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Id: biblio-1012312
Autor: Leitsmann, Conrad; Thelen, Paul; Schmid, Marianne; Meller, Johannes; Sahlmann, Carsten-Oliver; Meller, Birgit; Trojan, Lutz; Strauss, Arne.
Título: Enhancing PSMA-uptake with androgen deprivation therapy - a new way to detect prostate cancer metastases?
Fonte: Int. braz. j. urol;45(3):459-467, May-June 2019. tab, graf.
Idioma: en.
Resumo: ABSTRACT Purpose: 68Ga-PSMA PET/CT imaging is a promising modality for the staging of recurrent prostate cancer (PCa). Current evidence suggests limited diagnostic value of the 68Ga-PSMA PET/CT in PSA-levels ≤0.3ng/mL. Experimental data have demonstrated an increase in PSMA-expression in PCa metastases by androgen deprivation in vitro. The aim of the current study was to investigate a possible enhancing effect of PSMA with low-dose androgen deprivation in patients with BCR and low PSA-levels. Materials and Methods: Five patients with PCa and BCR, following radical prostatectomy, underwent 68Ga-PSMA PET/CT. A consecutive 68Ga-PSMA PET/CT was performed 6 to 11 days after injection of 80mg of Degarelix (Firmagon®). We recorded PSA and testosterone serum-levels and changes of PSMA-uptake in 68Ga-PSMA PET/CT images. Results: Median PSA prior 68Ga-PSMA PET/CT was 0.27ng/mL. All patients had a decrease in testosterone serum levels from median 2.95μg/l to 0.16μg/l following Degarelix injection. We observed an increase in the standardized uptake value (SUV) in PSMA-positive lymphogenous and osseous lesions in two patients following androgen deprivation. In another two patients, no PSMA positive signals were detected in either the first or the second scan. Conclusion: Our preliminary results of this feasibility assessment indicate a possible enhancing effect of PSMA-imaging induced by low-dose ADT. Despite several limitations and the small number of patients, this could be a new approach to improve staging by 68Ga-PSMA PET/CT in PCa patients with BCR after primary therapy. Further prospective studies with larger number of patients are needed to validate our findings.
Descritores: Compostos Organometálicos
Neoplasias da Próstata/patologia
Glicoproteínas de Membrana
Compostos Radiofarmacêuticos
Tomografia por Emissão de Pósitrons combinada à Tomografia Computadorizada/métodos
Antagonistas de Androgênios/uso terapêutico
Metástase Neoplásica/diagnóstico por imagem
-Oligopeptídeos/uso terapêutico
Valores de Referência
Fatores de Tempo
Reprodutibilidade dos Testes
Antígeno Prostático Específico/sangue
Gradação de Tumores
Pessoa de Meia-Idade
Recidiva Local de Neoplasia/patologia
Limites: Humanos
Masculino
Idoso
Tipo de Publ: Estudo de Avaliação
Responsável: BR1.1 - BIREME


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Id: biblio-1019888
Autor: Cihan, Yasemin Benderli.
Título: Re: The role of 68Ga-PSMA-PET/CT in radiotherapy planning in prostate cancer
Fonte: Int. braz. j. urol;45(4):863-865, July-Aug. 2019.
Idioma: en.
Descritores: Compostos Organometálicos/uso terapêutico
Neoplasias da Próstata/radioterapia
Neoplasias da Próstata/diagnóstico por imagem
Glicoproteínas de Membrana/uso terapêutico
Compostos Radiofarmacêuticos/uso terapêutico
Tomografia por Emissão de Pósitrons combinada à Tomografia Computadorizada/métodos
-Neoplasias da Próstata/patologia
Estadiamento de Neoplasias
Limites: Humanos
Masculino
Tipo de Publ: Carta
Responsável: BR1.1 - BIREME


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Id: biblio-1134336
Autor: Yamaga, Lilian Yuri Itaya; Cunha, Marcelo Livorsi da.
Título: Atypical metastases from prostate cancer detected on 68Ga-PSMA PET/CT: a case series
Fonte: Int. braz. j. urol;47(1):205-209, Jan.-Feb. 2021. graf.
Idioma: en.
