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Id: biblio-1020958
Autor: Yin, Jiaoyang; Ma, Yegang; Vogel, Ulla; Wang, Chunhong; Zhang, Ying; Wang, Huiwen.
Título: Methylation status of the PPP1R13L promoter region among lung cancer patients and healthy controls. Analytical cross-sectional study
Fonte: Säo Paulo med. j;137(3):255-261, May-June 2019. tab, graf.
Idioma: en.
Projeto: National Natural Science Foundation of China.
Resumo: ABSTRACT BACKGROUND: There is evidence that genetic predisposition and epigenetic alteration (e.g. DNA methylation) play major roles in lung cancer. In our genetic epidemiological studies, rs1970764 in oncogene PPP1R13L was most consistently associated with lung cancer risk. Here, we explored the role of PPP1R13L methylation in lung cancer development. DESIGN AND SETTING: Analytical cross-sectional study (45 lung cancer cases and 45 controls), conducted in China. METHODS: We investigated the DNA methylation status of 2,160 cytosine-phosphate-guanine (CpG) sites in the PPP1R13L promoter region using the EpiTYPER assay of the Sequenom MassARRAY platform. RESULTS: In the whole study group, the methylation levels of CpG-6, CpG-9, CpG-20 and CpG-21 were significantly lower and those of CpG-16 were significantly higher in cases than in controls. Among smokers, the methylation levels at five CpG sites (CpG-6, CpG-11, CpG-15, CpG-20 and CpG-21) were statistically significantly lower among cases. Among men, the methylation levels at four CpG sites (CpG-11, CpG-15, CpG-20 and CpG-21) were significantly lower among cases. Regarding smokers, the methylation levels at CpG-7.8 and CpG-21 among cases and at CpG-22 among controls were significantly lower, compared with nonsmokers. The frequency of positivity for methylation was not significantly different between lung cancer cases and controls (68.22% for cases and 71.87% for controls; P = 0.119). CONCLUSION: Our study on a Chinese population suggests that lung cancer patients have aberrant methylation status (hypomethylation tended to be more frequent) in peripheral blood leukocytes at several CpG sites in the PPP1R13L promoter region and that exposure to smoking may influence methylation status.
Descritores: Proteínas Repressoras/genética
Metilação de DNA/genética
Predisposição Genética para Doença/genética
Peptídeos e Proteínas de Sinalização Intracelular/genética
Neoplasias Pulmonares/genética
-Estudos de Casos e Controles
Estudos Transversais
Regiões Promotoras Genéticas
Limites: Humanos
Masculino
Feminino
Pessoa de Meia-Idade
Idoso
Responsável: BR1.1 - BIREME


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Id: biblio-1048187
Autor: Jiménez-Guillen, Doribet; Pérez-Pascual, Daniel; Souza-Perera, Ramón; Godoy-Hernández, Gregorio; Zúñiga-Aguilar, José Juan.
Título: Cloning of the Coffea canephora SERK1 promoter and its molecular analysis during the cell-to-embryo transition
Fonte: Electron. j. biotechnol;36:34-46, nov. 2018. tab, ilus.
Idioma: en.
Projeto: Consejo Nacional de Ciencia y Tecnología; . Comisión Intersecretarial de Bioseguridad de los Organismos Genéticamente Modificados; . DJG and DPP received CONACYT Ph.D..
Resumo: Background: Somatic embryogenesis receptor-like kinase 1 (SERK1) is a cell membrane receptor active in different plant tissues and involved in cell differentiation activities including somatic embryogenesis. The identification of promoter elements responsible for SERK1 expression during the onset of somatic embryogenesis can be useful to understand the molecular regulation of the cell-to embryo transition, and these promoter elements represent biotechnological tools in plant organ tissue culture. Results: A −1,620 bp DNA sequence located upstream of the Coffea canephora SERK1 gene homologue (CcSERK1) was isolated, and then, different segments containing key response elements (REs) for somatic embryogenesis onset and development were fused to the uidA (encoding a ß-glucuronidase, GUS) reporter gene to evaluate its expression in transgenic leaf explants. DNA segments of −1,620 and −1048 bp in length directed uidA expression with patterns in leaf explants similar to those occurring during somatic embryogenesis. When a −792-bp fragment was used, uidA expression disappeared only in leaf explants and pro-embryogenic mass but persisted in developing embryos. No uidA expression was detected in any embryogenic stage when a −618-bp fragment was used. Conclusion: DNA deletions showed that a −1048-bp sequence located upstream of the CcSERK1 gene is sufficient to direct gene expression during the onset and the development of C. canephora somatic embryogenesis. The DNA segment located between −1048 and −792 bp (containing BBM and WUS REs) is needed for gene expression before embryogenesis onset but not during embryo development. The promoter segment between −792 and −618 bp (including GATA, ARR1AT, and ANT REs) regulates gene expression in developing embryos.
