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  1 / 13701 MEDLINE  
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[PMID]:27772622
[Au] Autor:Trofe-Clark J; Sawinski D
[Ad] Endereço:Renal Electrolyte and Hypertension Division, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA; Department of Pharmacy Services, Hospital of the University of Pennsylvania, Philadelphia, PA. Electronic address: Jennifer.trofe-clark@uphs.upenn.edu.
[Ti] Título:BK and Other Polyomaviruses in Kidney Transplantation.
[So] Source:Semin Nephrol;36(5):372-385, 2016 09.
[Is] ISSN:1558-4488
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:For more than 40 years, polyomaviruses (BK virus and JC virus) have been known to cause disease in human beings. Recently, 11 new polyomaviruses were discovered. However, the majority of these viruses are rare in renal transplant recipients and BK and JC viruses remain the most important polyomaviruses to impact this population. BK virus presents as BK virus nephropathy and has, in rare instances, been associated with hemorrhagic cystitis or ureteral strictures. JC virus can cause progressive multifocal leukoencephalopathy or nephropathy in this population as well, but is uncommon. Antiviral prophylactic and therapeutic interventions for these diseases are lacking to date, although reduction of immunosuppression has been associated with success in treating both BK virus nephropathy and JC virus-induced disease. Risk factors are not well defined and vary across studies. However, the cumulative degree of immunosuppression is regarded universally as an important contributor to BK virus replication. For these reasons, it is recommended to screen all renal transplant recipients prospectively for BK virus infection. Multicenter trials using standardized BK and JC virus screening methods are necessary to define risk factors better, and to determine the effect of prophylaxis and treatments for these polyomaviruses affecting renal transplant recipients.
[Mh] Termos MeSH primário: Rejeição de Enxerto/prevenção & controle
Imunossupressores/efeitos adversos
Falência Renal Crônica/cirurgia
Transplante de Rim
Infecções por Polyomavirus/induzido quimicamente
Infecções Tumorais por Vírus/induzido quimicamente
[Mh] Termos MeSH secundário: Antivirais/uso terapêutico
Vírus BK
Seres Humanos
Vírus JC
Polyomavirus
Infecções por Polyomavirus/diagnóstico
Infecções por Polyomavirus/tratamento farmacológico
Infecções por Polyomavirus/prevenção & controle
Infecções Tumorais por Vírus/diagnóstico
Infecções Tumorais por Vírus/tratamento farmacológico
Infecções Tumorais por Vírus/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Immunosuppressive Agents)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  2 / 13701 MEDLINE  
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Zalis, Mariano G
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[PMID]:29106916
[Au] Autor:Varella RB; Zalona ACJ; Diaz NC; Zalis MG; Santoro-Lopes G
[Ad] Endereço:Laboratory of Virology, Department of Microbiology and Parasitology, Universidade Federal Fluminense, Brazil. Electronic address: rvarella@id.uff.br.
[Ti] Título:BK polyomavirus genotypes Ia and Ib1 exhibit different biological properties in renal transplant recipients.
[So] Source:Virus Res;243:65-68, 2018 01 02.
[Is] ISSN:1872-7492
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BK polyomavirus (BKV) is an opportunist agent associated with nephropathy (BKVAN) in 1-10% of kidney transplant recipients. BKV is classified into genotypes or subgroups according to minor nucleotidic variations with unknown biological implications. Studies assessing the possible association between genotypes and the risk of BKVAN in kidney transplant patients have presented conflicting results. In these studies, genotype Ia, which is highly prevalent in Brazil, was less frequently found and, thus, comparative data on the biological properties of this genotype are lacking. In this study, BKV Ia and Ib1 genotypes were compared according to their viral load, genetic evolution (VP1 and NCCR) - in a cohort of renal transplant recipients. The patients infected with Ia (13/23; 56.5%) genotype exhibited higher viral loads in urine [>1.4 log over Ib1 (10/23; 43.5%); p=0.025]. In addition, genotype Ia was associated with diverse mutations at VP1 loops and sites under positive selection outside loops, which were totally absent in Ib1. Although the number of viremic patients was similar, the three patients who had BK nephropathy (BKVAN) were infected with Ia genotype. NCCR architecture (ww or rr) were not distinctive between Ia and Ib1 genotypes. Ia genotype, which is rare in other published BKV cohorts, presented some diverse biological properties in transplanted recipients in comparison to Ib1.