Descritores: Compostos Organometálicos
Neoplasias da Próstata/diagnóstico por imagem
-Oligopeptídeos
Glicoproteínas de Membrana
Ácido Edético/análogos & derivados
Tomografia por Emissão de Pósitrons combinada à Tomografia Computadorizada
Limites: Humanos
Masculino
Tipo de Publ: Relatos de Casos
Responsável: BR1.1 - BIREME


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Id: biblio-950801
Autor: Cai, Guilan; Qiao, Shanshan; Chen, Kui.
Título: Suppression of miR-221 inhibits glioma cells proliferation and invasion via targeting SEMA3B
Fonte: Biol. Res;48:1-8, 2015. ilus, graf.
Idioma: en.
Resumo: BACKGROUND: Gliomas are the most common primary tumors in the central nervous system. Due to complicated signaling pathways involved in glioma progression, effective targets for treatment and biomarkers for prognosis prediction are still scant. RESULTS: In this study we revealed that a new microRNA (miR), the miR-221, was highly expressed in the glioma cells, and suppression of miR-221 resulted in decreased cellular proliferation, migration, and invasion in glioma cells. Mechanistic experiments validated that miR-221 participates in regulating glioma cells proliferation and invasion via suppression of a direct target gene, the Semaphorin 3B (SEMA3B). The rescue experiment with miR-221 and SEMA3B both knockdown results in significant reversion of miR-221 induced phenotypes. CONCLUSION: Taken together, our findings highlight an unappreciated role for miR-221 and SEMA3B in glioma.
Descritores: Neoplasias Encefálicas/patologia
Glicoproteínas de Membrana/farmacologia
Apoptose
Semaforinas/farmacologia
MicroRNAs/antagonistas & inibidores
Proliferação de Células
Glioma/patologia
-Neoplasias Encefálicas/metabolismo
Glicoproteínas de Membrana/genética
Transdução de Sinais
Regulação Neoplásica da Expressão Gênica
Movimento Celular
Western Blotting
Semaforinas/genética
MicroRNAs/metabolismo
Linhagem Celular Tumoral
Reação em Cadeia da Polimerase em Tempo Real
Glioma/metabolismo
Luciferases/metabolismo
Invasividade Neoplásica
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-950809
Autor: Lee, Seahyoung; Yun, Ina; Ham, Onju; Lee, Se-Yeon; Lee, Chang Yeon; Park, Jun-Hee; Lee, Jiyun; Seo, Hyang-Hee; Choi, Eunhyun; Hwang, Ki-Chul.
Título: Suppression of miR-181 a attenuates H2O2-induced death of mesenchymal stem cells by maintaining hexokinase II expression
Fonte: Biol. Res;48:1-7, 2015. graf.
Idioma: en.
Projeto: Korea Science and Engineering Foundation; . Ministry of Health and Welfare. Grant from the Korea Health 21 R&´D Project.
Resumo: BACKGROUND: Low survival rate of transplanted cells compromises the efficacy of cell therapy. Hexokinase II (HKII) is known to have anti-apoptotic activity through its interaction with mitochondria. The objective was to identify miRNAs targeting HKII and investigate whether miRNA-mediated modulation of HKII could improve the survival of mesenchymal stem cells (MSCs) exposed to H2O2. The expression of HKII in MSCs exposed to H2O2 was evaluated, and HKII-targeting miRNA was screened based on miRNA-target prediction databases. The effect of H2O2 on the expression of the selected HKII-targeting miRNA was examined and the effect of modulation of the selected HKII-targeting miRNA using anti-miRNA on H2O2-induced apoptosis of MSC was evaluated. RESULTS: H2O2 (600 µM) induced cell death of MSCs and decreased mitochondrial HKII expression. We have identified miR-181a as a HKII-targeting miRNA and H2O2 increased the expression of miR-181a in MSCs. Delivery of anti-miR-181a, which neutralizes endogenous miR-181a, significantly attenuated H2O2-induced decrease of HKII expression and disruption of mitochondrial membrane potential, improving the survival of MSCs exposed to H2O2. CONCLUSIONS: These findings suggest that H2O2-induced up-regulation of miR-181a contributes to the cell death of MSCs by down-regulating HKII. Neutralizing miR-181a can be an effective way to prime MSCs for transplantation into ischemic tissues.
