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  1 / 69219 MEDLINE  
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[PMID]:29394261
[Au] Autor:Patel N; Garikapati KR; Makani VKK; Nair AD; Vangara N; Bhadra U; Pal Bhadra M
[Ad] Endereço:Centre for Chemical Biology, CSIR-Indian Institute of Chemical Technology, Tarnaka, Hyderabad, Telangana State, India.
[Ti] Título:Regulating BMI1 expression via miRNAs promote Mesenchymal to Epithelial Transition (MET) and sensitizes breast cancer cell to chemotherapeutic drug.
[So] Source:PLoS One;13(2):e0190245, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Polycomb group (PcG) proteinB lymphoma Mo-MLV insertion region 1 homolog (BMI1) is a transcriptional repressor that plays an important role in human carcinogenesis. MicroRNAs (miRNAs) are endogenous small non-coding RNAsthat implicate a negative regulation on gene expression. Deregulation of the expression of miRNAs has been implicated in tumorigenesis. Here, we have shown that knock-down ofBMI1increases theexpression of tumor-suppressivemiRNAs. Elevated levels of expression of miR-200a, miR-200b, miR-15a, miR-429, miR-203were observed upon knock-down of BMI1. Up-regulation of these miRNAsleads to down-regulation ofPRC1 group of proteins i.e. BMI1, RING1A, RING1B and Ub-H2A. Interestingly, overexpression of miR-200a, miR-200b and miR-15aalso produced decreased BMI1 and Ub-H2A protein expression in the CD44+ Cancer Stem Cellpopulation of MDAMB-231cells. Also,elevating the levels of BMI1 regulated miRNAspromoted Mesenchymal to Epithelial transition by regulating the expression of N-Cadherin, Vimentin, ß-Catenin, Zeb, Snail thereby resulting in decreased invasion, migration and proliferation. Here, we also report that miR-200a, miR-200b, miR-203 accretes the sensitivity of MDAMB-231 cells to the histone deacetylase inhibitor (HDACi) SAHA and miR-15a sensitized breast cancer cells to the chemotherapeutic drug cisplatin leading to apoptosis. These findings suggest that modulatingspecific miRNAs may serve as a therapeutic approach for the treatment of breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Transição Epitelial-Mesenquimal/genética
Regulação Neoplásica da Expressão Gênica/genética
Complexo Repressor Polycomb 1/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Resistência a Medicamentos Antineoplásicos
Feminino
Seres Humanos
Invasividade Neoplásica
Metástase Neoplásica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (BMI1 protein, human); EC 2.3.2.27 (Polycomb Repressive Complex 1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190245


  2 / 69219 MEDLINE  
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[PMID]:29366479
[Au] Autor:Xia E; Bhandari A; Shen Y; Zhou X; Sindan N; Xiang J; Guan Y; Yang F; Wang O
[Ad] Endereço:Department of Thyroid & Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, PR China.
[Ti] Título:LncRNA CCND2-AS1 promotes proliferation, migration, and invasion in papillary thyroid carcinoma.
[So] Source:Biochem Biophys Res Commun;496(2):628-632, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In decades, a lot of long non-coding RNAs (LncRNAs) have been proven to exert influences on tumorigenesis in vitro and in vivo. Many lncRNAs have been reported as effective therapeutic targets and biomarkers in various cancers. However, whether LncRNAs are associated with the progression of PTC remains largely unknown. In this study, we measured the expression of CCND2-AS1 in PTC cell lines by quantitative real-time polymerase chain reaction (qRT-PCR).We found that CCND2-AS1 expression was significantly over-expressed in PTC cell lines compared to normal thyroid epithelial cells. Gain-and loss-of-function experiments were performed to investigate the role of CCND2-AS1 in PTC cells. In vitro experiments, we proved that CCND2-AS1 knockdown in TPC1 significantly suppressed cell proliferation, migration, and invasion, while CCND2-AS1 overexpression in BCPAP had the opposite effects. Meanwhile, we also found that CCND2-AS1 could regulate N-cadherin and Vimentin expression, which may influence invasion and migration. Our findings indicate that the lncRNA CCND2-AS1 is a gene associated with PTC and might become a potential therapeutic target.