[Mh] Termos MeSH primário: Vírus BK/isolamento & purificação
Transplante de Rim/efeitos adversos
Infecções por Polyomavirus/virologia
Infecções Tumorais por Vírus/virologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Vírus BK/classificação
Vírus BK/genética
Vírus BK/fisiologia
Genótipo
Seres Humanos
Rim/cirurgia
Rim/virologia
Masculino
Meia-Idade
Filogenia
Infecções por Polyomavirus/etiologia
Transplantados/estatística & dados numéricos
Infecções Tumorais por Vírus/etiologia
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171107
[St] Status:MEDLINE


  3 / 13701 MEDLINE  
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[PMID]:27777772
[Au] Autor:Michel Ortega RM; Wolff DJ; Schandl CA; Drabkin HA
[Ad] Endereço:Division of Hematology and Oncology, Medical University of South Carolina, 173 Ashley Ave, Suite 102 BSB, Charleston, SC 29425 USA.
[Ti] Título:Urothelial carcinoma of donor origin in a kidney transplant patient.
[So] Source:J Immunother Cancer;4:63, 2016.
[Is] ISSN:2051-1426
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Malignancy after transplantation is an uncommon multifactorial occurrence. Immunosuppression to prevent graft rejection is described as a major risk factor in malignancy development in the post-transplant state. Donor-derived malignancy is a rare reported complication. Herein, we review our patient history and discuss diagnostic strategies and the implications of immunosuppression for donor-derived malignancy. CASE PRESENTATION: This is a 69-year-old man with post-renal-transplant urothelial carcinoma determined to be of donor origin. His course was complicated by BK virus at six years post-transplant; urothelial carcinoma was identified nine years post-transplant. Cystectomy was performed, but because of immunosuppression and underlying chronic kidney disease, the patient was considered ineligible for adjuvant chemotherapy. Two years after resection, screening MRI demonstrated retroperitoneal lymphadenopathy and a right upper pole mass in the transplanted kidney. Urine cytology confirmed the presence of malignant cells; FISH showed 2-8 copies of the X chromosome and no Y chromosome consistent with female origin of the malignant cells. CT-guided renal mass and paraaortic lymph node biopsies demonstrated that about 50 % of cells had an XY complement, while the remainder showed a XX genotype by chromosomal SNP microarray analysis. Immunosuppression was discontinued and the donor kidney removed. X/Y FISH of the urothelial carcinoma identified in the explanted kidney confirmed that the malignant cells were of female donor origin. Follow-up at 3, 6 and 12 months after discontinuation of immunosuppression and surgery demonstrated normalization of the lymphadenopathy and absence of new lesions. CONCLUSIONS: Immunosuppression is a major risk factor for development of malignancy in transplant recipients. Donor-derived malignancy can arise and current molecular studies allow an accurate diagnosis. Withdrawal of immunosuppression and surgical resection of the transplant kidney proved an effective treatment in our case.
[Mh] Termos MeSH primário: Transplante de Rim/efeitos adversos
Doadores de Tecidos
Neoplasias Urológicas/diagnóstico
Neoplasias Urológicas/etiologia
[Mh] Termos MeSH secundário: Idoso
Vírus BK
Aberrações Cromossômicas
Seres Humanos
Imunossupressão
Imunossupressores/efeitos adversos
Hibridização in Situ Fluorescente
Imagem por Ressonância Magnética
Masculino
Infecções por Polyomavirus/complicações
Infecções por Polyomavirus/virologia
Tomografia Computadorizada por Raios X
Transplante Homólogo
Infecções Tumorais por Vírus/complicações
Infecções Tumorais por Vírus/virologia
Neoplasias Urológicas/genética
Neoplasias Urológicas/terapia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunosuppressive Agents)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  4 / 13701 MEDLINE  
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Texto completo SciELO Brasil
[PMID]:29186254
[Au] Autor:Góes HFO; Lima CDS; Issa MCA; Luz FB; Pantaleão L; Paixão JGMD
[Ad] Endereço:Department of Dermatology, Universidade Federal Fluminense (UFF) - Niterói (RJ), Brazil.
[Ti] Título:Merkel cell carcinoma in an immunosuppressed patient.
[So] Source:An Bras Dermatol;92(3):386-388, 2017 May-Jun.