Descritores: Apoptose
MicroRNAs/metabolismo
Células-Tronco Mesenquimais/patologia
Glioma/patologia
Hexoquinase/metabolismo
Peróxido de Hidrogênio/toxicidade
-Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/metabolismo
Diferenciação Celular
Movimento Celular
Sobrevivência Celular
Espécies Reativas de Oxigênio
Semaforinas/genética
Semaforinas/metabolismo
MicroRNAs/antagonistas & inibidores
Células-Tronco Mesenquimais/efeitos dos fármacos
Células-Tronco Mesenquimais/enzimologia
Reação em Cadeia da Polimerase em Tempo Real
Glioma/metabolismo
Peróxido de Hidrogênio/administração & dosagem
Mitocôndrias/enzimologia
Invasividade Neoplásica
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-950816
Autor: Liang, Yangui; Hua, Qiang; Pan, Pengwei; Yang, Jie; Zhang, Qi.
Título: Development of a novel method to evaluate sialylation of glycoproteins and analysis of gp96 sialylation in Hela, SW1990 and A549 cell lines
Fonte: Biol. Res;48:1-9, 2015. ilus, graf.
Idioma: en.
Projeto: National Natural Science Foundation of China.
Resumo: BACKGROUND: Glycoproteins play a critical role in the cellular activities of eukaryotes. Sialic acid is typically the outermost monosaccharide of glycolipids and glycoproteins, and is necessary for normal development. RESULTS: A strategy based on avidin-biotin affinity was established to enrich sialylated glycoproteins from HeLa cervical carcinoma, SW1990 pancreatic adenocarcinoma, and A549 lung adenocarcinoma cells. Using HPLC-MS/MS, western blot, real-time PCR, and enzyme-linked immunosorbent assay, gp96 was identified in all three cell lines. No significant difference in the protein expression of gp96 was detected at the whole cell level, but the amount of bioti-nylated gp96 in SW1990 cells was 30-40 % lower than that in A549 and HeLa cells, and the amount of sialylated gp96 in SW1990 cells was 30 % lower than that in A549 and HeLa cells. Immunoblotting results showed that the expression of sialyltransferase proteins in the total cell lysates from HeLa and A549 cells were higher than that in SW1990 cells. CONCLUSIONS: We established a new method for investigating the expression and sialylation of glycoproteins using metabolic labeling, click chemistry, and avidin-biotin affinity. We successfully used this method to purify sialylated glycoproteins from cancer cell lines. Our results showed that the levels of gp96 sialylation varied across different cancer cell lines, and this may be because of differences in sialyltransferase expression.
Descritores: Ácidos Siálicos/metabolismo
Glicoproteínas de Membrana/metabolismo
Glicosiltransferases/metabolismo
Proteínas de Neoplasias/metabolismo
-Ensaio de Imunoadsorção Enzimática
Células HeLa
Espectrometria de Massas em Tandem
Reação em Cadeia da Polimerase em Tempo Real
Células A549
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-950823
Autor: Chen, Haide; Li, Yang; Lin, Xijuan; Cui, Di; Cui, Chun; Li, Hui; Xiao, Lei.
Título: Functional disruption of human leukocyte antigen II in human embryonic stem cell
Fonte: Biol. Res;48:1-9, 2015. ilus, graf.
Idioma: en.
Projeto: Ministry of Agriculture; . National Natural Science Foundation of China; . Zhejiang Provincial Natural Science Foundation of China; . Agricultural Variety Breeding Project of Zhejiang Province; . Ministry of Science and Technology of China.
Resumo: BACKGROUND: Theoretically human embryonic stem cells (hESCs) have the capacity to self-renew and differentiate into all human cell types. Therefore, the greatest promise of hESCs-based therapy is to replace the damaged tissues of patients suffering from traumatic or degenerative diseases by the exact same type of cells derived from hESCs. Allo-graft immune rejection is one of the obstacles for hESCs-based clinical applications. Human leukocyte antigen (HLA) II leads to CD4+ T cells-mediated allograft rejection. Hence, we focus on optimizing hESCs for clinic application through gene modification. RESULTS: Transcription activator-like effector nucleases (TALENs) were used to target MHC class II transactivator (CIITA) in hESCs efficiently. CIITA(-/-)hESCs did not show any difference in the differentiation potential and self-renewal capacity. Dendritic cells (DCs) derived from CIITA(-/-)hESCs expressed CD83 and CD86 but without the constitutive HLA II. Fibroblasts derived from CIITA(-/-)hESCs were powerless in IFN-γ inducible expression of HLA II. CONCLUSION: We generated HLA II defected hESCs via deleting CIITA, a master regulator of constitutive and IFN-γ inducible expression of HLA II genes. CIITA(-/-)hESCs can differentiate into tissue cells with non-HLA II expression. It's promising that CIITA(-/-)hESCs-derived cells could be used in cell therapy (e.g., T cells and DCs) and escape the attack of receptors' CD4+ T cells, which are the main effector cells of cellular immunity in allograft.