Descritores: Proteínas de Plantas/genética
Proteínas Quinases/genética
Coffea/genética
-Biotecnologia
Expressão Gênica
Regiões Promotoras Genéticas
Plantas Geneticamente Modificadas
Clonagem Molecular
Genes Reporter
Regulação da Expressão Gênica de Plantas
Desenvolvimento Embrionário
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1253093
Autor: Umer, Noroza; Zahra Naqvi, Rubab; Rauf, Imran; Anjum, Naveed; Keen, Patricia R; Van Eck, Joyce; Jander, Georg; Asif, Muhammad.
Título: Expression of Pinellia ternata leaf agglutinin under rolC promoter confers resistance against a phytophagous sap sucking aphid, Myzus persicae
Fonte: Electron. j. biotechnol;47:72-82, sept. 2020. tab, ilus, graf.
Idioma: en.
Projeto: International Research Support Initiative Program of Higher Education Commission (HEC) of; . Pakistan; . United States Department of Agriculture (USDA).
Resumo: BACKGROUND: Piercing/sucking insect pests in the order Hemiptera causes substantial crop losses by removing photoassimilates and transmitting viruses to their host plants. Cloning and heterologous expression of plantderived insect resistance genes is a promising approach to control aphids and other sap-sucking insect pests. While expression from the constitutive 35S promoter provides broad protection, the phloem-specific rolC promoter provides better defense against sap sucking insects. The selection of plant-derived insect resistance genes for expression in crop species will minimize bio-safety concerns. RESULTS: Pinellia ternata leaf agglutinin gene (pta), encodes an insecticidal lectin, was isolated and cloned under the 35S and rolC promoters in the pGA482 plant transformation vector for Agrobacterium-mediated tobacco transformation. Integration and expression of the transgene was validated by Southern blotting and qRT-PCR, respectively. Insect bioassays data of transgenic tobacco plants showed that expression of pta under rolC promoter caused 100% aphid mortality and reduced aphid fecundity up to 70% in transgenic tobacco line LRP9. These results highlight the better effectivity of pta under rolC promoter to control phloem feeders, aphids. CONCLUSIONS: These findings suggested the potential of PTA against aphids and other sap sucking insect pests. Evaluation of gene in tobacco under two different promoters; 35S constitutive promoter and rolC phloemspecific promoter could be successfully use for other crop plants particularly in cotton. Development of transgenic cotton plants using plant-derived insecticidal, PTA, would be key step towards commercialization of environmentally safe insect-resistant crops.
Descritores: Afídeos/patogenicidade
Controle Biológico de Vetores
Pinellia/química
-Vírus de Plantas
Tabaco
Southern Blotting
Reação em Cadeia da Polimerase
Regiões Promotoras Genéticas
Plantas Geneticamente Modificadas
Folhas de Planta/química
Transgenes
Resistência à Doença
Proteção de Cultivos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-974952
Autor: Ribeiro, Aline Lopes; Caodaglio, Amanda Schiersner; Sichero, Laura.
Título: Regulation of HPV transcription
Fonte: Clinics;73(supl.1):e486s, 2018. graf.
Idioma: en.
Resumo: Human papillomavirus infection is associated with the development of malignant and benign neoplasms. Approximately 40 viral types can infect the anogenital mucosa and are categorized into high- and low-risk oncogenic human papillomavirus, depending on their association with the development of cervical carcinoma. High-risk human papillomavirus 16 and 18 are detected in 55% and 15% of all invasive cervical squamous cell carcinomas worldwide, respectively. Low-risk human papillomavirus 6 and 11 are responsible for 90% of genital warts and are also associated with the development of recurrent respiratory papillomatosis. Human papillomavirus preferentially infects mitotic active cells of the basal layer from both mucosal and cutaneous epithelium through microabrasions. The viral life cycle synchronizes with the epithelial differentiation program, which may be due, in part, to the binding of differentially expressed cellular transcription factors to the long control region throughout the various epithelial layers. This review aimed to summarize the current knowledge regarding the mechanisms by which viral gene expression is regulated and the influence of human papillomavirus heterogeneity upon this phenomenon. A better understanding of the regulatory mechanisms may elucidate the particularities of human papillomavirus-associated pathogenesis and may provide new tools for antiviral therapy.