[Is] ISSN:1806-4841
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Merkel cell carcinoma is an uncommon neuroendocrine carcinoma with a rising incidence and an aggressive behavior. It predominantly occurs in older patients, with onset occurring at a mean age of 75-80 years. Recognized risk factors are ultraviolet sunlight exposure, immunosuppression, and, more recently, Merkel cell polyomavirus. We report a case of Merkel cell carcinoma in a young HIV positive patient with Merkel Cell polyomavirus detected in the tumor.
[Mh] Termos MeSH primário: Infecções Oportunistas Relacionadas com a AIDS/diagnóstico
Carcinoma de Célula de Merkel/diagnóstico
Poliomavírus das Células de Merkel
Infecções por Polyomavirus/diagnóstico
Neoplasias Cutâneas/diagnóstico
Infecções Tumorais por Vírus/diagnóstico
[Mh] Termos MeSH secundário: Infecções Oportunistas Relacionadas com a AIDS/virologia
Carcinoma de Célula de Merkel/virologia
Seres Humanos
Hospedeiro Imunocomprometido
Masculino
Meia-Idade
Neoplasias Cutâneas/virologia
[Pt] Tipo de publicação:CASE REPORTS
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE


  5 / 13701 MEDLINE  
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[PMID]:27774637
[Au] Autor:Chou TC; Tsai KB; Wu CY; Hong CH; Lee CH
[Ad] Endereço:Department of Dermatology, Cathay General Hospital, Taipei, Taiwan.
[Ti] Título:Presence of the Merkel cell polyomavirus in Merkel cell carcinoma combined with squamous cell carcinoma in a patient with chronic arsenism.
[So] Source:Clin Exp Dermatol;41(8):902-905, 2016 Dec.
[Is] ISSN:1365-2230
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We present a case of Merkel cell carcinoma (MCC) coincident with squamous cell carcinoma (SCC) on the breast of a woman with chronic arsenism. This case demonstrates the distinct association of chronic arsenism with two different primary cutaneous carcinomas. Merkel cell polyomavirus (MCPyV) was identified in the lesional skin of the MCC but not in that of the SCC, suggesting there are different interactions of MCPyV in the pathogenesis of SCC and MCC related to arsenic. Physicians need to be vigilant in the occurrence of both SCC and MCC in patients with chronic arsenism. To our knowledge, this is the first study to show the presence of MCPyV in the MCC but not the SCC portion of an arsenic-induced tumour.
[Mh] Termos MeSH primário: Arsênico/toxicidade
Doença de Bowen/induzido quimicamente
Neoplasias da Mama/virologia
Carcinoma de Célula de Merkel/virologia
Carcinoma de Células Escamosas/virologia
Poliomavírus das Células de Merkel/isolamento & purificação
Neoplasias Primárias Múltiplas/virologia
Infecções por Polyomavirus/virologia
Neoplasias Cutâneas/induzido quimicamente
Infecções Tumorais por Vírus/virologia
[Mh] Termos MeSH secundário: Idoso
Feminino
Seres Humanos
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
N712M78A8G (Arsenic)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1111/ced.12954


  6 / 13701 MEDLINE  
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[PMID]:28455138
[Au] Autor:Behdarvand A; Zamani MS; Sadeghi F; Yahyapour Y; Vaziri F; Jamnani FR; Nowruzi B; Fateh A; Siadat SD
[Ad] Endereço:Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
[Ti] Título:Evaluation of Merkel cell polyomavirus in non-small cell lung cancer and adjacent normal cells.
[So] Source:Microb Pathog;108:21-26, 2017 Jul.