Descritores: Proteínas Nucleares/genética
Transativadores/genética
Diferenciação Celular/genética
Deleção de Genes
Desoxirribonucleases/metabolismo
Células-Tronco Embrionárias Humanas/metabolismo
-Teratoma
Células Dendríticas/metabolismo
Imunoglobulinas/metabolismo
Imuno-Histoquímica
Glicoproteínas de Membrana/metabolismo
Células Tumorais Cultivadas
Antígenos de Histocompatibilidade Classe II/genética
Antígenos CD/metabolismo
Interferon gama/metabolismo
Camundongos SCID
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Desoxirribonucleases/classificação
Antígeno B7-2/metabolismo
Corpos Embrioides/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Cariótipo
Fibroblastos/metabolismo
Autorrenovação Celular
Células Apresentadoras de Antígenos/metabolismo
Limites: Humanos
Animais
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1178191
Autor: Baptistella, Antuani Rafael.
Título: Marcadores e mecanismos de resistência à terapia neoadjuvante e o papel das vesículas extracelulares secretadas pelas células tumorais no câncer de reto / Biomarkers and mechanisms of resistance to neoadjuvnat therapy and the role of extracelular vesicles secreted by tumor cells in rectal cancer.
Fonte: São Paulo; s.n; 2016. 208 p. ilust, tabelas.
Idioma: pt.
Tese: Apresentada a Fundação Antônio Prudente para obtenção do grau de Doutor.
Resumo: O câncer de reto é o segundo tumor mais comum no intestino grosso correspondendo a um terço do total de casos de câncer colorretal (CCR). Pacientes com câncer de reto em estádios II e III são tratados com radioquimioterapia neoadjuvante seguida de ressecção cirúrgica do tumor. Análises das peças cirúrgicas ressecadas mostraram que apenas 10-45% dos pacientes obtém resposta patológica completa (RCp) à terapia neoadjuvante, estando essa associada com uma diminuição da recorrência local, melhora da sobrevida livre de doença e aumento na preservação esfincteriana. Apesar da melhora na sobrevida nas últimas décadas, a resposta à terapia neoadjuvante continua variável e imprevisível e não é possível identificar e separar clinicamente os grupos de pacientes que terão ou não resposta completa ao tratamento neoadjuvante. Além disso, os mecanismos de resistência à radioquimioterapia nos tumores de reto são pouco compreendidos. Dessa forma, o objetivo principal deste estudo foi identificar marcadores e mecanismos celulares relacionados à resistência à terapia neoadjuvante em adenocarcinoma de reto e o papel das vesículas extracelulares (VEs) nesse processo. O estudo proteômico comparativo entre biópsias obtidas de tumores pré-tratamento com o tumor residual removido cirurgicamente pós-tratamento radioquimioterápico mostrou uma importante alteração no perfil de expressão proteica. Entre as proteínas que aumentam a expressão após a neoadjuvância estão as proteínas de reparo de dano de DNA, Ku70 e Ku80, e a proteína de tráfego intracelular Rab5C. Em um modelo in vitro, foi demonstrado que Rab5C orquestra um mecanismo de resistência à radioterapia nos tumores de reto através da modulação da internalização de EGFR promovida por radiação ionizante (RI). O EGRF intracelular por sua vez é essencial para regular a expressão de Ku70 e Ku80 e a resistência celular à RI. Estes dados apontam Rab5C e EGFR como potenciais alvos terapêuticos para sensibilizar células de câncer de reto resistentes ao tratamento neoadjuvante. Também foi observado que a RI promove alterações epigenéticas predominantemente de hipometilação, e entre os genes alterados estão SPG20 e TBC1D16, sendo o primeiro importante para a internalização de EGFR e o segundo para a regulação de Rab5C e modulação de EGFR. O perfil de expressão proteica foi ainda comparado entre biópsias pré-tratamento de pacientes com RCp e sem resposta patológica, e o resultado mostrou que esses dois grupos de pacientes apresentam um diferente perfil de expressão proteica. Nos pacientes com RCp as proteínas com aumento da expressão estão atuando em vias que favorecem a resposta à terapia, como a detoxificação de glutationa