[Mh] Termos MeSH primário: Carcinoma Papilar/genética
Regulação Neoplásica da Expressão Gênica
Invasividade Neoplásica/genética
RNA Longo não Codificante/genética
Neoplasias da Glândula Tireoide/genética
[Mh] Termos MeSH secundário: Carcinoma Papilar/patologia
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Seres Humanos
Invasividade Neoplásica/patologia
Glândula Tireoide/patologia
Neoplasias da Glândula Tireoide/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Long Noncoding)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE


  3 / 69219 MEDLINE  
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[PMID]:29337059
[Au] Autor:Lin L; Li M; Lin L; Xu X; Jiang G; Wu L
[Ad] Endereço:Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China; Tongji University School of Medicine, Shanghai 200092, China.
[Ti] Título:FPPS mediates TGF-ß1-induced non-small cell lung cancer cell invasion and the EMT process via the RhoA/Rock1 pathway.
[So] Source:Biochem Biophys Res Commun;496(2):536-541, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Farnesyl pyrophosphate synthase (FPPS), a key enzyme in the mevalonate pathway, was recently shown to play a role in cancer progression. However, its role in non-small cell lung cancer (NSCLC) metastasis and the underlying mechanism remain unclear. In this study, FPPS expression was significantly correlated with TNM stage, and metastasis. Inhibition or knockdown of FPPS blocked TGF-ß1-induced cell invasion and epithelial-to-mesenchymal transition (EMT) process. FPPS expression of FPPS was induced by TGF-ß1 and FPPS promoted cell invasion and EMT via the RhoA/Rock1 pathway. In conclusion, FPPS mediates TGF-ß1-induced lung cancer cell invasion and EMT via the RhoA/Rock1 pathway. These findings suggest new treatment strategies to reduce mortality associated with metastasis in patients with NSCLC.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/metabolismo
Transição Epitelial-Mesenquimal
Geraniltranstransferase/metabolismo
Neoplasias Pulmonares/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
Quinases Associadas a rho/metabolismo
Proteína rhoA de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Idoso
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Linhagem Celular Tumoral
Feminino
Regulação Neoplásica da Expressão Gênica
Geraniltranstransferase/análise
Geraniltranstransferase/genética
Seres Humanos
Pulmão/metabolismo
Pulmão/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Masculino
Meia-Idade
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Transforming Growth Factor beta1); EC 2.5.1.10 (Geranyltranstransferase); EC 2.7.11.1 (ROCK1 protein, human); EC 2.7.11.1 (rho-Associated Kinases); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE


  4 / 69219 MEDLINE  
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[PMID]:29400040
[Au] Autor:Lechien JR; Doyen J; Deleuze M; Khalife M; Saussez S
[Ti] Título:Giant metastasis invading pharyngeal wall, pterygo­maxillary space, submaxillary and parotid glands.
[So] Source:Rev Laryngol Otol Rhinol (Bord);136(4):167-8, 2015.
[Is] ISSN:0035-1334
[Cp] País de publicação:France
[La] Idioma:eng
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/patologia
Neoplasias de Cabeça e Pescoço/patologia
Neoplasias Primárias Desconhecidas/patologia
Faringe/patologia
Neoplasias das Glândulas Salivares/secundário
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Meia-Idade
Invasividade Neoplásica
Glândula Parótida/patologia
Glândula Submandibular/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180206
[St] Status:MEDLINE


  5 / 69219 MEDLINE  
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[PMID]:29330228
[Au] Autor:McCormack A; Dekkers OM; Petersenn S; Popovic V; Trouillas J; Raverot G; Burman P; ESE survey collaborators
[Ad] Endereço:St Vincent's Hospital and Garvan Institute of Medical ResearchSydney, Australia.
[Ti] Título:Treatment of aggressive pituitary tumours and carcinomas: results of a European Society of Endocrinology (ESE) survey 2016.
