reticuloendotheliosis virus (REV) at the early stages of infection. In contrast, the expression of the ALVE1 env gene was significantly induced in CEFs and MSB1 cells infected with Marek's disease virus (MDV). However, the methylation and expression levels of the ALVE1 long terminal repeat (LTR) did not show obvious alterations in response to viral infection. The present study revealed the expression patterns of ALVE1 in a variety of chicken organs and tissues and in chicken cells in response to avian tumour virus infection. These findings may be of significance for understanding the role and function of ERVs that are present in the host genome.
[Mh] Termos MeSH primário: Coinfecção/veterinária
Retrovirus Endógenos/genética
Regulação Viral da Expressão Gênica
Interações Microbianas
Vírus Oncogênicos/genética
Infecções por Retroviridae/complicações
Infecções Tumorais por Vírus/veterinária
[Mh] Termos MeSH secundário: Estruturas Animais/virologia
Animais
Células Cultivadas
Embrião de Galinha
Galinhas
Coinfecção/virologia
Metilação de DNA
Retrovirus Endógenos/crescimento & desenvolvimento
Fibroblastos/virologia
Perfilação da Expressão Gênica
Vírus Oncogênicos/crescimento & desenvolvimento
Reação em Cadeia da Polimerase em Tempo Real
Infecções por Retroviridae/virologia
Análise de Sequência de DNA
Infecções Tumorais por Vírus/virologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170127
[Lr] Data última revisão:
170127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161001
[St] Status:MEDLINE
[do] DOI:10.1007/s00705-016-3086-2


  7 / 3519 MEDLINE  
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[PMID]:28038674
[Au] Autor:Walsh SR; Gerpe MC; Wootton SK
[Ad] Endereço:Department of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, Ontario, Canada.
[Ti] Título:Construction of a molecular clone of ovine enzootic nasal tumor virus.
[So] Source:Virol J;13(1):209, 2016 Dec 30.
[Is] ISSN:1743-422X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Enzootic nasal tumor virus (ENTV-1) is an ovine betaretrovirus that has been linked to enzootic nasal adenocarcinoma (ENA), a contagious tumor of the ethmoid turbinates of sheep. Transmission experiments performed using virus isolated from cell free nasal tumor homogenates suggest that ENTV-1 is the causative agent of ENA; however, this etiological relationship has not been conclusively proven due to the fact that the virus cannot be propagated in vitro nor is there an infectious molecular clone of the virus. METHODS: Here we report construction of a molecular clone of ENTV-1 and demonstrate that transfection of this molecular clone into HEK 293T cells produces mature virus particles. RESULTS: Analysis of recombinant virus particles derived from the initial molecular clone revealed a defect in the proteolytic processing of Gag; however, this defect could be corrected by co-expression of the Gag-Pro-Pol polyprotein from the highly related Jaagsiekte sheep retrovirus (JSRV) suggesting that the polyprotein cleavage sites in the ENTV-1 molecular clone were functional. Mutagenesis of the molecular clone to correct amino acid variants identified within the pro gene did not restore proteolytic processing; whereas deletion of one proline residue from a polyproline tract located in variable region 1 (VR1) of the matrix resulted in production of CA protein of the mature (cleaved) size strongly suggesting that normal virion morphogenesis and polyprotein cleavage took place. Finally, electron microscopy revealed the presence of spherical virus particles with an eccentric capsid and an average diameter of about 100 nm. CONCLUSION: In summary, we have constructed the first molecular clone of ENTV-1 from which mature virus particles can be produced. Future experiments using virus produced from this molecular clone can now be conducted to fulfill Koch's postulates and demonstrate that ENTV-1 is necessary and sufficient to induce ENA in sheep.
[Mh] Termos MeSH primário: Betaretrovirus/crescimento & desenvolvimento
Betaretrovirus/genética
Clonagem Molecular
Vírus Oncogênicos/crescimento & desenvolvimento
Vírus Oncogênicos/genética
[Mh] Termos MeSH secundário: Animais
Betaretrovirus/isolamento & purificação
Betaretrovirus/ultraestrutura
Linhagem Celular
Análise Mutacional de DNA
Células Epiteliais/virologia
Seres Humanos
Microscopia Eletrônica de Transmissão
Vírus Oncogênicos/isolamento & purificação
Vírus Oncogênicos/ultraestrutura
Poliproteínas/genética
Poliproteínas/metabolismo
Processamento de Proteína Pós-Traducional
Genética Reversa
Ovinos
Transfecção
Proteínas Virais/genética
Proteínas Virais/metabolismo
Vírion/ultraestrutura
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Polyproteins); 0 (Viral Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170101
[St] Status:MEDLINE
[do] DOI:10.1186/s12985-016-0660-x