[Is] ISSN:1096-1208
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Several risk factors have been linked to lung cancer (LC). Nevertheless, a viral etiology has been mentioned for a subset of patients developing LC. The aim of this study was to evaluate the effect of Merkel cell polyomavirus (MCPyV) on developing non-small cell lung cancer (NSCLCs). In total, 96 paraffin-embedded NSCLC biopsies and 96 adjacent non-LC normal specimens were analyzed by quantitative real-time polymerase chain reaction (PCR) for the existence of the MCPyV DNA and the expressions of RNA transcripts. Among the 96 enrolled participants, 42 patients were adenocarcinomas (ADs) and 54 patients were squamous cell carcinoma (SCC). Of the 42 ADs, MCPyV DNA was determined in 15 (35.7%) samples and of the 54 SCC, MCPyV DNA was detected in 22 (40.7%) samples. Only one non-cancerous sample in SCC subjects was positive for MCPyV LT-Ag DNA load (0.216 × 10 ). In MCPyV-positive subjects, the median MCPyV copy number was higher in the patients with ADs (0.016 × 10 copies/cell) compared to SCCs (0.005 × 10 copies/cell); but this difference was not statistically significant (P = 0.913). In the seven stages of LC, the MCPyV LT-Ag was quantified in stage IV (0.204 × 10 copies/cell) more than in other stages. There was statistically significant difference between stages of cancer and MCPyV LT-Ag DNA load (P = 0.002). These results revealed for the first time the presence of MCPyV in a subset of patients with NSCLCs in Iran. Further studies should be carried out to clarify the role of MCPyV in lung carcinogenesis.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/epidemiologia
Carcinoma Pulmonar de Células não Pequenas/virologia
Neoplasias Pulmonares/epidemiologia
Neoplasias Pulmonares/virologia
Poliomavírus das Células de Merkel/patogenicidade
Infecções Tumorais por Vírus/complicações
[Mh] Termos MeSH secundário: Adenocarcinoma/diagnóstico
Adenocarcinoma/epidemiologia
Adenocarcinoma/virologia
Idoso
Carcinoma Pulmonar de Células não Pequenas/diagnóstico
Carcinoma de Células Escamosas/diagnóstico
Carcinoma de Células Escamosas/epidemiologia
Carcinoma de Células Escamosas/virologia
DNA Viral/genética
DNA Viral/isolamento & purificação
Feminino
Seres Humanos
Irã (Geográfico)/epidemiologia
Neoplasias Pulmonares/diagnóstico
Masculino
Poliomavírus das Células de Merkel/genética
Meia-Idade
Prevalência
RNA Viral
Reação em Cadeia da Polimerase em Tempo Real
Fatores de Risco
Fumar
Infecções Tumorais por Vírus/genética
Infecções Tumorais por Vírus/virologia
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Viral); 0 (RNA, Viral)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


  7 / 13701 MEDLINE  
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[PMID]:29028833
[Au] Autor:Cheng J; Park DE; Berrios C; White EA; Arora R; Yoon R; Branigan T; Xiao T; Westerling T; Federation A; Zeid R; Strober B; Swanson SK; Florens L; Bradner JE; Brown M; Howley PM; Padi M; Washburn MP; DeCaprio JA
[Ad] Endereço:Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, United States of America.
[Ti] Título:Merkel cell polyomavirus recruits MYCL to the EP400 complex to promote oncogenesis.
[So] Source:PLoS Pathog;13(10):e1006668, 2017 Oct.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Merkel cell carcinoma (MCC) frequently contains integrated copies of Merkel cell polyomavirus DNA that express a truncated form of Large T antigen (LT) and an intact Small T antigen (ST). While LT binds RB and inactivates its tumor suppressor function, it is less clear how ST contributes to MCC tumorigenesis. Here we show that ST binds specifically to the MYC homolog MYCL (L-MYC) and recruits it to the 15-component EP400 histone acetyltransferase and chromatin remodeling complex. We performed a large-scale immunoprecipitation for ST and identified co-precipitating proteins by mass spectrometry. In addition to protein phosphatase 2A (PP2A) subunits, we identified MYCL and its heterodimeric partner MAX plus the EP400 complex. Immunoprecipitation for MAX and EP400 complex components confirmed their association with ST. We determined that the ST-MYCL-EP400 complex binds together to specific gene promoters and activates their expression by integrating chromatin immunoprecipitation with sequencing (ChIP-seq) and RNA-seq. MYCL and EP400 were required for maintenance of cell viability and cooperated with ST to promote gene expression in MCC cell lines. A genome-wide CRISPR-Cas9 screen confirmed the requirement for MYCL and EP400 in MCPyV-positive MCC cell lines. We demonstrate that ST can activate gene expression in a EP400 and MYCL dependent manner and this activity contributes to cellular transformation and generation of induced pluripotent stem cells.
