Base de dados : MEDLINE
Pesquisa : B04.280.210 [Categoria DeCS]
Referências encontradas : 119 [refinar]
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  1 / 119 MEDLINE  
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[PMID]:27034740
[Au] Autor:Mushtaq M; Darekar S; Kashuba E
[Ad] Endereço:Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institute, 17177 Stockholm, Sweden.
[Ti] Título:DNA Tumor Viruses and Cell Metabolism.
[So] Source:Oxid Med Cell Longev;2016:6468342, 2016.
[Is] ISSN:1942-0994
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Viruses play an important role in cancerogenesis. It is estimated that approximately 20% of all cancers are linked to infectious agents. The viral genes modulate the physiological machinery of infected cells that lead to cell transformation and development of cancer. One of the important adoptive responses by the cancer cells is their metabolic change to cope up with continuous requirement of cell survival and proliferation. In this review we will focus on how DNA viruses alter the glucose metabolism of transformed cells. Tumor DNA viruses enhance "aerobic" glycolysis upon virus-induced cell transformation, supporting rapid cell proliferation and showing the Warburg effect. Moreover, viral proteins enhance glucose uptake and controls tumor microenvironment, promoting metastasizing of the tumor cells.
[Mh] Termos MeSH primário: Transformação Celular Viral
Vírus de DNA Tumorais/metabolismo
Neoplasias/metabolismo
Neoplasias/virologia
Infecções Tumorais por Vírus/metabolismo
Proteínas Virais/metabolismo
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Sobrevivência Celular
Glicólise
Seres Humanos
Neoplasias/patologia
Infecções Tumorais por Vírus/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Viral Proteins)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160402
[St] Status:MEDLINE
[do] DOI:10.1155/2016/6468342


  2 / 119 MEDLINE  
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[PMID]:26405230
[Au] Autor:Lau L; Gray EE; Brunette RL; Stetson DB
[Ad] Endereço:Department of Immunology, University of Washington School of Medicine, Seattle, WA 98109, USA.
[Ti] Título:DNA tumor virus oncogenes antagonize the cGAS-STING DNA-sensing pathway.
[So] Source:Science;350(6260):568-71, 2015 Oct 30.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS) detects intracellular DNA and signals through the adapter protein STING to initiate the antiviral response to DNA viruses. Whether DNA viruses can prevent activation of the cGAS-STING pathway remains largely unknown. Here, we identify the oncogenes of the DNA tumor viruses, including E7 from human papillomavirus (HPV) and E1A from adenovirus, as potent and specific inhibitors of the cGAS-STING pathway. We show that the LXCXE motif of these oncoproteins, which is essential for blockade of the retinoblastoma tumor suppressor, is also important for antagonizing DNA sensing. E1A and E7 bind to STING, and silencing of these oncogenes in human tumor cells restores the cGAS-STING pathway. Our findings reveal a host-virus conflict that may have shaped the evolution of viral oncogenes.
[Mh] Termos MeSH primário: Proteínas E1A de Adenovirus/metabolismo
Vírus de DNA Tumorais/imunologia
Proteínas de Ligação a DNA/metabolismo
Proteínas de Membrana/antagonistas & inibidores
Nucleotídeos Cíclicos/antagonistas & inibidores
Proteínas Oncogênicas Virais/metabolismo
Evasão Tumoral
[Mh] Termos MeSH secundário: Proteínas E1A de Adenovirus/química
Proteínas E1A de Adenovirus/genética
Motivos de Aminoácidos
Sequência de Aminoácidos
DNA de Neoplasias/imunologia
Proteínas de Ligação a DNA/química
Proteínas de Ligação a DNA/genética
Evolução Molecular
Células HEK293
Células HeLa
Interações Hospedeiro-Patógeno
Seres Humanos
Redes e Vias Metabólicas
Dados de Sequência Molecular
Proteínas Oncogênicas Virais/química
Proteínas Oncogênicas Virais/genética
Proteína do Retinoblastoma/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adenovirus E1A Proteins); 0 (DNA, Neoplasm); 0 (DNA-Binding Proteins); 0 (E7 protein, Human papillomavirus type 18); 0 (MPYS protein, human); 0 (Membrane Proteins); 0 (Nucleotides, Cyclic); 0 (Oncogene Proteins, Viral); 0 (Retinoblastoma Protein); 0 (cyclic guanosine monophosphate-adenosine monophosphate)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:151030
[Lr] Data última revisão:
151030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150926
[St] Status:MEDLINE
[do] DOI:10.1126/science.aab3291