e degradação de glicogênio, enquanto as proteínas com aumento da expressão em pacientes sem RCp estão envolvidas em vias do metabolismo energético do tumor as quais contribuem para a resistência tumoral à terapia. As diferenças observadas nestes grupos devem ser amplamente exploradas uma vez que podem ser marcadores preditivos de resposta ao tratamento radioquimioterápico. A realização de estudos funcionais foi viabilizada pela geração de um modelo celular de tumor de reto resistente à radioterapia. Ao analisar as VEs secretadas por estas células foi observado que a RI não altera a quantidade e o tamanho médio das VEs secretadas, porém é capaz de alterar o carregamento proteico das mesmas. De fato, as VEs de células irradiadas apresentam um perfil proteico diferente quando comparadas as VEs de células não irradiadas, onde encontramos aumento da expressão de Ku70, Ku80 e Rab5C, além das metiltransferases NSUN2 e GLYM nas VEs de células pós RI. Interessantemente, as VEs secretadas por células irradiadas são capazes de transmitir a resistência à RI às células não irradiadas. Além disso os resultados mostraram que o tratamento com VEs de células irradiadas promove metilação em 98% do DNA avaliado em células SW837 em comparação ao tratamento com VEs de células não irradiadas. Os genes hipermetilados estão envolvidos em vias relacionadas ao sistema imune, como a apresentação de antígeno, sinalização de imunodeficiência primária e maturação de células dendríticas. Por fim, foi identificado que a expressão da proteína A33 está relacionada ao grau de diferenciação dos tumores colorretais, e que essa proteína está presente em VEs secretadas por células de adenocarcinoma de reto, indicando que a mesma pode ser usada para isolar VEs específicas do tecido colorretal. Os dados obtidos neste trabalho apontam mecanismos relacionados à resistência à terapia neoadjuvante no adenocarcinoma de reto e que em conjunto permitirão identificar novos alvos terapêuticos com potencial de melhorar a resposta à radioquimioterapia, além de identificar marcadores de resposta à terapia neoadjuvante antes do tratamento e dessa forma, poupar os pacientes não respondedores de terapias tóxicas e melhorar a sustentabilidade na saúde poupando os custos com drogas não eficientes para um grupo de pacientes.

Rectal cancer is the second most common cancer in large intestine, corresponding to one third of total cases of colorectal cancer (CRC). Patients with rectal cancer in stage II and III are treated with neoadjuvant chemoradiation followed by surgical resection. Analyzes of the resected tumor demonstrated that only 10-45% of the patients achieve pathological complete response (pCR) after neoadjuvant therapy, which is associated with a decrease in local recurrence, improvement of disease free survival and increase in sphincter preservation. Despite the improvement in survival in the last decades, the response to neoadjuvant therapy is still variable and unpredictable, and before the surgery it is not possible to identify and separate clinically the group of patients that will or will not have complete response to neoadjuvant treatment. Moreover, the mechanisms of resistance of rectal tumors to chemoradiation are poorly understood. Thus, the main objective of this work was to identify biomarkers and cellular mechanisms related to the resistance to neoadjuvant therapy in rectal adenocarcinomas and the role of extracellular vesicles (EVs) in this process. The comparative proteomic study between biopsy obtained from tumors pretreatment with residual tumor, post chemoradiation treatment, removed by surgery showed an important alteration in the protein expression profile. Among the proteins with increased expression after neoadjuvant therapy are the DNA repair proteins Ku70 and Ku80, and the protein involved in the intracellular trafficking, Rab5C. It was demonstrated in vitro that Rab5C orchestrates a mechanism of radioresistance in rectal tumors by modulating the EGFR internalization promoted by