  8 / 3519 MEDLINE  
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[PMID]:27723397
[Au] Autor:Weiss RA
[Ad] Endereço:Emeritus Professor of Viral Oncology, University College London, London WC1E 6BT.
[Ti] Título:Tumour-inducing viruses.
[So] Source:Br J Hosp Med (Lond);77(10):565-568, 2016 Oct.
[Is] ISSN:1750-8460
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Virus infections are an important factor in the global burden of human cancer. The discovery and mode of action of human tumour viruses is briefly reviewed together with the promise of prevention through vaccination.
[Mh] Termos MeSH primário: Neoplasias/virologia
Vírus Oncogênicos
Infecções Tumorais por Vírus/prevenção & controle
Vacinas Virais/uso terapêutico
[Mh] Termos MeSH secundário: Adenocarcinoma/prevenção & controle
Adenocarcinoma/virologia
Carcinoma/prevenção & controle
Carcinoma/virologia
Carcinoma Hepatocelular/prevenção & controle
Carcinoma Hepatocelular/virologia
Epidermodisplasia Verruciforme/prevenção & controle
Infecções por Vírus Epstein-Barr/prevenção & controle
Feminino
Hepacivirus
Vírus da Hepatite B
Herpesvirus Humano 4
Seres Humanos
Leiomiossarcoma/prevenção & controle
Leiomiossarcoma/virologia
Neoplasias Hepáticas/prevenção & controle
Neoplasias Hepáticas/virologia
Linfoma/prevenção & controle
Linfoma/virologia
Masculino
Neoplasias Nasofaríngeas/prevenção & controle
Neoplasias Nasofaríngeas/virologia
Neoplasias/prevenção & controle
Papillomaviridae
Infecções por Papillomavirus/prevenção & controle
Neoplasias Cutâneas/prevenção & controle
Neoplasias Cutâneas/virologia
Neoplasias Gástricas/prevenção & controle
Neoplasias Gástricas/virologia
Neoplasias do Colo do Útero/prevenção & controle
Neoplasias do Colo do Útero/virologia
Neoplasias Vulvares/prevenção & controle
Neoplasias Vulvares/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Viral Vaccines)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170309
[Lr] Data última revisão:
170309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161011
[St] Status:MEDLINE


  9 / 3519 MEDLINE  
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[PMID]:27655063
[Au] Autor:Figueroa T; Boumart I; Coupeau D; Rasschaert D
[Ad] Endereço:Equipe Transcription et Lymphome Viro-Induit (TLVI), UMR 7261 CNRS/Université François Rabelais de Tours, Tours, France.
[Ti] Título:Hyperediting by ADAR1 of a new herpesvirus lncRNA during the lytic phase of the oncogenic Marek's disease virus.
[So] Source:J Gen Virol;97(11):2973-2988, 2016 Nov.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Marek's disease virus, or Gallid herpesvirus 2 (GaHV-2), is an avian alphaherpesvirus that induces T-cell lymphoma in chickens. During transcriptomic studies of the RL region of the genome, we characterized the 7.5 kbp gene of the ERL lncRNA (edited repeat-long, long non-coding RNA), which may act as a natural antisense transcript (NAT) of the major GaHV-2 oncogene meq and of two of the three miRNA clusters. During infections in vivo and in vitro, we detected hyperediting of the ERL lncRNA that appeared to be directly correlated with ADAR1 expression levels. The ERL lncRNA was expressed equally during the lytic and latent phases of infection and during viral reactivation, but its hyperediting increased only during the lytic infection of chicken embryo fibroblasts. We also showed that chicken ADAR1 expression was controlled by the JAK/STAT IFN-response pathway, through an inducible promoter containing IFN-stimulated response elements that were functional during stimulation with IFN-α or poly(I:C). Like the human and murine miR-155-5p, the chicken gga-miR-155-5p and the GaHV-2 analogue mdv1-miR-M4-5p deregulated this pathway by targeting and repressing expression of suppressor of cytokine signalling 1, leading to the upregulation of ADAR1. Finally, we hypothesized that the natural antisense transcript role of the ERL lncRNA could be disrupted by its hyperediting, particularly during viral lytic replication, and that the observed deregulation of the innate immune system by mdv1-miR-M4-5p might contribute to the viral cycle.
[Mh] Termos MeSH primário: Adenosina Desaminase/metabolismo
Herpesvirus Galináceo 2/genética
Doença de Marek/enzimologia
Doença de Marek/virologia
Vírus Oncogênicos/genética
RNA Longo não Codificante/genética
RNA Viral/genética
[Mh] Termos MeSH secundário: Adenosina Desaminase/genética
Animais
Galinhas
Fibroblastos/enzimologia
Fibroblastos/metabolismo
Fibroblastos/virologia
Regulação Viral da Expressão Gênica
Herpesvirus Galináceo 2/fisiologia
Doença de Marek/genética
MicroRNAs/genética
MicroRNAs/metabolismo
Vírus Oncogênicos/fisiologia
Regiões Promotoras Genéticas
Edição de RNA
RNA Longo não Codificante/metabolismo
RNA Viral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (RNA, Long Noncoding); 0 (RNA, Viral); EC 3.5.4.4 (Adenosine Deaminase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170503
[Lr] Data última revisão:
170503
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160923
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000606