[So] Source:Eur J Endocrinol;178(3):265-276, 2018 03.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To collect outcome data in a large cohort of patients with aggressive pituitary tumours (APT)/carcinomas (PC) and specifically report effects of temozolomide (TMZ) treatment. DESIGN: Electronic survey to ESE members Dec 2015-Nov 2016. RESULTS: Reports on 166 patients (40 PC, 125 APT, 1 unclassified) were obtained. Median age at diagnosis was 43 (range 4-79) years. 69% of the tumours were clinically functioning, and the most frequent immunohistochemical subtype were corticotroph tumours (45%). Ki-67 index did not distinguish APT from PC, median 7% and 10% respectively. TMZ was first-line chemotherapy in 157 patients. At the end of the treatment (median 9 cycles), radiological evaluation showed complete response (CR) in 6%, partial response (PR) in 31%, stable disease (SD) in 33% and progressive disease in 30%. Response was more frequent in patients receiving concomitant radiotherapy and TMZ. CR was seen only in patients with low MGMT expression. Clinically functioning tumours were more likely to respond than non-functioning tumours, independent of MGMT status. Of patients with CR, PR and SD, 25, 40 and 48% respectively progressed after a median of 12-month follow-up. Other oncological drugs given as primary treatment and to TMZ failures resulted in PR in 20%. CONCLUSION: This survey confirms that TMZ is established as first-line chemotherapeutic treatment of APT/PC. Clinically functioning tumours, low MGMT and concurrent radiotherapy were associated with a better response. The limited long-term effect of TMZ and the poor efficacy of other drugs highlight the need to identify additional effective therapies.
[Mh] Termos MeSH primário: Adenoma/terapia
Antineoplásicos Alquilantes/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Carcinoma/terapia
Irradiação Craniana
Dacarbazina/análogos & derivados
Procedimentos Neurocirúrgicos
Neoplasias Hipofisárias/terapia
[Mh] Termos MeSH secundário: Adenoma/metabolismo
Adenoma/patologia
Adolescente
Adulto
Idoso
Bevacizumab/administração & dosagem
Capecitabina/administração & dosagem
Carcinoma/metabolismo
Carcinoma/patologia
Carmustina/administração & dosagem
Criança
Pré-Escolar
Metilases de Modificação do DNA/metabolismo
Enzimas Reparadoras do DNA/metabolismo
Dacarbazina/administração & dosagem
Dacarbazina/uso terapêutico
Endocrinologia
Europa (Continente)
Feminino
Seres Humanos
Antígeno Ki-67/metabolismo
Masculino
Meia-Idade
Invasividade Neoplásica
Neoplasias Hipofisárias/metabolismo
Neoplasias Hipofisárias/patologia
Sociedades Médicas
Inquéritos e Questionários
Talidomida/administração & dosagem
Proteínas Supressoras de Tumor/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (Ki-67 Antigen); 0 (Tumor Suppressor Proteins); 2S9ZZM9Q9V (Bevacizumab); 4Z8R6ORS6L (Thalidomide); 6804DJ8Z9U (Capecitabine); 7GR28W0FJI (Dacarbazine); EC 2.1.1.- (DNA Modification Methylases); EC 2.1.1.63 (MGMT protein, human); EC 6.5.1.- (DNA Repair Enzymes); U68WG3173Y (Carmustine); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180114
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0933


  6 / 69219 MEDLINE  
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[PMID]:29267504
[Au] Autor:Mendes GA; Haag T; Trott G; Rech CGSL; Ferreira NP; Oliveira MC; Kohek MB; Pereira-Lima JFS
[Ad] Endereço:Programa de Pós-Graduação em Patologia, Universidade Federal de Ciências da Saúde de Porto Alegre, Porto Alegre, RS, Brasil.
[Ti] Título:Expression of E-cadherin, Slug and NCAM and its relationship to tumor invasiveness in patients with acromegaly.
[So] Source:Braz J Med Biol Res;51(2):e6808, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Pituitary adenomas account for 10-15% of primary intracranial tumors. Growth hormone (GH)-secreting adenomas account for 13% of all pituitary adenomas and cause acromegaly. These tumors can be aggressive, invade surrounding structures and are highly recurrent. The objective of this study was to evaluate E-cadherin, Slug and neural cell adhesion molecule (NCAM) expression in GH-secreting pituitary adenomas and its relationship to tumor invasiveness. A cross-sectional study of patients who underwent hypophysectomy due to GH-secreting pituitary adenoma from April 2007 to December 2014 was carried out. The medical records were reviewed to collect clinical data. Immediately after surgery, tumor samples were frozen in liquid nitrogen and stored in a biofreezer at -80°C for assessment of E-cadherin 1 (CDH1), SLUG (SNAI2), and NCAM (NCAM1) by real-time PCR. The samples were fixed in formalin and embedded in paraffin for immunohistochemical analysis of E-cadherin and NCAM. Thirty-five patients with acromegaly were included in the study. Of these, 65.7% had invasive tumors. Immunohistochemically, E-cadherin was expressed in 96.7% of patients, and NCAM in 80% of patients. There was no statistically significant relationship between tumor grade or invasiveness and immunohistochemical expression of these markers. Regarding gene expression, 50% of cases expressed CDH1, none expressed SNAI2, and 53.3% expressed NCAM1. There was no statistically significant relationship between tumor grade or invasiveness and gene expression of CDH1, SNAI2, and NCAM1. The absence of Slug overexpression and of E-cadherin and NCAM suppression suggests that expression of these markers is not associated with tumor invasiveness in GH-secreting pituitary adenomas.