ionizing radiation (IR). The intracellular EGFR is essential to regulate Ku70 and Ku80 expression and the cell resistance to IR. These data pointed Rab5C and EGFR as potential therapeutic targets to sensitize rectal cancer cells resistant to neoadjuvant treatment. It was also observed that IR promotes epigenetic alterations, predominantly hypomethylation, and between the altered genes are SPG20 and TBC1D16, the first is important to EGFR internalization, while the second regulates Rab5C and modulates EGFR. The protein expression profile was further compared between biopsy pretreatment of patients with and without pCR, and the results showed that these two groups of patients present a different protein expression profile. In patients with pCR the proteins with increased expression are involved in pathways favoring the response to therapy, as glutathione-mediated detoxification and glycogen degradation, while the proteins with increased expression in patients without pCR are involved in tumor energetic metabolism pathways that contribute to tumor resistance to therapy. The observed differences in these groups should be widely explored since they may be predictive markers of response to chemoradiation treatment. The performance of functional studies was possible by generation of a cellular model of rectal tumor resistant to radiotherapy. The analysis of the EVs secreted by these cells showed that IR does not alter the amount and the medium size of secreted EVs, but is able to change their protein content. EVs from irradiated cells presented a different protein profile when compared to EVs from non-irradiated cells, where it was found the increased expression of Ku70, Ku80 and Rab5C, besides the methyltransferases NSUN2 and GLYM in EVs after irradiation. Interestingly, the EVs secreted by irradiated cells are capable of transfering resistance to IR to non-irradiated cells. Moreover, the results showed that the treatment of SW837 cells with EVs from irradiated cells promoted methylation in 98% of the analyzed DNA in comparison with the treatment with EVs from non-irradiated cells. The hypermethylated genes are involved in pathways related to immune system, as antigen presentation, primary immunodeficiency signaling and dendritic cells maturation. Lastly, it was identified that the A33 expression is related to the colorectal tumors differentiation degree, and this protein is present in EVs secreted by rectal adenocarcinoma, indicating that it may be used to isolate EVs specific from colorectal tissues. The data obtained in this work pointed to mechanisms related to resistance to neoadjuvant therapy in rectal adenocarcinoma that together will allow to identify new therapeutic targets with the potential to improve the response to chemoradiation, as well as to identify markers of response to neoadjuvant therapy before the treatment, and, in this way, avoid the non-responder patients to receive toxic therapies and improve health sustainability, sparing cost with non-efficient drugs for a group of patients.
Descritores: Neoplasias Retais/patologia
Neoplasias Retais/terapia
Adenocarcinoma/patologia
Adenocarcinoma/terapia
Terapia Neoadjuvante
Vesículas Extracelulares/patologia
-Neoplasias Retais/genética
Glicoproteínas de Membrana/análise
Biomarcadores
Adenocarcinoma/genética
Proteínas/análise
Expressão Gênica
Linhagem Celular
Sobrevivência Celular
Resultado do Tratamento
Genes erbB-1
Proliferação de Células
Vesículas Extracelulares/genética
Metilação
Invasividade Neoplásica
Limites: Humanos
Masculino
Feminino
Adulto
Pessoa de Meia-Idade
Idoso
Responsável: BR30.1 - Biblioteca
BR30.1


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Id: biblio-950904
Autor: Xiong, Xilin; Li, Yang; Liu, Ling; Qi, Kai; Chen, Yueqin; Fang, Jianpei; Zhang, Chi.
Título: Arsenic trioxide induces cell cycle arrest and affects Trk receptor expression in human neuroblastoma SK-N-SH cells
Fonte: Biol. Res;51:18, 2018. tab, graf.
Idioma: en.
Projeto: Guangdong Science and Technology Department.
