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  1 / 18616 MEDLINE  
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[PMID]:29377939
[Au] Autor:Budzyn M; Iskra M; Turkiewicz W; Krasinski Z; Gryszczynska B; Kasprzak MP
[Ad] Endereço:Department of General Chemistry, Chair of Chemistry and Clinical Biochemistry, Poznan University of Medical Sciences, Poznan, Poland.
[Ti] Título:Plasma concentration of selected biochemical markers of endothelial dysfunction in women with various severity of chronic venous insufficiency (CVI)-A pilot study.
[So] Source:PLoS One;13(1):e0191902, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Although the endothelial dysfunction is considered to be implicated in the pathogenesis of chronic venous insufficiency (CVI) the endothelial status in patients with venous disorders is still not fully evaluated. Therefore the aim of the study was to measure the concentration of selected markers of endothelial dysfunction: von Willebrand factor (vWf), soluble P-selectin (sP-selectin), soluble thrombomodulin (sTM) and soluble VE-cadherin (sVE-cadherin) in CVI women who constitute the most numerous group of patients suffering from venous disease. MATERIALS AND METHODS: Forty four women with CVI were involved in the study and divided into subgroups based on CEAP classification. Concentration of vWf, sP-selectin, sTM and sVE-cadherin were measured and compared with those obtained in 25 healthy age and sex-matched women. RESULTS: It was found that the concentration of sTM increased and sVEcadherin decreased along with disease severity in CVI women. A significant rise of sTM was observed especially in CVI women, with the highest inflammation status reflected by hsCRP or elastase concentration, and in CVI women with a high oxidative stress manifested by an increased plasma MDA. A significant fall of circulating sVE-cadherin was reported in CVI women with moderate to highest intensity of inflammation and oxidative stress. There was no change in vWF and sP-selectin concentration at any stage of CVI severity. CONCLUSIONS: The results of the present study demonstrate the presence of endothelial dysfunction in women suffering from CVI which seems to progress with the disease severity and may be associated with inflammation and enhanced oxidative stress.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Endotélio Vascular/fisiopatologia
Insuficiência Venosa/sangue
[Mh] Termos MeSH secundário: Adulto
Antígenos CD/sangue
Caderinas/sangue
Doença Crônica
Feminino
Seres Humanos
Meia-Idade
Selectina-P/sangue
Projetos Piloto
Índice de Gravidade de Doença
Trombomodulina/sangue
Fator de von Willebrand/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Biomarkers); 0 (Cadherins); 0 (P-Selectin); 0 (Thrombomodulin); 0 (cadherin 5); 0 (von Willebrand Factor)
[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:180130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191902


  2 / 18616 MEDLINE  
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[PMID]:28452702
[Au] Autor:Shin JM; Kang JH; Lee SA; Park IH; Lee HM
[Ad] Endereço:Department of Otorhinolaryngology-Head and Neck Surgery, Seoul, South Korea.
[Ti] Título:Effect of doxycycline on epithelial-mesenchymal transition the p38/Smad pathway in respiratory epithelial cells.
[So] Source:Am J Rhinol Allergy;31(2):71-77, 2017 Mar 01.