[Mh] Termos MeSH primário: Acromegalia/patologia
Adenoma/patologia
Caderinas/análise
Moléculas de Adesão de Célula Nervosa/análise
Neoplasias Hipofisárias/patologia
Fatores de Transcrição da Família Snail/análise
[Mh] Termos MeSH secundário: Acromegalia/genética
Acromegalia/metabolismo
Adenoma/química
Adenoma/genética
Adolescente
Adulto
Idoso
Biomarcadores Tumorais/análise
Antígeno CD56/análise
Estudos Transversais
Feminino
Expressão Gênica
Seres Humanos
Imuno-Histoquímica
Masculino
Meia-Idade
Gradação de Tumores
Invasividade Neoplásica
Neoplasias Hipofisárias/química
Neoplasias Hipofisárias/genética
Reação em Cadeia da Polimerase em Tempo Real
Estatísticas não Paramétricas
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CD56 Antigen); 0 (Cadherins); 0 (NCAM1 protein, human); 0 (Neural Cell Adhesion Molecules); 0 (SNAI1 protein, human); 0 (Snail Family Transcription Factors)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


  7 / 69219 MEDLINE  
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[PMID]:28460061
[Au] Autor:Papaleontiou M; Hughes DT; Guo C; Banerjee M; Haymart MR
[Ad] Endereço:Division of Metabolism, Endocrinology, and Diabetes, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48106.
[Ti] Título:Population-Based Assessment of Complications Following Surgery for Thyroid Cancer.
[So] Source:J Clin Endocrinol Metab;102(7):2543-2551, 2017 Jul 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: As thyroid cancer incidence rises, more patients undergo thyroid surgery. Although postoperative complication rates have been reported in single institution studies, population-based data are limited. Objective: To determine thyroid cancer surgery complication rates and identify at-risk populations. Design/Setting/Patients: Using the Surveillance, Epidemiology, and End Results-Medicare database, we evaluated general complications within 30 days and thyroid surgery-specific complications within 1 year in 27,912 patients who underwent surgery for differentiated or medullary thyroid cancer between 1998 and 2011. Multivariable analyses of patient characteristics associated with postoperative complications were performed. Main Outcome Measures: General and thyroid surgery-specific complications. Results: Overall, 1820 (6.5%) patients developed general postoperative complications and 3427 (12.3%) developed thyroid surgery-specific complications. In multivariable analyses, general and thyroid surgery-specific complications were significantly higher in patients >65 years [odds ratio (OR), 2.61; 95% confidence interval (CI), 2.31 to 2.95; OR, 3.12; 95% CI, 2.85 to 3.42], those with a Charlson/Deyo comorbidity score of 1 (OR, 2.40; 95% CI, 1.66 to 3.49; OR, 1.88; 95% CI, 1.53 to 2.31) and ≥2 (OR, 7.05; 95% CI, 5.33 to 9.56; OR, 3.62; 95% CI, 3.11 to 4.25), and those with regional (OR, 1.18; 95% CI, 1.03 to 1.35; OR, 1.31; 95% CI, 1.19 to 1.45) or distant disease (OR, 2.83; 95% CI, 2.30 to 3.47; OR, 1.85; 95% CI, 1.54 to 2.21), respectively. Conclusions: The rates of thyroid cancer surgery complications are higher than predicted, and patients with older age, more comorbidities, and advanced disease are at greatest risk. Efforts to reduce complications are needed.