[Mh] Termos MeSH primário: Antígenos Virais de Tumores/metabolismo
Carcinoma de Célula de Merkel/virologia
Transformação Celular Viral/fisiologia
DNA Helicases/metabolismo
Proteínas de Ligação a DNA/metabolismo
Regulação Neoplásica da Expressão Gênica/fisiologia
Proteínas Proto-Oncogênicas c-myc/metabolismo
[Mh] Termos MeSH secundário: Antígenos Transformantes de Poliomavirus/metabolismo
Carcinoma de Célula de Merkel/genética
Carcinoma de Célula de Merkel/metabolismo
Linhagem Celular Tumoral
Seres Humanos
Immunoblotting
Imunoprecipitação
Poliomavírus das Células de Merkel
Infecções por Polyomavirus/complicações
Infecções por Polyomavirus/genética
Infecções por Polyomavirus/metabolismo
Infecções Tumorais por Vírus/complicações
Infecções Tumorais por Vírus/genética
Infecções Tumorais por Vírus/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Polyomavirus Transforming); 0 (Antigens, Viral, Tumor); 0 (DNA-Binding Proteins); 0 (MYCL1 protein, human); 0 (Proto-Oncogene Proteins c-myc); EC 3.6.4.- (DNA Helicases); EC 3.6.4.12 (EP400 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006668


  8 / 13701 MEDLINE  
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[PMID]:28794032
[Au] Autor:Bamunusinghe D; Liu Q; Plishka R; Dolan MA; Skorski M; Oler AJ; Yedavalli VRK; Buckler-White A; Hartley JW; Kozak CA
[Ad] Endereço:Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA.
[Ti] Título:Recombinant Origins of Pathogenic and Nonpathogenic Mouse Gammaretroviruses with Polytropic Host Range.
[So] Source:J Virol;91(21), 2017 Nov 01.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ecotropic, xenotropic, and polytropic mouse leukemia viruses (E-, X-, and P-MLVs) exist in mice as infectious viruses and endogenous retroviruses (ERVs) inserted into mouse chromosomes. All three MLV subgroups are linked to leukemogenesis, which involves generation of recombinants with polytropic host range. Although P-MLVs are deemed to be the proximal agents of disease induction, few biologically characterized infectious P-MLVs have been sequenced for comparative analysis. We analyzed the complete genomes of 16 naturally occurring infectious P-MLVs, 12 of which were typed for pathogenic potential. We sought to identify ERV progenitors, recombinational hot spots, and segments that are always replaced, never replaced, or linked to pathogenesis or host range. Each P-MLV has an E-MLV backbone with P- or X-ERV replacements that together cover 100% of the recombinant genomes, with different substitution patterns for X- and P-ERVs. Two segments are always replaced, both coding for envelope (Env) protein segments: the N terminus of the surface subunit and the cytoplasmic tail R peptide. Viral gene replacements are influenced by host restriction genes and Pathogenic potential maps to the transmembrane subunit segment encoding the N-heptad repeat (HR1). Molecular dynamics simulations identified three novel interdomain salt bridges in the lymphomagenic virus HR1 that could affect structural stability, entry or sensitivity to host immune responses. The long terminal repeats of lymphomagenic P-MLVs are differentially altered by recombinations, duplications, or mutations. This analysis of the naturally occurring, sometimes pathogenic P-MLV recombinants defines the limits and extent of intersubgroup recombination and identifies specific sequence changes linked to pathogenesis and host interactions. During virus-induced leukemogenesis, ecotropic mouse leukemia viruses (MLVs) recombine with nonecotropic endogenous retroviruses (ERVs) to produce polytropic MLVs (P-MLVs). Analysis of 16 P-MLV genomes identified two segments consistently replaced: one at the envelope N terminus that alters receptor choice and one in the R peptide at the envelope C terminus, which is removed during virus assembly. Genome-wide analysis shows that nonecotropic replacements in the progenitor ecotropic MLV genome are more extensive than previously appreciated, covering 100% of the genome; contributions from xenotropic and polytropic ERVs differentially alter the regions responsible for receptor determination or subject to APOBEC3 and Fv1 restriction. All pathogenic viruses had modifications in the regulatory elements in their long terminal repeats and differed in a helical segment of envelope involved in entry and targeted by the host immune system. Virus-induced leukemogenesis thus involves generation of complex recombinants, and specific replacements are linked to pathogenesis and host restrictions.