  3 / 119 MEDLINE  
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[PMID]:25884932
[Au] Autor:Fimereli D; Gacquer D; Fumagalli D; Salgado R; Rothé F; Larsimont D; Sotiriou C; Detours V
[Ad] Endereço:IRIBHM - Université Libre de Bruxelles, ULB, Campus Erasme CP602, 808 route de Lennik, 1070, Brussels, Belgium. dfimerel@ulb.ac.be.
[Ti] Título:No significant viral transcription detected in whole breast cancer transcriptomes.
[So] Source:BMC Cancer;15:147, 2015 Mar 18.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Studies evaluating the presence of viral sequences in breast cancer (BC), including various strains of human papillomavirus and human herpes virus, have yielded conflicting results. Most were based on RT-PCR and in situ hybridization. METHODS: In this report we searched for expressed viral sequences in 58 BC transcriptomes using five distinct in silico methods. In addition, we complemented our RNA sequencing results with exome sequencing, PCR and immunohistochemistry (IHC) analyses. A control sample was used to test our in silico methods. RESULTS: All of the computational methods correctly detected viral sequences in the control sample. We identified a small number of viral sequences belonging to human herpesvirus 4 and 6 and Merkel cell polyomavirus. The extremely low expression levels-two orders of magnitude lower than in a typical hepatitis B virus infection in hepatocellular carcinoma-did not suggest active infections. The presence of viral elements was confirmed in sample-matched exome sequences, but could not be confirmed by PCR or IHC. CONCLUSIONS: Our results show that no viral sequences are expressed in significant amounts in the BC investigated. The presence of non-transcribed viral DNA cannot be excluded.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Vírus de DNA Tumorais/genética
Transcrição Genética/genética
Transcriptoma/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Neoplasias da Mama/patologia
Feminino
Herpesvirus Humano 4/genética
Seres Humanos
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1601
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150418
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-015-1176-2


  4 / 119 MEDLINE  
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[PMID]:24781742
[Au] Autor:Doolittle JM; Webster-Cyriaque J
[Ti] Título:Polymicrobial infection and bacterium-mediated epigenetic modification of DNA tumor viruses contribute to pathogenesis.
[So] Source:MBio;5(3):e01015-14, 2014 Apr 29.
[Is] ISSN:2150-7511
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ABSTRACT The human body plays host to a wide variety of microbes, commensal and pathogenic. In addition to interacting with their host, different microbes, such as bacteria and viruses, interact with each other, sometimes in ways that exacerbate disease. In particular, gene expression of a number of viruses, including Kaposi's sarcoma-associated herpesvirus (KSHV), Epstein-Barr virus (EBV), and human immunodeficiency virus (HIV), is known to be regulated by epigenetic modifications induced by bacteria. These viruses establish latent infection in their host cells and can be reactivated by bacterial products. Viral reactivation has been suggested to contribute to periodontal disease and AIDS. In addition, bacterium-virus interactions may play a role in cancers, such as Kaposi's sarcoma, gastric cancer, and head and neck cancer. It is important to consider the effects of coexisting bacterial infections when studying viral diseases in vivo.
[Mh] Termos MeSH primário: Infecções Bacterianas/microbiologia
Coinfecção/microbiologia
Coinfecção/virologia
Vírus de DNA Tumorais/genética
Epigênese Genética
Interações Hospedeiro-Patógeno
Infecções Tumorais por Vírus/virologia
[Mh] Termos MeSH secundário: Seres Humanos
Ativação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Em] Mês de entrada:1501
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140501
[St] Status:MEDLINE