[Is] ISSN:1945-8932
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Doxycycline has antibacterial and anti-inflammatory effects, and it also suppresses collagen biosynthesis. This study aimed to confirm the effects and mechanism of doxycycline on transforming growth factor (TGF) beta 1 induced epithelial-mesenchymal transition and cell migration in A549 and primary nasal epithelial cells. METHODS: A 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay and phalloidin-fluorescein isothiocyanate staining were used to evaluate cytotoxicity and cellular morphologic changes. Western blot and immunofluorescence staining were used to determine the expression levels of E-cadherin, vimentin, alpha-smooth muscle actin, fibronectin, phosphorylated Smad2/3, and mitogen-activated protein kinases. Scratch and transwell migration assays were used to assess cellular migration ability. RESULTS: Doxycycline (0-10 µg/mL) had no significant cytotoxic effects in A549 and primary nasal epithelial cells. Increased expression of mesenchymal markers, including vimentin, alpha-smooth muscle actin, and fibronectin in TGF beta 1 induced A549 cells were downregulated by doxycycline treatment. In contrast, E-cadherin expression was upregulated in TGF beta 1 induced A549 cells. An in vitro cell migration assay showed that doxycycline also inhibited the ability of TGF beta 1 induced migration. Doxycycline treatment suppressed the activation of Smad2/3 and p38, whereas its inhibitory effects were similar to each element-specific inhibitor in A549 and primary nasal epithelial cells. CONCLUSION: Doxycycline inhibited TGF beta 1 induced epithelial-to-mesenchymal transition and migration by targeting Smad2/3 and p38 signal pathways in respiratory epithelial cells.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Doxiciclina/farmacologia
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Mucosa Respiratória/efeitos dos fármacos
[Mh] Termos MeSH secundário: Células A549
Caderinas/metabolismo
Movimento Celular/efeitos dos fármacos
Regulação da Expressão Gênica
Seres Humanos
Sistema de Sinalização das MAP Quinases
Cultura Primária de Células
Mucosa Respiratória/patologia
Proteína Smad2/metabolismo
Proteína Smad3/metabolismo
Fator de Crescimento Transformador beta/metabolismo
Vimentina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cadherins); 0 (Smad2 Protein); 0 (Smad3 Protein); 0 (Transforming Growth Factor beta); 0 (Vimentin); N12000U13O (Doxycycline)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.2500/ajra.2017.31.4410


  3 / 18616 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


  4 / 18616 MEDLINE  
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[PMID]:29429180
[Au] Autor:Hu J; Chen ZC; Zhang YZ; Han P; Ma WJ; Zhang Q; Xu M
[Ad] Endereço:Department of Otorhinolaryngology Head and Neck Surgery, Second Affiliated Hospital, Xi'an Jiaotong University School of Medicine, Xi'an 710004, China.
[Ti] Título:[The experimental study on endoplasmic reticulum stress-participated outer hair cell apoptosis in cadherin 23 gene mutant mice].
[So] Source:Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi;53(2):110-117, 2018 Feb 07.
[Is] ISSN:1673-0860
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To test the mechanism and upstream pathway of outer hair cell apoptosis in Cadherin 23 (Cdh23) gene mutant mice. The mutant 23 ( ) 57 /6 ( 6) . 70 . - ( ) . ( ) ( ) . - - ( ) / ( ) . . . 23 . The ABR thresholds in mice were significantly higher than those in B6 mice at the age of 1 and 3 months (both <0.05). The surface preparation with TUNEL staining confirmed OHC apoptosis in mouse cochleae which showed a higher TUNEL positive cell ratio than B6 mouse( =11.291, <0.01). The ER stress marker and mRNA were upregulated in the mouse inner ear, when compared with those in the B6 mouse(both <0.05). The BiP protein extracted from the mouse cochleae was significantly higher than that of B6 mouse measured by Western blot ( =3.66, =0.02). Immunostaining showed that BiP and CHOP were highly detected in the OHC in mouse cochleae, and was mainly detected in the perinuclear region of OHC. However, a bare BiP and CHOP signal were shown in B6 mouse cochleae. The CDH23 protein was specifically localized at the top of the OHC in B6 mice, indicating the localization of the tip links in hair bundle stereocilia. On the contrary, the CDH23 protein was found to be localized from the top to the nuclei of the OHC in mice. Portions of the CDH23 proteins failed to reach the top of the hair bundles and remained in the OHC cytoplasm. As the downstream response of the Cdh23 gene mutation, portions of the mutant CDH23 protein was accumulated in ER lumen resulting in the increase of ER loading and ultimately triggered ER stress and hair cell apoptosis in mouse cochleae.