[Mh] Termos MeSH primário: Complicações Pós-Operatórias/epidemiologia
Neoplasias da Glândula Tireoide/patologia
Neoplasias da Glândula Tireoide/cirurgia
Tireoidectomia/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Idoso
Intervalo Livre de Doença
Feminino
Seres Humanos
Incidência
Modelos Logísticos
Masculino
Medicare/estatística & dados numéricos
Meia-Idade
Análise Multivariada
Invasividade Neoplásica/patologia
Estadiamento de Neoplasias
Complicações Pós-Operatórias/fisiopatologia
Estudos Retrospectivos
Medição de Risco
Programa de SEER
Análise de Sobrevida
Neoplasias da Glândula Tireoide/mortalidade
Tireoidectomia/métodos
Estados Unidos
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-00255


  8 / 69219 MEDLINE  
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[PMID]:29305865
[Au] Autor:Yin K; Dang S; Cui L; Fan X; Xie R; Qu J; Shang M; Chen J
[Ad] Endereço:Department of General Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
[Ti] Título:Netrin-1 promotes metastasis of gastric cancer by regulating YAP activity.
[So] Source:Biochem Biophys Res Commun;496(1):76-82, 2018 01 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Yes-associated protein (YAP) is a major downstream molecular of the Hippo pathway, which plays important role in cancer development. Netrin-1 conveys oncogenic activity in many types of malignant tumors. However, the downstream signaling of netrin-1 mediating its oncogenic effects in gastric cancer (GC) is not well defined. Here, we aim to investigate the role of netrin-1 in metastasis potential of GC by regulating YAP. In this study, we showed that netrin-1 inhibition significantly decreased migration and invasion abilities of GC cells, while netrin-1 overexpression effectively reversed this effect. We also demonstrated that netrin-1 upregulated YAP expression via its transmembrane receptor neogenin. Furthermore, our in vitro and in vivo results showed that the effect of netrin-1 on GC cells migration and invasion abilities was regulated by YAP. Collectively, our results defined netrin-1 as a positive regulator of malignant tumor metastasis in GC by activating the YAP signaling, with potential implications for new approaches to GC therapy.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Regulação Neoplásica da Expressão Gênica
Netrina-1/metabolismo
Fosfoproteínas/metabolismo
Neoplasias Gástricas/metabolismo
Neoplasias Gástricas/patologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Invasividade Neoplásica
Metástase Neoplásica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (NTN1 protein, human); 0 (Phosphoproteins); 0 (YAP1 (Yes-associated) protein, human); 158651-98-0 (Netrin-1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


  9 / 69219 MEDLINE  
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[PMID]:27779203
[Au] Autor:Villalobos-Hernandez A; Bobbala D; Kandhi R; Khan MG; Mayhue M; Dubois CM; Ferbeyre G; Saucier C; Ramanathan S; Ilangumaran S
[Ad] Endereço:Immunology Division, Department of Pediatrics, Faculty of Medicine and Health Sciences, University of Sherbrooke, Sherbrooke, Quebec, Canada.
[Ti] Título:SOCS1 inhibits migration and invasion of prostate cancer cells, attenuates tumor growth and modulates the tumor stroma.
[So] Source:Prostate Cancer Prostatic Dis;20(1):36-47, 2017 Mar.
[Is] ISSN:1476-5608
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The suppressor of cytokine signaling 1 (SOCS1) gene is repressed in prostate cancer (PCa) by epigenetic silencing and microRNA miR30d. Increased expression of the SOCS1-targeting miR30d correlates with higher biochemical recurrence, suggesting a tumor suppressor role of SOCS1 in PCa, but the underlying mechanisms are unclear. We have shown that SOCS1 inhibits MET receptor kinase signaling, a key oncogenic pathway in cancer progression. Here we evaluated the role of SOCS1 in attenuating MET signaling in PCa cells and tumor growth in vivo. METHODS: MET-overexpressing human DU145 and PC3 PCa cell lines were stably transduced with SOCS1, and their growth, migration and invasion of collagen matrix were evaluated in vitro. Cells expressing SOCS1 or the control vector were evaluated for tumor growth in NOD.scid.gamma mice as xenograft or orthotopic tumors. RESULTS: HGF-induced MET signaling was attenuated in SOCS1-expressing DU145 and PC3 cells. Compared with vector control cells, SOCS1-expressing cells showed reduced proliferation and impaired migration following HGF stimulation. DU145 and PC3 cells showed marked ability to invade the collagen matrix following HGF stimulation and this was attenuated by SOCS1. As xenografts, SOCS1-expressing PCa cells showed significantly reduced tumor growth compared with vector control cells. In the orthotopic tumor model, SOCS1 reduced the growth of primary tumors and metastatic spread. Intriguingly, the SOCS1-expressing DU145 and PC3 tumors showed increased collagen deposition, associated with increased frequency of myofibroblasts. CONCLUSIONS: Our findings support the tumor suppressor role of SOCS1 in PCa and suggest that attenuation of MET signaling is one of the underlying mechanisms. SOCS1 in PCa cells also appears to prevent the tumor-promoting functions of cancer-associated fibroblasts.