  5 / 119 MEDLINE  
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[PMID]:23686238
[Au] Autor:McFadden K; Luftig MA
[Ad] Endereço:Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710, USA.
[Ti] Título:Interplay between DNA tumor viruses and the host DNA damage response.
[So] Source:Curr Top Microbiol Immunol;371:229-57, 2013.
[Is] ISSN:0070-217X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Viruses encounter many challenges within host cells in order to replicate their nucleic acid. In the case of DNA viruses, one challenge that must be overcome is recognition of viral DNA structures by the host DNA damage response (DDR) machinery. This is accomplished in elegant and unique ways by different viruses as each has specific needs and sensitivities dependent on its life cycle. In this review, we focus on three DNA tumor viruses and their interactions with the DDR. The viruses Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV), and human papillomavirus (HPV) account for nearly all of the virus-associated human cancers worldwide. These viruses have also been excellent models for the study of oncogenic virus-mediated cell transformation. In this review, we will discuss how each of these viruses engage and subvert aspects of the host DDR. The first level of DDR engagement is a result of the genetic linkage between the oncogenic potential of these viruses and their ability to replicate. Namely, the promotion of cells from quiescence into the cell cycle to facilitate virus replication can be sensed through aberrant cellular DNA replication structures which activate the DDR and hinder cell transformation. DNA tumor viruses subvert this growth-suppressive DDR through changes in viral oncoprotein expression which ultimately facilitate virus replication. An additional level of DDR engagement is through direct detection of replicating viral DNA. These interactions parallel those observed in other DNA virus systems in that the need to subvert these intrinsic sensors of aberrant DNA structure in order to replicate must be in place. DNA tumor viruses are no exception. This review will cover the molecular features of DNA tumor virus interactions with the host DDR and the consequences for virus replication.
[Mh] Termos MeSH primário: Dano ao DNA
Vírus de DNA Tumorais/genética
Infecções Tumorais por Vírus/genética
Infecções Tumorais por Vírus/virologia
Replicação Viral/genética
[Mh] Termos MeSH secundário: Animais
Dano ao DNA/fisiologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Em] Mês de entrada:1308
[Cu] Atualização por classe:161026
[Lr] Data última revisão:
161026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130521
[St] Status:MEDLINE
[do] DOI:10.1007/978-3-642-37765-5_9


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[PMID]:21856415
[Au] Autor:Guergnon J; Godet AN; Galioot A; Falanga PB; Colle JH; Cayla X; Garcia A
[Ad] Endereço:Laboratoire E3 Phosphatases-Unité Signalisation Moléculaire et Activation Cellulaire, Institut Pasteur 25, rue du Dr Roux, 75015 Paris, France.
[Ti] Título:PP2A targeting by viral proteins: a widespread biological strategy from DNA/RNA tumor viruses to HIV-1.
[So] Source:Biochim Biophys Acta;1812(11):1498-507, 2011 Nov.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Protein phosphatase 2A (PP2A) is a large family of holoenzymes that comprises 1% of total cellular proteins and accounts for the majority of Ser/Thr phosphatase activity in eukaryotic cells. Although initially viewed as constitutive housekeeping enzymes, it is now well established that PP2A proteins represent a family of highly and sophistically regulated phosphatases. The past decade, multiple complementary studies have improved our knowledge about structural and functional regulation of PP2A holoenzymes. In this regard, after summarizing major cellular regulation, this review will mainly focus on discussing a particulate biological strategy, used by various viruses, which is based on the targeting of PP2A enzymes by viral proteins in order to specifically deregulate, for their own benefit, cellular pathways of their hosts. The impact of such PP2A targeting for research in human diseases, and in further therapeutic developments, is also discussed.
[Mh] Termos MeSH primário: Vírus de DNA Tumorais/fisiologia
HIV-1/fisiologia
Proteína Fosfatase 2/antagonistas & inibidores
Proteína Fosfatase 2/metabolismo
Retroviridae/fisiologia
Proteínas Virais/farmacologia
[Mh] Termos MeSH secundário: Seres Humanos
Transporte Proteico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Viral Proteins); EC 3.1.3.16 (Protein Phosphatase 2)
[Em] Mês de entrada:1111
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110823
[St] Status:MEDLINE
[do] DOI:10.1016/j.bbadis.2011.07.001