[Mh] Termos MeSH primário: Apoptose/genética
Caderinas/genética
Estresse do Retículo Endoplasmático/genética
Células Ciliadas Auditivas Externas/patologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Cóclea/patologia
Estresse do Retículo Endoplasmático/fisiologia
Potenciais Evocados Auditivos do Tronco Encefálico
Células Ciliadas Vestibulares
Marcação In Situ das Extremidades Cortadas
Linfocinas/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Mutação
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fator de Transcrição CHOP/genética
Fator de Transcrição CHOP/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (Cdh23 protein, mouse); 0 (Lymphokines); 0 (RNA, Messenger); 0 (immunoglobulin-binding factors); 147336-12-7 (Transcription Factor CHOP)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1673-0860.2018.02.006


  5 / 18616 MEDLINE  
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[PMID]:29429165
[Au] Autor:Zhou JX; He XR; Song GX; Zou ZG; Wang LH; Hu R; Li HX
[Ad] Endereço:Department of Pathology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
[Ti] Título:[Clinicopathologic features with collecting duct carcinoma of kidney: report of 10 cases].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(2):123-127, 2018 Feb 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To study the pathological features, immunophenotypes, differential diagnoses and prognostic parameters of collecting duct carcinoma of the kidney (CDC). Clinical imaging, histopathology, immunohistochemistry, and survival data of 10 patients at First Affiliated Hospital of Nanjing Medical University from January 2009 to August 2017 were retrospectively analyzed along with a review of literatures. The clinical symptoms of CDC were not specific, and image examinations showed space-occupying mass lesions. Tumors were mainly located in renal medulla with grey and firm cut face and the presence of focal hemorrhage and necrosis. Microscopically, there were predominant tubular or tubular-papillary structures with associated focal sarcomatoid areas, desmoplastic stromal reaction and lymphoplasmacytic cells infiltration. Tumor cells had marked cytological atypia with high grade nuclei, conspicuous nucleolus and numerous mitoses. Immunohistochemically, tumor cells were strongly positive for CK19, E-cadherin, vimentin, HCK, CK7 and PAX8. The main treatment was radical nephrectomy in the patients. Seven cases died of CDC with median survival of 10 months. CDC is a rare, highly aggressive malignancy of kidney with poor prognosis. Definitive diagnosis should be made by histology and immunohistochemistry. Differential diagnoses include papillary renal cell carcinoma(type â…¡), renal medullary carcinoma, infiltrating high grade urothelial carcinoma, renal pelvis adenocarcinoma and metastatic adenocarcinomas.
[Mh] Termos MeSH primário: Carcinoma de Células Renais/patologia
Neoplasias Renais/patologia
Túbulos Renais Coletores/patologia
[Mh] Termos MeSH secundário: Caderinas/análise
Carcinoma de Células Renais/química
Carcinoma de Células de Transição/patologia
Nucléolo Celular
Núcleo Celular
Diagnóstico Diferencial
Seres Humanos
Imuno-Histoquímica
Neoplasias Renais/química
Túbulos Renais Coletores/química
Necrose/patologia
Vimentina/análise
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDH1 protein, human); 0 (Cadherins); 0 (Vimentin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.02.009


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[PMID]:29237530
[Au] Autor:Zhu XH; Li QG; Wang J; Hu GZ; Liu ZQ; Hu QH; Wu G
[Ad] Endereço:School of Medicine, Nanchang University, Nanchang 330006, China. nclqg2017@163.com.
[Ti] Título:[Mechanism of action of BET bromodomain inhibitor JQ1 in treating airway remodeling in asthmatic mice].
[So] Source:Zhongguo Dang Dai Er Ke Za Zhi;19(12):1278-1284, 2017 Dec.
[Is] ISSN:1008-8830
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To investigate the molecular mechanism of action of BET bromodomain inhibitor JQ1 in treating airway remodeling in asthmatic mice. METHODS: A total of 24 mice were randomly divided into control group, ovalbumin (OVA)-induced asthma group (OVA group), and JQ1 intervention group (JQ1+OVA group), with 8 mice in each group. OVA sensitization/challenge was performed to establish a mouse model of asthma. At 1 hour before challenge, the mice in the JQ1+OVA group were given intraperitoneal injection of JQ1 solution (50 µg/g). Bronchoalveolar lavage fluid (BALF) and lung tissue samples were collected at 24 hours after the last challenge, and the total number of cells and percentage of eosinophils in BALF were calculated. Pathological staining was performed to observe histopathological changes in lung tissue. RT-PCR and Western blot were used to measure the mRNA and protein expression of E-cadherin and vimentin during epithelial-mesenchymal transition (EMT). RESULTS: Compared with the control group, the OVA group had marked infiltration of inflammatory cells in the airway, thickening of the airway wall, increased secretion of mucus, and increases in the total number of cells and percentage of eosinophils in BALF (P<0.01). Compared with the OVA group, the JQ1+OVA group had significantly alleviated airway inflammatory response and significant reductions in the total number of cells and percentage of eosinophils in BALF (P<0.01). Compared with the control group, the OVA group had significant reductions in the mRNA and protein expression of E-cadherin and significant increases in the mRNA and protein expression of vimentin (P<0.01); compared with the OVA group, the JQ1+OVA group had significant increases in the mRNA and protein expression of E-cadherin and significant reductions in the mRNA and protein expression of vimentin (P<0.01); there were no significant differences in these indices between the JQ1+OVA group and the control group (P>0.05). CONCLUSIONS: Mice with OVA-induced asthma have airway remodeling during EMT. BET bromodomain inhibitor JQ1 can reduce airway inflammation, inhibit EMT, and alleviate airway remodeling, which provides a new direction for the treatment of asthma.