  10 / 3519 MEDLINE  
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[PMID]:27415011
[Au] Autor:Robinson LA; Jaing CJ; Pierce Campbell C; Magliocco A; Xiong Y; Magliocco G; Thissen JB; Antonia S
[Ad] Endereço:Department of Thoracic Oncology, Moffitt Cancer Center, Tampa, Florida 33612-9416, USA.
[Ti] Título:Molecular evidence of viral DNA in non-small cell lung cancer and non-neoplastic lung.
[So] Source:Br J Cancer;115(4):497-504, 2016 Aug 09.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Although ∼20% of human cancers are caused by microorganisms, only suspicion exists for a microbial cause of lung cancer. Potential infectious agents were investigated in non-small cell lung cancer (NSCLC) and non-neoplastic lung. METHODS: Seventy NSCLC tumours (33 squamous cell carcinomas, 17 adenocarcinomas, 10 adenocarcinomas with lepidic spread, and 10 oligometastases) and 10 non-neoplastic lung specimens were evaluated for molecular evidence of microorganisms. Tissues were subjected to the Lawrence Livermore Microbial Detection Array, an oncovirus panel of the International Agency for Research on Cancer, and human papillomavirus (HPV) genotyping. Associations were examined between microbial prevalence, clinical characteristics, and p16 and EGFR expression. RESULTS: Retroviral DNA was observed in 85% squamous cell carcinomas, 47% adenocarcinomas, and 10% adenocarcinomas with lepidic spread. Human papillomavirus DNA was found in 69% of squamous cell carcinomas with 30% containing high-risk HPV types. No significant viral DNA was detected in non-neoplastic lung. Patients with tumours containing viral DNA experienced improved long-term survival compared with patients with viral DNA-negative tumours. CONCLUSIONS: Most squamous cell carcinomas and adenocarcinomas contained retroviral DNA and one-third of squamous cell carcinomas contained high-risk HPV DNA. Viral DNA was absent in non-neoplastic lung. Trial results encourage further study of the viral contribution to lung carcinogenesis.
[Mh] Termos MeSH primário: Adenocarcinoma/virologia
Carcinoma Pulmonar de Células não Pequenas/virologia
Carcinoma de Células Escamosas/virologia
DNA Viral/análise
Neoplasias Pulmonares/virologia
Pulmão/virologia
Papillomaviridae/genética
Retroviridae/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/complicações
Adenocarcinoma/metabolismo
Idoso
Idoso de 80 Anos ou mais
Carcinoma Pulmonar de Células não Pequenas/complicações
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Carcinoma de Células Escamosas/complicações
Carcinoma de Células Escamosas/metabolismo
Inibidor p16 de Quinase Dependente de Ciclina/metabolismo
Feminino
Genótipo
Seres Humanos
Pulmão/metabolismo
Neoplasias Pulmonares/complicações
Neoplasias Pulmonares/metabolismo
Masculino
Meia-Idade
Vírus Oncogênicos/genética
Infecções por Papillomavirus/complicações
Infecções por Papillomavirus/metabolismo
Infecções por Papillomavirus/virologia
Reação em Cadeia da Polimerase
Receptor do Fator de Crescimento Epidérmico/metabolismo
Infecções por Retroviridae/complicações
Infecções por Retroviridae/metabolismo
Infecções por Retroviridae/virologia
Infecções Tumorais por Vírus/complicações
Infecções Tumorais por Vírus/metabolismo
Infecções Tumorais por Vírus/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin-Dependent Kinase Inhibitor p16); 0 (DNA, Viral); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160715
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2016.213



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