  7 / 119 MEDLINE  
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[PMID]:20530433
[Au] Autor:Zheng Y; Xia P; Zheng HC; Takahashi H; Masuda S; Takano Y
[Ad] Endereço:Department of Diagnostic Pathology, Graduate School of Medicine and Pharmaceutical Science, University of Toyama, Toyama, Japan.
[Ti] Título:The screening of viral risk factors in tongue and pharyngolaryngeal squamous carcinoma.
[So] Source:Anticancer Res;30(4):1233-8, 2010 Apr.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The oral cavity and pharyngolarynx is readily open to the environment, which provides a good atmosphere to viral infection and subsequently links to the local carcinogenesis. The aim of this study is to clarify the viral risk factors for tongue and pharyngolaryngeal squamous carcinomas and the oncogenic role of DNA viruses. MATERIALS AND METHODS: Tongue, pharyngeal and laryngeal carcinomas, and corresponding non-neoplastic mucosa (NNM) were collected and subjected to microdissection and DNA extraction with integrity detected by beta-globin polymerase chain reaction(PCR). Additionally, we examined genomic DNA copies of Epstein-Barr virus (EBV), human papilloma virus (HPV) 16 and 18, and John Cunningham virus (JCV) by real-time PCR with a comparison of the clinicopathological features of the tumors. RESULTS: All the extracted DNA samples showed good integrity. Compared with NNM, EBV and HPV16 copies were higher in the three kinds of head and neck carcinoma respectively (p<0.05). The same situation was also observed in tongue and pharyngeal carcinoma for HPV18, and pharyngeal carcinoma for JCV (p<0.05). There were fewer EBV copies in tongue than pharyngeal and laryngeal carcinoma (p<0.05). Pharyngeal carcinoma had a higher HPV16 copy number than tongue and laryngeal carcinoma (p<0.05). Moderately differentiated carcinoma of the head and neck had more EBV copies than well-differentiated (p<0.05). CONCLUSION: The viruses studied here might play an important role in the carcinogenesis of tongue and pharyngolaryngeal squamous carcinomas.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/virologia
Vírus de DNA Tumorais/isolamento & purificação
Neoplasias Laríngeas/virologia
Neoplasias Faríngeas/virologia
Neoplasias da Língua/virologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Linhagem Celular Tumoral
Vírus de DNA Tumorais/genética
DNA Viral/análise
DNA Viral/genética
Feminino
Herpesvirus Humano 4/genética
Herpesvirus Humano 4/isolamento & purificação
Papillomavirus Humano 16/genética
Papillomavirus Humano 16/isolamento & purificação
Seres Humanos
Vírus JC/genética
Vírus JC/isolamento & purificação
Masculino
Meia-Idade
Infecções Tumorais por Vírus/patologia
Infecções Tumorais por Vírus/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Viral)
[Em] Mês de entrada:1006
[Cu] Atualização por classe:100609
[Lr] Data última revisão:
100609
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100610
[St] Status:MEDLINE


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[PMID]:19588547
[Au] Autor:Greber UF; Puntener D
[Ad] Endereço:Institute of Zoology, University of Zürich, Switzerland.
[Ti] Título:DNA-tumor virus entry--from plasma membrane to the nucleus.
[So] Source:Semin Cell Dev Biol;20(5):631-42, 2009 Jul.
[Is] ISSN:1096-3634
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:DNA-tumor viruses comprise enveloped and non-enveloped agents that cause malignancies in a large variety of cell types and tissues by interfering with cell cycle control and immortalization. Those DNA-tumor viruses that replicate in the nucleus use cellular mechanisms to transport their genome and newly synthesized viral proteins into the nucleus. This requires cytoplasmic transport and nuclear import of their genome. Agents that employ this strategy include adenoviruses, hepadnaviruses, herpesviruses, and likely also papillomaviruses, and polyomaviruses, but not poxviruses which replicate in the cytoplasm. Here, we discuss how DNA-tumor viruses enter cells, take advantage of cytoplasmic transport, and import their DNA genome through the nuclear pore complex into the nucleus. Remarkably, nuclear import of incoming genomes does not necessarily follow the same pathways used by the structural proteins of the viruses during the replication and assembly phases of the viral life cycle. Understanding the mechanisms of DNA nuclear import can identify new pathways of cell regulation and anti-viral therapies.
[Mh] Termos MeSH primário: Membrana Celular/virologia
Núcleo Celular/virologia
Vírus de DNA Tumorais/metabolismo
Internalização do Vírus
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular
Membrana Celular/metabolismo
Núcleo Celular/metabolismo
Poro Nuclear/metabolismo
Poro Nuclear/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Mês de entrada:0909
[Cu] Atualização por classe:091027
[Lr] Data última revisão:
091027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090710
[St] Status:MEDLINE