Resumo: BACKGROUND: Arsenic trioxide (As2O3), a drug that has been used in China for approximately two thousand years, induces cell death in a variety of cancer cell types, including neuroblastoma (NB). The tyrosine kinase receptor (Trk) family comprises three members, namely TrkA, TrkB and TrkC. Various studies have confirmed that TrkA and TrkC expression is associated with a good prognosis in NB, while TrkB overexpression can lead to tumor cell growth and invasive metastasis. Previous studies have shown that As2O3 can inhibit the growth and proliferation of a human NB cell line and can also affect the N-Myc mRNA expression. It remains unclear whether As2O3 regulates Trks for the purposes of treating NB. METHODS: The aim of the present study was to investigate the effect of As2O3 on Trk expression in NB cell lines and its potential therapeutic efficacy. SK-N-SH cells were grown with increasing doses of As2O3 at different time points. We cultured SK-N-SH cells, which were treated with increasing doses of As2O3 at different time points. Trk expression in the NB samples was quantified by immunohistochemistry, and the cell cycle was analyzed by flow cytometry. TrkA, TrkB and TrkC mRNA expression was evaluated by real-time PCR analysis. RESULTS: Immunohistochemical and real-time PCR analyses indicated that TrkA and TrkC were over-expressed in NB, and specifically during stages 1, 2 and 4S of the disease progression. TrkB expression was increased in stage 3 and 4 NB. As2O3significantly arrested SK-N-SH cells in the G2/M phase. In addition, TrkA, TrkB and TrkC expression levels were significantly upregulated by higher concentrations of As2O3 treatment, notably in the 48-h treatment period. Our findings suggested that to achieve the maximum effect and appropriate regulation of Trk expression in NB stages 1, 2 and 4S, As2O3 treatment should be at relatively higher concentrations for longer delivery times;however, for NB stages 3 and 4, an appropriate concentration and infusion time for As2O3 must be carefully determined. CONCLUSION: The present findings suggested that As2O3 induced Trk expression in SK-N-SH cells to varying degrees and may be a promising adjuvant to current treatments for NB due to its apoptotic effects.
Descritores: Óxidos/farmacologia
Arsenicais/farmacologia
Glicoproteínas de Membrana/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Receptor trkB/efeitos dos fármacos
Proliferação de Células/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Neuroblastoma/metabolismo
-Glicoproteínas de Membrana/metabolismo
Receptor trkB/metabolismo
Linhagem Celular Tumoral/efeitos dos fármacos
Linhagem Celular Tumoral/metabolismo
Trióxido de Arsênio
Neuroblastoma/patologia
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-950905
Autor: Lin, Ruhui; Li, Long; Zhang, Yingzheng; Huang, Sheng; Chen, Shangjie; Shi, Jiao; Zhuo, Peiyuan; Jin, Hao; Li, Zuanfang; Liu, Weilin; Wang, Zhifu; Chen, Lidian; Tao, Jing.
Título: Electroacupuncture ameliorate learning and memory by improving N -acetylaspartate and glutamate metabolism in APP/PS1 mice
Fonte: Biol. Res;51:21, 2018. graf.
Idioma: en.
Projeto: National Natural Science Foundation of China; . Fujian Rehabilitation Technology of Collaborative Innovation Center; . Fujian Rehabilitation Technology of Collaborative Innovation Center; . Fujian Rehabilitation Technology of Collaborative Innovation Center; . Fujian Natural Science Foundation of China; . Fujian University of Traditional Chinese Medicine.
Resumo: OBJECTIVE: To explore the precise mechanism of electroacupuncture (EA) to delay cognitive impairment in Alzheimer disease. Methods N -Acetylaspartate (NAA), glutamate (Glu) and myoinositol (mI) metabolism were measured by magnetic resonance spectroscopy, learning and memory of APP/PS1 mouse was evaluated by the Morris water maze test and the step-down avoidance test, neuron survival number and neuronal structure in the hippocampus were observed by Nissl staining, and BDNF and phosphorylated TrkB detected by Western blot. RESULTS: EA at DU20 acupuncture significantly improve learning and memory in behavioral tests, up-regulate NAA, Glu and mI metabolism, increase the surviving neurons in hippocampus, and promote the expression of BDNF and TrkB in the APP/PS1 transgenic mice. CONCLUSION: These findings suggested that EA is a potential therapeutic for ameliorate cognitive dysfunction, and it might be due to EA could improve NAA and Glu metabolism by upregulation of BDNF in APP/PS1 mice.
Descritores: Eletroacupuntura/métodos
Ácido Aspártico/análogos & derivados
Ácido Glutâmico/metabolismo
Hipocampo/química
Aprendizagem/fisiologia
Memória/fisiologia
-Proteínas Tirosina Quinases/análise
Imageamento por Ressonância Magnética
Glicoproteínas de Membrana/análise
Camundongos Transgênicos
Espectroscopia de Ressonância Magnética
Distribuição Aleatória
Western Blotting
Ácido Aspártico/metabolismo
Aprendizagem em Labirinto
Fator Neurotrófico Derivado do Encéfalo
Modelos Animais
Teste de Esforço
Hipocampo/diagnóstico por imagem
Inositol/análise
Limites: Animais
Masculino
Camundongos
Responsável: CL1.1 - Biblioteca Central



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