[Mh] Termos MeSH primário: Remodelação das Vias Aéreas/efeitos dos fármacos
Asma/tratamento farmacológico
Azepinas/farmacologia
Triazóis/farmacologia
[Mh] Termos MeSH secundário: Animais
Caderinas/análise
Caderinas/genética
Transição Epitelial-Mesenquimal
Feminino
Camundongos
Proteínas Nucleares/antagonistas & inibidores
Ovalbumina/imunologia
RNA Mensageiro/análise
Fatores de Transcrição/antagonistas & inibidores
Vimentina/análise
Vimentina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((+)-JQ1 compound); 0 (Azepines); 0 (Brd4 protein, mouse); 0 (Cadherins); 0 (E-cadherin protein, mouse); 0 (Nuclear Proteins); 0 (RNA, Messenger); 0 (Transcription Factors); 0 (Triazoles); 0 (Vimentin); 9006-59-1 (Ovalbumin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE


  7 / 18616 MEDLINE  
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[PMID]:28460635
[Au] Autor:Chen I; Mathews-Greiner L; Li D; Abisoye-Ogunniyan A; Ray S; Bian Y; Shukla V; Zhang X; Guha R; Thomas C; Gryder B; Zacharia A; Beane JD; Ravichandran S; Ferrer M; Rudloff U
[Ad] Endereço:Thoracic and Gastrointestinal Oncology Branch, National Cancer Institute, National Institutes for Health, CCR 4 West/4-3740, 10 Center Drive, Bethesda, MD, 20892-0001, USA.
[Ti] Título:Transcriptomic profiling and quantitative high-throughput (qHTS) drug screening of CDH1 deficient hereditary diffuse gastric cancer (HDGC) cells identify treatment leads for familial gastric cancer.
[So] Source:J Transl Med;15(1):92, 2017 May 01.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Patients with hereditary diffuse gastric cancer (HDGC), a cancer predisposition syndrome associated with germline mutations of the CDH1 (E-cadherin) gene, have few effective treatment options. Despite marked differences in natural history, histopathology, and genetic profile to patients afflicted by sporadic gastric cancer, patients with HDGC receive, in large, identical systemic regimens. The lack of a robust preclinical in vitro system suitable for effective drug screening has been one of the obstacles to date which has hampered therapeutic advances in this rare disease. METHODS: In order to identify therapeutic leads selective for the HDGC subtype of gastric cancer, we compared gene expression profiles and drug phenotype derived from an oncology library of 1912 compounds between gastric cancer cells established from a patient with metastatic HDGC harboring a c.1380delA CDH1 germline variant and sporadic gastric cancer cells. RESULTS: Unsupervised hierarchical cluster analysis shows select gene expression alterations in c.1380delA CDH1 SB.mhdgc-1 cells compared to a panel of sporadic gastric cancer cell lines with enrichment of ERK1-ERK2 (extracellular signal regulated kinase) and IP3 (inositol trisphosphate)/DAG (diacylglycerol) signaling as the top networks in c.1380delA SB.mhdgc-1 cells. Intracellular phosphatidylinositol intermediaries were increased upon direct measure in c.1380delA CDH1 SB.mhdgc-1 cells. Differential high-throughput drug screening of c.1380delA CDH1 SB.mhdgc-1 versus sporadic gastric cancer cells identified several compound classes with enriched activity in c.1380 CDH1 SB.mhdgc-1 cells including mTOR (Mammalian Target Of Rapamycin), MEK (Mitogen-Activated Protein Kinase), c-Src kinase, FAK (Focal Adhesion Kinase), PKC (Protein Kinase C), or TOPO2 (Topoisomerase II) inhibitors. Upon additional drug response testing, dual PI3K (Phosphatidylinositol 3-Kinase)/mTOR and topoisomerase 2A inhibitors displayed up to >100-fold increased activity in hereditary c.1380delA CDH1 gastric cancer cells inducing apoptosis most effectively in cells with deficient CDH1 function. CONCLUSION: Integrated pharmacological and transcriptomic profiling of hereditary diffuse gastric cancer cells with a loss-of-function c.1380delA CDH1 mutation implies various pharmacological vulnerabilities selective to CDH1-deficient familial gastric cancer cells and suggests novel treatment leads for future preclinical and clinical treatment studies of familial gastric cancer.