  9 / 119 MEDLINE  
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[PMID]:19400863
[Au] Autor:Kalland KH; Ke XS; Øyan AM
[Ad] Endereço:The Gade Institute, University of Bergen, Norway.
[Ti] Título:Tumour virology--history, status and future challenges.
[So] Source:APMIS;117(5-6):382-99, 2009 May.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Viruses enter host cells in order to complete their life cycles and have evolved to exploit host cell structures, regulatory factors and mechanisms. The virus and host cell interactions have consequences at multiple levels, spanning from evolution through disease to models and tools for scientific discovery and treatment. Virus-induced human cancers arise after a long duration of time and are monoclonal or oligoclonal in origin. Cancer is therefore a side effect rather than an essential part of viral infections in humans. Still, 15-20% of all human cancers are caused by viruses. A review of tumour virology shows its close integration in cancer research. Viral tools and experimental models have been indispensible for the progress of molecular biology. In particular, retroviruses and DNA tumour viruses have played major roles in our present understanding of the molecular biology of both viruses and the host. Recently, additional complex relationships due to virus and host co-evolution have appeared and may lead to a further understanding of the overall regulation of gene expression programmes in cancer.
[Mh] Termos MeSH primário: Interações Hospedeiro-Patógeno/fisiologia
Vírus Oncogênicos/fisiologia
Infecções Tumorais por Vírus/virologia
[Mh] Termos MeSH secundário: Animais
Leucose Aviária/virologia
Evolução Biológica
Transformação Celular Neoplásica
Galinhas
Vírus de DNA Tumorais/genética
Vírus de DNA Tumorais/patogenicidade
Vírus de DNA Tumorais/fisiologia
Epigênese Genética
Regulação Neoplásica da Expressão Gênica
Regulação Viral da Expressão Gênica
Genes Virais
Seres Humanos
Mamíferos/virologia
Camundongos
Neoplasias/etiologia
Neoplasias/virologia
Oncogenes
Vírus Oncogênicos/genética
Vírus Oncogênicos/patogenicidade
Interferência de RNA
Pesquisa
Retroviridae/genética
Retroviridae/fisiologia
Infecções por Retroviridae/fisiopatologia
Infecções por Retroviridae/virologia
Infecções Tumorais por Vírus/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:0906
[Cu] Atualização por classe:101118
[Lr] Data última revisão:
101118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090430
[St] Status:MEDLINE
[do] DOI:10.1111/j.1600-0463.2009.02452.x


  10 / 119 MEDLINE  
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[PMID]:19230560
[Au] Autor:zur Hausen H; de Villiers EM
[Ad] Endereço:Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280,69120 Heidelberg, Germany. zurhausen@dkfz-heidelberg.de
[Ti] Título:TT viruses: oncogenic or tumor-suppressive properties?
[So] Source:Curr Top Microbiol Immunol;331:109-16, 2009.
[Is] ISSN:0070-217X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Torque teno (TT) viruses have been more frequently reported in malignant biopsies when compared to normal control tissue. The possible contribution of TT virus infection to human carcinogenesis or the potential oncolytic functions of these virus infections are being discussed based on available experimental evidence. The data could suggest an involvement of TT virus infections as an indirect carcinogen by modulating T cell immune responses. Significant oncolytic functions, potentially mediated by the inhibition of nuclear factor (NF)-kappaB transcription factor or by apoptin-like gene activities, are emerging to be less likely.
[Mh] Termos MeSH primário: Transformação Celular Viral
Vírus de DNA Tumorais/fisiologia
Infecções por Vírus de DNA/virologia
Neoplasias/virologia
Torque teno virus/fisiologia
Infecções Tumorais por Vírus/virologia
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:0903
[Cu] Atualização por classe:161026
[Lr] Data última revisão:
161026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090224
[St] Status:MEDLINE



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