Descritores: Papillomaviridae/genética
Fatores de Transcrição/genética
Regulação Viral da Expressão Gênica
Infecções por Papillomavirus/virologia
-Papillomaviridae/fisiologia
Proteínas Oncogênicas Virais/genética
Regiões Promotoras Genéticas/genética
Limites: Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Id: biblio-989638
Autor: Wang, Changyi; Xu, Guodong; Wen, Qi; Peng, Xiaolin; Chen, Hongen; Zhang, Jingwen; Xu, Shan; Zhang, Chunhui; Zhang, Min; Ma, Jianping; Hui, Zhaohui; Wu, Guifu; Ma, Min.
Título: CBS promoter hypermethylation increases the risk of hypertension and stroke
Fonte: Clinics;74:e630, 2019. tab, graf.
Idioma: en.
Projeto: China Postdoctoral Science Foundation; . Natural Science Foundation of Guangdong Province, China; . Shenzhen Science and Technology Innovation Committee; . SanMing Project of Medicine in Shenzhen; . The fourth batch of TCM clinical Outstanding talent program of China; . Health and Family Planning Commission of Shenzhen Municipality; . National Natural Science Foundation of China; . Project of Science and Technology Innovation for College Students in Zhejiang Province.
Resumo: OBJECTIVES: Cystathionine β-synthase is a major enzyme in the metabolism of plasma homocysteine. Hyperhomocysteinemia is positively associated with hypertension and stroke. The present study was performed to examine the possible effects of Cystathionine β-synthase promoter methylation on the development of hypertension and stroke. METHODS: Using quantitative methylation-specific PCR, we determined the Cystathionine β-synthase methylation levels in 218 healthy individuals and 132 and 243 age- and gender-matched stroke and hypertensive patients, respectively. The relative changes in Cystathionine β-synthase promoter methylation were analyzed using the 2-ΔΔCt method. The percent of the methylated reference of Cystathionine β-synthase was used to represent the Cystathionine β-synthase promoter methylation levels. RESULTS: In this study, the Cystathionine β-synthase promoter methylation levels of hypertensive and stroke participants were both higher than that of the healthy individuals (median percentages of the methylated reference were 50.61%, 38.05% and 30.53%, respectively, all p<0.001). Multivariable analysis showed that Cystathionine β-synthase promoter hypermethylation increased the risk of hypertension [odds ratio, OR (95% confidence interval, CI)=1.035 (1.025-1.045)] and stroke [OR (95% CI)=1.015 (1.003-1.028)]. The area under the curve of Cystathionine β-synthase promoter methylation was 0.844 (95% CI: 0.796-0.892) in male patients with hypertension and 0.722 (95% CI: 0.653-0.799) in male patients with stroke. CONCLUSION: Cystathionine β-synthase promoter hypermethylation increases the risk of hypertension and stroke, especially in male patients.
Descritores: Regiões Promotoras Genéticas
Metilação de DNA
Acidente Vascular Cerebral/enzimologia
Cistationina beta-Sintase/metabolismo
Hipertensão/enzimologia
-Biomarcadores/metabolismo
Estudos de Casos e Controles
Fatores Sexuais
Fatores Etários
Medição de Risco
Grupo com Ancestrais do Continente Asiático/genética
Homocisteína/metabolismo
Limites: Humanos
Masculino
Feminino
Adulto
Pessoa de Meia-Idade
Idoso
Responsável: BR1.1 - BIREME


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Id: biblio-950787
Autor: Song, Bin; Bian, Qi; Shao, Cheng-Hao; Liu, An-An; Jing, Wei; Liu, Rui; Zhang, Yi-Jie; Zhou, Ying-Qi; Li, Gang; Jin, Gang.
Título: Sox2 function as a negative regulator to control HAMP expression
Fonte: Biol. Res;48:1-8, 2015. graf.
Idioma: en.
Projeto: Shanghai Municipal Natural Science Foundation.