[Mh] Termos MeSH primário: Caderinas/deficiência
Avaliação Pré-Clínica de Medicamentos
Perfilação da Expressão Gênica
Ensaios de Triagem em Larga Escala
Neoplasias Gástricas/tratamento farmacológico
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Adulto
Caderinas/genética
Linhagem Celular Tumoral
Diglicerídeos/metabolismo
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica
Predisposição Genética para Doença
Mutação em Linhagem Germinativa/genética
Seres Humanos
Fosfatos de Inositol/metabolismo
Masculino
Linhagem
Reprodutibilidade dos Testes
Neoplasias Gástricas/patologia
Regulação para Cima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDH1 protein, human); 0 (Cadherins); 0 (Diglycerides); 0 (Inositol Phosphates); 0 (inositol 3,4,5-trisphosphate); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[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:170503
[St] Status:MEDLINE
[do] DOI:10.1186/s12967-017-1197-5


  8 / 18616 MEDLINE  
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[PMID]:28743796
[Au] Autor:Roberts SL; Dun XP; Doddrell RDS; Mindos T; Drake LK; Onaitis MW; Florio F; Quattrini A; Lloyd AC; D'Antonio M; Parkinson DB
[Ad] Endereço:Plymouth University Peninsula Schools of Medicine and Dentistry, John Bull Building, Plymouth Science Park, Plymouth PL6 8BU, UK.
[Ti] Título:Sox2 expression in Schwann cells inhibits myelination and induces influx of macrophages to the nerve.
[So] Source:Development;144(17):3114-3125, 2017 09 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Correct myelination is crucial for the function of the peripheral nervous system. Both positive and negative regulators within the axon and Schwann cell function to ensure the correct onset and progression of myelination during both development and following peripheral nerve injury and repair. The Sox2 transcription factor is well known for its roles in the development and maintenance of progenitor and stem cell populations, but has also been proposed as a negative regulator of myelination in Schwann cells. We wished to test fully whether Sox2 regulates myelination and show here that, in mice, sustained Sox2 expression blocks myelination in the peripheral nerves and maintains Schwann cells in a proliferative non-differentiated state, which is also associated with increased inflammation within the nerve. The plasticity of Schwann cells allows them to re-myelinate regenerated axons following injury and we show that re-myelination is also blocked by Sox2 expression in Schwann cells. These findings identify Sox2 as a physiological regulator of Schwann cell myelination and its potential to play a role in disorders of myelination in the peripheral nervous system.
[Mh] Termos MeSH primário: Macrófagos/metabolismo
Bainha de Mielina/metabolismo
Nervos Periféricos/metabolismo
Fatores de Transcrição SOXB1/metabolismo
Células de Schwann/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Caderinas/metabolismo
Proliferação Celular
Proteína 2 de Resposta de Crescimento Precoce/metabolismo
Proteínas de Fluorescência Verde/metabolismo
Camundongos Transgênicos
Atividade Motora
Condução Nervosa
Traumatismos dos Nervos Periféricos/metabolismo
Traumatismos dos Nervos Periféricos/patologia
Nervos Periféricos/patologia
Nervos Periféricos/ultraestrutura
Proteínas Proto-Oncogênicas c-jun/metabolismo
Ratos
Recuperação de Função Fisiológica
Células de Schwann/patologia
Transgenes
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cadherins); 0 (Early Growth Response Protein 2); 0 (Proto-Oncogene Proteins c-jun); 0 (SOXB1 Transcription Factors); 0 (beta Catenin); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1242/dev.150656


  9 / 18616 MEDLINE  
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[PMID]:28742884
[Au] Autor:Borzym-Kluczyk M; Radziejewska I; Cechowska-Pasko M; Darewicz B
[Ad] Endereço:Department of Pharmaceutical Biochemistry, Medical University of Bialystok, Bialystok, Poland.
[Ti] Título:Reduced expression of E-cadherin and increased sialylation level in clear cell renal cell carcinoma.
[So] Source:Acta Biochim Pol;64(3):465-470, 2017.