[Mh] Termos MeSH primário: Neoplasias da Próstata/metabolismo
Neoplasias da Próstata/patologia
Células Estromais/metabolismo
Proteína 1 Supressora da Sinalização de Citocina/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/metabolismo
Colágeno/metabolismo
Metilação de DNA
Modelos Animais de Doenças
Epigênese Genética
Expressão Gênica
Fator de Crescimento de Hepatócito/metabolismo
Xenoenxertos
Seres Humanos
Masculino
Camundongos
Invasividade Neoplásica
Metástase Neoplásica
Neoplasias da Próstata/genética
Proteínas Proto-Oncogênicas c-met/metabolismo
Transdução de Sinais
Células Estromais/patologia
Proteína 1 Supressora da Sinalização de Citocina/genética
Carga Tumoral
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HGF protein, human); 0 (SOCS1 protein, human); 0 (Suppressor of Cytokine Signaling 1 Protein); 67256-21-7 (Hepatocyte Growth Factor); 9007-34-5 (Collagen); EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1038/pcan.2016.50


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[PMID]:27775851
[Au] Autor:van Weert S; Reinhard R; Bloemena E; Buter J; Witte BI; Vergeer MR; Leemans CR
[Ad] Endereço:Department of Otolaryngology - Head and Neck Surgery, VU University Medical Center, Amsterdam, The Netherlands.
[Ti] Título:Differences in patterns of survival in metastatic adenoid cystic carcinoma of the head and neck.
[So] Source:Head Neck;39(3):456-463, 2017 Mar.
[Is] ISSN:1097-0347
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We examined the assumption in conventional teaching about metastatic adenoid cystic carcinoma (ACC) being an indolent type of disease. METHODS: A single center analysis of 105 cases of ACC was performed. Radiographs were reviewed and tumor response to chemotherapy was measured. Distant disease-free survival (DDFS) and time to death since distant metastases diagnosis were analyzed. RESULTS: Forty-two percent of the patients were diagnosed with distant metastases. DDFS showed significant negative associations with advanced T classification, N+ classification, solid type tumor, and positive surgical margins. Distant metastases (91%) developed in the first 5 years after presentation. Median distant metastatic survival was 13.8 months. The most frequent organ sited was the lung. Solid type ACC showed a preponderance for multiorgan metastases (17/28; 61%). Distant metastases seemed not to occur in case of clear surgical margins. Solid type ACC had a significant poorer survival after development of distant metastases. CONCLUSION: Metastatic ACC is not always an indolent disease. © 2016 Wiley Periodicals, Inc. Head Neck 39: 456-463, 2017.
[Mh] Termos MeSH primário: Carcinoma Adenoide Cístico/mortalidade
Carcinoma Adenoide Cístico/patologia
Causas de Morte
Neoplasias de Cabeça e Pescoço/mortalidade
Neoplasias de Cabeça e Pescoço/patologia
Linfonodos/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Carcinoma Adenoide Cístico/diagnóstico por imagem
Carcinoma Adenoide Cístico/terapia
Estudos de Coortes
Intervalo Livre de Doença
Feminino
Seguimentos
Neoplasias de Cabeça e Pescoço/diagnóstico por imagem
Neoplasias de Cabeça e Pescoço/terapia
Seres Humanos
Metástase Linfática
Imagem por Ressonância Magnética/métodos
Masculino
Meia-Idade
Invasividade Neoplásica/patologia
Recidiva Local de Neoplasia/mortalidade
Recidiva Local de Neoplasia/patologia
Recidiva Local de Neoplasia/terapia
Estadiamento de Neoplasias
Estudos Retrospectivos
Análise de Sobrevida
Fatores de Tempo
Tomografia Computadorizada por Raios X/métodos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1002/hed.24613



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