Resumo: BACKGROUND: Hepcidin, encoding by HAMP gene, is the pivotal regulator of iron metabolism, controlling the systemic absorption and transportation of irons from intracellular stores. Abnormal levels of HAMP expression alter plasma iron parameters and lead to iron metabolism disorders. Therefore,itis animportant goal to understand the mechanisms controlling HAMP gene expression. RESULTS: Overexpression of Sox2 decrease basal expression of HAMP or induced by IL-6 or BMP-2, whereas, knockdown of Sox2 can increase HAMP expression, furthermore, two potential Sox2-binding sites were identified within the human HAMP promoter. Indeed, luciferase experiments demonstrated that deletion of any Sox2-binding site impaired the negative regulation of Sox2 on HAMP promoter transcriptional activity in basal conditions. ChIP experiments showed that Sox2 could directly bind to these sites. Finally, we verified the role of Sox2 to negatively regulate HAMP expression in human primary hepatocytes. CONCLUSION: We found that Sox2 as a novel factor to bind with HAMP promoter to negatively regulate HAMP expression, which may be further implicated as a therapeutic option for the amelioration of HAMP-overexpression-related diseases, including iron deficiency anemia.
Descritores: Regulação Neoplásica da Expressão Gênica/genética
Hepatócitos/metabolismo
Fatores de Transcrição SOXB1/genética
Hepcidinas/genética
-Plasmídeos/genética
Sítios de Ligação
Interleucina-6/metabolismo
Regiões Promotoras Genéticas/genética
Proteína Morfogenética Óssea 2/metabolismo
Fatores de Transcrição SOXB1/metabolismo
Técnicas de Silenciamento de Genes
Células Hep G2
Hepcidinas/metabolismo
Vetores Genéticos
Anemia/genética
Anemia/metabolismo
Ferro/metabolismo
Luciferases
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


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Carvalho, Maria da Glória da Costa
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Id: biblio-950814
Autor: Almeida, Fabiana Greyce Oliveira; Aquino, Priscila Ferreira de; Souza, Afonso Duarte Leäo de; Souza, Antonia Queiroz Lima de; Vinhote, Sonia do Carmo; Mac-Cormick, Thais Messias; Silva, Marcelo Soares da Mota; Chalub, Sidney Raimundo Silva; Fischer, Juliana de Saldanha da Gama; Carvalho, Paulo Costa; Carvalho, Maria da Gloria da Costa.
Título: Colorectal cancer DNA methylation patterns from patients in Manaus, Brazil
Fonte: Biol. Res;48:1-6, 2015. ilus, tab.
Idioma: en.
Resumo: BACKGROUND: DNA methylation is commonly linked with the silencing of the gene expression for many tumor suppressor genes. As such, determining DNA methylation patterns should aid, in times to come, in the diagnosis and personal treatment for various types of cancers. Here, we analyzed the methylation pattern from five colorectal cancer patients from the Amazon state in Brazil for four tumor suppressor genes, viz.: DAPK, CDH1, CDKN2A, and TIMP2 by employing a polymerase chain reaction (PCR) specific to methylation. Efforts in the study of colorectal cancer are fundamental as it is the third most of highest incidence in the world. RESULTS: Tumor biopsies were methylated in 1/5 (20 %), 2/5 (40 %), 4/5 (80 %), and 4/5 (80 %) for CDH1, CDKN2A, DAPK, and TIMP2 genes, respectively. The margin biopsies were methylated in 3/7 (43 %), 2/7 (28 %), 7/7 (100 %), and 6/7 (86 %) for CDH1, CDKN2A, DAPK, and TIMP2, respectively. CONCLUSIONS: Our findings showed DAPK and TIMP2 to be methylated in most samples from both tumor tissues and adjacent non-neoplastic margins; thus presenting distinct methylation patterns. This emphasizes the importance of better understanding of the relation of these patterns with cancer in the context of different populations.
Descritores: Neoplasias Colorretais/genética
Genes Supressores de Tumor
Metilação de DNA/genética
-Brasil
Reação em Cadeia da Polimerase
Regiões Promotoras Genéticas
Inativação Gênica
Limites: Humanos
Masculino
Feminino
Adulto
Pessoa de Meia-Idade
Idoso
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


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Id: lil-794563
Autor: Zuo, Hong-Peng; Guo, Ying-Yu; Che, Lin; Wu, Xian-Zheng.
Título: Hypomethylation of Interleukin-6 Promoter is Associated with the Risk of Coronary Heart Disease / Hipometilação do Promotor de Interleucina-6 Associada com Risco de Doença Arterial Coronariana
Fonte: Arq. bras. cardiol;107(2):131-136, Aug. 2016. tab, graf.