[Is] ISSN:1734-154X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Cancer cells are characterized by an aberrant increase in protein N-glycosylation and by disruption of E-cadherin-mediated adherens junctions. However, the relationship between alterations in N-glycosylation process and loss of E-cadherin adhesion in cancer remains unclear. The mechanisms of altered expression of adhesive glycoproteins in cancer cells have not been fully elucidated. Thus, the aim of this study was to examine the expression of E-cadherin and sialyl Lewis / , NeuAcα2-3Gal, NeuAcα2-6Gal/GalNAc structures in the normal renal tissue and intermediate and cancerous tissues from patients with clear cell RCC. Moreover, we attempted to correlate the E-cadherin expression with some specific sugar residues of renal cancer tissue glycoproteins. The expression of E-cadherin was analysed using ELISA test and immunoblotting. Oligosaccharide structures and sialylation level were detected with ELISA test using specific biotinylated lectins or antibodies. A significant decrease of E-cadherin expression as well as a significant increase in sialylated oligosaccharides level in intermediate zone and renal cancer tissue in comparison to normal renal tissue are reported. Significant decrease in expression of cadherins and increase in sialylation of oligosaccharide structures in renal cancer tissue in comparison to normal renal tissue, and in renal cancer tissue in comparison to intermediate zone of renal tissue, are important for the future research concerning detection and quantification of cadherins and sialylated oligosaccharide structures in urine and cells of urinary sediment as possible non-invasive marker of early RCC.
[Mh] Termos MeSH primário: Caderinas/metabolismo
Carcinoma de Células Renais/metabolismo
Neoplasias Renais/metabolismo
[Mh] Termos MeSH secundário: Acetilglucosamina/metabolismo
Idoso
Carcinoma de Células Renais/patologia
Feminino
Glicoconjugados/metabolismo
Glicoproteínas/metabolismo
Seres Humanos
Rim/metabolismo
Neoplasias Renais/patologia
Antígeno Lewis X/metabolismo
Masculino
Meia-Idade
Valores de Referência
Ácidos Siálicos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDH1 protein, human); 0 (Cadherins); 0 (Glycoconjugates); 0 (Glycoproteins); 0 (Lewis X Antigen); 0 (Sialic Acids); V956696549 (Acetylglucosamine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.18388/abp.2015_1215


  10 / 18616 MEDLINE  
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[PMID]:29374706
[Au] Autor:Ceausu AR; Ciolofan A; Cimpean AM; Magheti A; Mederle O; Raica M
[Ad] Endereço:Department of Microscopic Morphology/Histology, Angiogenesis Research Center Timisoara, Victor Babes University of Medicine and Pharmacy, Timisoara, Romania.
[Ti] Título:The Mesenchymal-Epithelial and Epithelial-Mesenchymal Cellular Plasticity of Liver Metastases with Digestive Origin.
[So] Source:Anticancer Res;38(2):811-816, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Few data are available regarding the epithelial to mesenchymal transition (EMT) /mesenchymal to epitheilal transition (MET) in the liver metastasis of digestive cancers. The aim of this study was to establish EMT/MET metastatic tumor cell plasticity according to the histological growth pattern of liver metastases. MATERIALS AND METHODS: Biopsies from 25 patients with liver metastasis (desmoplastic, replacement and pushing type) were evaluated. Double immunostaining of E-cadherin/vimentin, keratin 8,18/vimentin and E-cadherin/ keratin 8,18 were performed. RESULTS: The following cell types were noted: epithelial, mesenchymal, non-differentiated and differentiated hybrid mesenchymal/ epithelial and non-hybrid phenotype. All cases had mesenchymal/ epithelial phenotype cells. A significant correlation was found between the non-differentiated hybrid mesenchymal/ epithelial phenotype metastatic cells and histological growth pattern for gastric and colorectal cancer. CONCLUSION: A MET-targeting strategy, in conjunction with conventional chemotherapy, may be useful for the treatment of liver metastases.
[Mh] Termos MeSH primário: Neoplasias do Sistema Digestório/patologia
Neoplasias Hepáticas/secundário
[Mh] Termos MeSH secundário: Caderinas/metabolismo
Plasticidade Celular/fisiologia
Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/patologia
Neoplasias do Sistema Digestório/metabolismo
Transição Epitelial-Mesenquimal/fisiologia
Seres Humanos
Imuno-Histoquímica
Queratinas/metabolismo
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Neoplasias Pancreáticas/metabolismo
Neoplasias Pancreáticas/patologia
Neoplasias Gástricas/metabolismo
Neoplasias Gástricas/patologia
Vimentina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDH1 protein, human); 0 (Cadherins); 0 (Vimentin); 68238-35-7 (Keratins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE



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