[Mh] Termos MeSH primário: Especificidade de Hospedeiro/genética
Vírus da Leucemia Murina/classificação
Vírus da Leucemia Murina/patogenicidade
Leucemia Experimental/virologia
Infecções por Retroviridae/virologia
Infecções Tumorais por Vírus/virologia
Proteínas Virais/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência de Bases
Evolução Molecular
Genoma Viral
Vírus da Leucemia Murina/genética
Camundongos
Simulação de Dinâmica Molecular
Conformação Proteica
Receptores Virais/genética
Receptores Virais/metabolismo
Homologia de Sequência
Sequências Repetidas Terminais
Proteínas Virais/química
Proteínas Virais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Virus); 0 (Viral Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE


  9 / 13701 MEDLINE  
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[PMID]:28763479
[Au] Autor:Haymerle G; Janik S; Fochtmann A; Pammer J; Schachner H; Nemec L; Mildner M; Houben R; Grasl MC; Erovic BM
[Ad] Endereço:Department of Otolaryngology Head and Neck Surgery, Medical University of Vienna, Vienna, Austria.
[Ti] Título:Expression of Merkelcell polyomavirus (MCPyV) large T-antigen in Merkel cell carcinoma lymph node metastases predicts poor outcome.
[So] Source:PLoS One;12(8):e0180426, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The aim of this study was to determine the prevalence of MCPyV in Merkel cell carcinoma (MCC) primaries versus lymph node metastasis and to evaluate possible prognostic factors. METHODS: Samples of MCC primaries and lymph node metastases were stained immunohistochemically for the MCPyV large T-antigen and expression was compared to patients´ clinical outcome. RESULTS: 41 MCC patients were included. 33 (61%) out of 54 specimens were MCPyV-positive in the immunohistochemistry. 15 (47%) out of 32 primary tumors were positive compared to 18 (82%) out of 22 lymph node metastases. Eleven patients with positive polyomavirus expression died from the carcinoma compared to 4 patients without virus expression. Cox regression analysis showed worse disease-free survival in patients with MCPyV compared to virus-negative lymph nodes (p = 0.002). CONCLUSIONS: To our knowledge this is the first study to describe a negative prognostic effect of the MCPyV expression in lymph node metastasis in MCC patients.
[Mh] Termos MeSH primário: Antígenos Virais de Tumores/metabolismo
Carcinoma de Célula de Merkel/patologia
Infecções por Polyomavirus/patologia
Neoplasias Cutâneas/patologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Carcinoma de Célula de Merkel/virologia
Intervalo Livre de Doença
Feminino
Regulação Neoplásica da Expressão Gênica
Regulação Viral da Expressão Gênica
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Metástase Linfática
Masculino
Poliomavírus das Células de Merkel/genética
Meia-Idade
Polyomavirus/genética
Prevalência
Prognóstico
Modelos de Riscos Proporcionais
Neoplasias Cutâneas/virologia
Resultado do Tratamento
Infecções Tumorais por Vírus/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Viral, Tumor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180426


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[PMID]:28640744
[Au] Autor:Moens U; Calvignac-Spencer S; Lauber C; Ramqvist T; Feltkamp MCW; Daugherty MD; Verschoor EJ; Ehlers B; Ictv Report Consortium
[Ad] Endereço:1​University of Tromsø, 9037 Tromsø, Norway.
[Ti] Título:ICTV Virus Taxonomy Profile: Polyomaviridae.
[So] Source:J Gen Virol;98(6):1159-1160, 2017 Jun.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The Polyomaviridae is a family of small, non-enveloped viruses with circular dsDNA genomes of approximately 5 kbp. The family includes four genera whose members have restricted host range, infecting mammals and birds. Polyomavirus genomes have also been detected recently in fish. Merkel cell polyomavirus and raccoon polyomavirus are associated with cancer in their host; other members are human and veterinary pathogens. Clinical manifestations are obvious in immunocompromised patients but not in healthy individuals. This is a summary of the International Committee on Taxonomy of Viruses (ICTV) Report on the taxonomy of the Polyomaviridae, which is available at www.ictv.global/report/polyomaviridae.
[Mh] Termos MeSH primário: Polyomaviridae/classificação
Polyomaviridae/genética
Infecções por Polyomavirus/veterinária
Infecções por Polyomavirus/virologia
Infecções Tumorais por Vírus/veterinária
Infecções Tumorais por Vírus/virologia
[Mh] Termos MeSH secundário: Animais
Aves
Peixes
Seres Humanos
Mamíferos
Infecções por Polyomavirus/complicações
Infecções por Polyomavirus/patologia
Infecções Tumorais por Vírus/complicações
Infecções Tumorais por Vírus/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000839



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