Idioma: en.
Resumo: Abstract Background: Interleukin-6 (IL-6) is implicated in the pathogenesis of coronary heart disease (CHD), and IL-6 expression has associated with reduced DNA methylation of its gene promoter. However, there are no data on IL-6 promoter methylation and the risk of CHD. Objective: To examine whether IL-6 promoter methylation measured in blood leukocyte DNA is associated with CHD risk. Methods: A total of 212 cases with CHD and 218 controls were enrolled. Methylation at two CpG sites in IL-6 promoter was measured by bisulfite pyrosequencing, and the mean IL-6 methylation was calculated by averaging the methylation measures of the two CpGs. Results: Mean methylation level in IL-6 promoter in CHD cases was significantly lower than that in controls (p = 0.023). Logistic regression analysis showed that IL-6 methylation was inversely associated with the risk of CHD. The odds ratios (ORs) of CHD for subjects in the second and first (lowest) tertile of IL-6 methylation were 1.87 (95% CI = 1.10‑3.20) and 2.01 (95% CI = 1.19-3.38) (ptrend = 0.013), respectively, compared to subjects in the third (highest) tertile. The IL-6 hypomethylation-related risk estimates tended to be stronger for acute myocardial infarction (ptrend = 0.006). CpG position-specific analysis showed that hypomethylation of position 1 conferred a more pronounced increase in CHD risk than that of position 2. Conclusion: These findings suggest that DNA hypomethylation of IL-6 promoter is associated with the increased risk for CHD, especially for acute myocardial infarction. The two distinct CpGs in IL-6 may contribute differently to the development of CHD.

Resumo Fundamento: Interleucina-6 (IL-6) está implicada na patogênese de doença arterial coronariana (DAC), sendo sua expressão associada com redução da metilação de DNA do promotor do seu gene. Entretanto, não há dados sobre metilação do promotor de IL-6 e risco de DAC. Objetivo: Verificar se a metilação do promotor de IL-6 medida no DNA de leucócitos sanguíneos acha-se associada com risco de DAC. Métodos: este estudo arrolou 212 casos com DAC e 218 controles. Metilação em dois sítios de CpG no promotor de IL-6 foi medida por pirosequenciamento de bissulfito, sendo a metilação média de IL-6 calculada pela média das medidas de metilação dos dois CpGs. Resultados: A média do nível de metilação no promotor de IL-6 nos casos de DAC foi significativamente mais baixa do que nos controles (p = 0,023). Análise de regressão logística mostrou associação inversa entre metilação de IL-6 e risco de DAC. As razões de chance (OR) de DAC para indivíduos no segundo e no primeiro (mais baixo) tercis de metilação de IL-6 foram 1,87 (IC 95%: 1,10-3,20) e 2,01 (IC 95%: 1,19-3,38) (ptrend = 0,013), respectivamente, comparadas à de indivíduos no terceiro (mais alto) tercil. As estimativas de risco relacionado à hipometilação de IL-6 tenderam a ser mais fortes para infarto agudo do miocárdio (ptrend = 0,006). Análise com especificidade de posição de CpG mostrou que hipometilação na posição 1 conferiu maior elevação no risco de DAC do que na posição 2. Conclusão: Tais achados sugerem que a hipometilação de DNA do promotor de IL-6 está associada com elevado risco de DAC, especialmente para infarto agudo do miocárdio. Os dois CpGs distintos no promotor de IL-6 podem contribuir de modo diferente para o desenvolvimento de DAC.
Descritores: Interleucina-6/genética
Regiões Promotoras Genéticas
Ilhas de CpG
Metilação de DNA
Doença das Coronárias/genética
Predisposição Genética para Doença/genética
-Interleucina-6/metabolismo
Análise de Sequência de DNA
Angina Instável/genética
Infarto do Miocárdio/genética
Limites: Humanos
Masculino
Feminino
Idoso
Responsável: BR1.1 - BIREME


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Id: biblio-1019497
Autor: Yang, Ju-Hong; Lin, Lie-Kun; Zhang, Song.
Título: Effects of DACT1 methylation status on invasion and metastasis of nasopharyngeal carcinoma
Fonte: Biol. Res;52:31, 2019. graf.
Idioma: en.
Projeto: Shenzhen Medical Research Project funding.
Resumo: BACKGROUND: The purpose of the present study was to investigate the role of the methylation status of the DACT1 gene on the invasion and metastasis of nasopharyngeal carcinoma cells. METHODS: The levels of methylation and expression of the DACT1 gene in nasopharyngeal carcinoma tissues and CNE2 cells were determined by methylation-specific PCR and RT-PCR, respectively. CNE2 cells were treated with 5-aza-2-deoxycytidine, and the variation in the methylation status of the DACT1 gene was detected, as well as the influence of methylation on invasiveness of nasopharyngeal carcinoma cells. RESULTS: The DACT1 gene was hyper-methylated in 44 of 62 cases of nasopharyngeal carcinoma. The DACT1 gene was hyper-methylated in 32 of 38 cases of nasopharyngeal carcinoma with lymph node metastasis, and the DACT1 gene was hyper-methylated in 7 of 24 cases of nasopharyngeal carcinoma without lymph node metastasis. The DACT1 mRNA level was weakly expressed or not expressed in all nasopharyngeal carcinoma tissues with hyper-methylated DACT1 genes; however, the DACT1 mRNA level was highly expressed in nasopharyngeal carcinoma tissues with low expression of the methylated DACT1 gene. The DACT1 gene was hyper-methylated and not expressed in CNE2 cells that did not have 5-aza-2-deoxycytidine treatment. After 5-aza-2-deoxycytidine treatment, the DACT1 gene was demethylated and the expression of DACT1 was restored. Moreover, the invasion ability was inhibited in CNE2 cells treated with 5-aza-2-deoxycytidine. CONCLUSION: The expression of DACT1 was related to the methylation status. High expression of DACT1 may inhibit the invasion and metastasis of nasopharyngeal carcinoma cells.
Descritores: Proteínas Nucleares/genética
Neoplasias Nasofaríngeas/patologia
Metilação de DNA/genética
Proteínas Adaptadoras de Transdução de Sinal/genética
Carcinoma Nasofaríngeo/secundário
-Proteínas Nucleares/metabolismo
Neoplasias Nasofaríngeas/genética
Regiões Promotoras Genéticas
Metilação de DNA/fisiologia
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Carcinoma Nasofaríngeo/genética
Invasividade Neoplásica
Proteínas de Neoplasias/metabolismo
Limites: Humanos
Masculino
Feminino
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1089306
Autor: Wang, Changyuan; Wei, Li; Chu, Weilin; Yu, Haiyang; Yu, Xinjuan; Li, Chunxia.
Título: Correlation of interleukin-18 gene polymorphism with the susceptibility of condyloma acuminatum in Chinese population
Fonte: Braz. j. infect. dis;23(6):388-394, Nov.-Dec. 2019. tab, graf.
Idioma: en.
Resumo: ABSTRACT Host immunogenetic setting is involved in the regulation of human papillomavirus (HPV) infection and development of condyloma acuminatum (CA). We investigated the correlation of two common single nucleotide polymorphisms (SNPs) (−607C/A and −137G/C) of IL-18 with the susceptibility of CA in a large Chinese cohort. Out of 408 CA patients analyzed, 300 had HPV infection transmitted through sexual contact (SC) and 108 through non-sexual contact (NSC). In addition, 360 healthy volunteers were enrolled as controls. SNPs at positions −607C/A and −137G/C in IL-18 promoter were analyzed. Comparing CA patients to healthy controls, no dominant relevance was found between the IL-18 promoter −607 C/A or −137G/C polymorphisms and the CA disease either identified genotypically (p > 0.05) or by allelically (p > 0.05). However, the IL-18 promoter −137G/C polymorphism genotype and allele frequencies in the NSC CA group, but not between in the SC group, were significantly higher than in the controls. There was no dominant relevance between IL-18-607C/A polymorphism genotype and allele frequencies among SC, NSC CA patients, and controls. Our study demonstrates that polymorphism −137G/C in IL-18 promoter is significantly correlated with risk of CA in NSC patients.
Descritores: Condiloma Acuminado/genética
Interleucina-18/genética
Polimorfismo de Nucleotídeo Único/genética
Infecções por Papillomavirus/complicações
-Polimorfismo Genético
Condiloma Acuminado/virologia
China
Estudos de Coortes
Regiões Promotoras Genéticas
Predisposição Genética para Doença
Infecções por Papillomavirus/transmissão
Grupo com Ancestrais do Continente Asiático/genética
Alelos
Genótipo
Limites: Humanos
Masculino
Feminino
Responsável: BR1.1 - BIREME



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