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[PMID]:28760868
[Au] Autor:Werneburg S; Fuchs HLS; Albers I; Burkhardt H; Gudi V; Skripuletz T; Stangel M; Gerardy-Schahn R; Hildebrandt H
[Ad] Endereço:Institute of Clinical Biochemistry, and.
[Ti] Título:Polysialylation at Early Stages of Oligodendrocyte Differentiation Promotes Myelin Repair.
[So] Source:J Neurosci;37(34):8131-8141, 2017 Aug 23.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Polysialic acid is a glycan modification of the neural cell adhesion molecule (NCAM) produced by the polysialyltransferases ST8SIA2 and ST8SIA4. Polysialic acid has been detected in multiple sclerosis plaques, but its beneficial or adverse role in remyelination is elusive. Here, we show that, despite a developmental delay, myelination at the onset and during cuprizone-induced demyelination was unaffected in male or mice. However, remyelination, restoration of oligodendrocyte densities, and motor recovery after the cessation of cuprizone treatment were compromised. Impaired differentiation of NCAM- or ST8SIA2-negative oligodendrocyte precursors suggested an underlying cell-autonomous mechanism. In contrast, premature differentiation in ST8SIA4-negative cultures explained the accelerated remyelination previously observed in mice. mRNA profiling during differentiation of human stem cell-derived and primary murine oligodendrocytes indicated that the opposing roles of ST8SIA2 and ST8SIA4 arise from sequential expression. We also provide evidence that potentiation of ST8SIA2 by 9- retinoic acid and artificial polysialylation of oligodendrocyte precursors by a bacterial polysialyltransferase are mechanisms to promote oligodendrocytic differentiation. Thus, differential targeting of polysialyltransferases and polysialic acid engineering are promising strategies to advance the treatment of demyelinating diseases. The beneficial or adverse role of polysialic acid (polySia) in myelin repair is a long-standing question. As a modification of the neural cell adhesion molecule (NCAM), polySia is produced by the polysialyltransferases ST8SIA2 and ST8SIA4. Here we demonstrate that NCAM and ST8SIA2 promote oligodendrocyte differentiation and myelin repair as well as motor recovery after cuprizone-induced demyelination. In contrast, ST8SIA4 delays oligodendrocyte differentiation, explaining its adverse role in remyelination. These opposing roles of the polysialyltransferases are based on different expression profiles. 9- retinoic acid enhances ST8SIA2 expression, providing a mechanism for understanding how it supports oligodendrocyte differentiation and remyelination. Furthermore, artificial polysialylation of the cell surface promotes oligodendrocyte differentiation. Thus, boosting ST8SIA2 and engineering of polySia are promising strategies for improving myelin repair.
[Mh] Termos MeSH primário: Antígeno CD56/biossíntese
Diferenciação Celular/fisiologia
Bainha de Mielina/metabolismo
Oligodendroglia/metabolismo
Sialiltransferases/biossíntese
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Doenças Desmielinizantes/metabolismo
Células-Tronco Embrionárias/metabolismo
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Atividade Motora/fisiologia
Molécula L1 de Adesão de Célula Nervosa
Distribuição Aleatória
Ácidos Siálicos/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD56 Antigen); 0 (Ncam1 protein, mouse); 0 (Neural Cell Adhesion Molecule L1); 0 (Sialic Acids); 0 (polysialic acid); 0 (polysialyl neural cell adhesion molecule); EC 2.4.99.- (CMP-N-acetylneuraminate-poly-alpha-2,8-sialosyl sialyltransferase); EC 2.4.99.- (Sialyltransferases); EC 2.4.99.8 (ST8SiaIV protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1147-17.2017


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[PMID]:28751757
[Au] Autor:Tangen IL; Kopperud RK; Visser NC; Staff AC; Tingulstad S; Marcickiewicz J; Amant F; Bjørge L; Pijnenborg JM; Salvesen HB; Werner HM; Trovik J; Krakstad C
[Ad] Endereço:Department of Gynaecology and Obstetrics, Haukeland University Hospital, 5053 Bergen, Norway.
[Ti] Título:Expression of L1CAM in curettage or high L1CAM level in preoperative blood samples predicts lymph node metastases and poor outcome in endometrial cancer patients.
[So] Source:Br J Cancer;117(6):840-847, 2017 Sep 05.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Several studies have identified L1 cell adhesion molecule (L1CAM) as a strong prognostic marker in endometrial cancer. To further underline the clinical usefulness of this biomarker, we investigated L1CAM as a predictive marker for lymph node metastases and its prognostic impact in curettage specimens and preoperative plasma samples. In addition, we aimed to validate the prognostic value of L1CAM in hysterectomy specimen. METHODS: Immunohistochemical staining of L1CAM was performed for 795 hysterectomy and 1134 curettage specimen from endometrial cancer patients. The L1CAM level in preoperative blood samples from 372 patients was determined using ELISA. RESULTS: Expression of L1CAM in curettage specimen was significantly correlated to L1CAM level in corresponding hysterectomy specimen (P<0.001). Both in curettage and preoperative plasma samples L1CAM upregulation was significantly associated with features of aggressive disease and poor outcome (P<0.001). The L1CAM was an independent predictor of lymph node metastases, after correction for curettage histology, both in curettage specimen (P=0.002) and plasma samples (P=0.048). In the hysterectomy samples L1CAM was significantly associated with poor outcome (P<0.001). CONCLUSIONS: We demonstrate that preoperative evaluation of L1CAM levels, both in curettage or plasma samples, predicts lymph node metastases and adds valuable information on patient prognosis.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/análise
Neoplasias do Endométrio/sangue
Neoplasias do Endométrio/química
Metástase Linfática
Molécula L1 de Adesão de Célula Nervosa/análise
[Mh] Termos MeSH secundário: Idoso
Biomarcadores Tumorais/sangue
Distribuição de Qui-Quadrado
Curetagem
Neoplasias do Endométrio/mortalidade
Neoplasias do Endométrio/patologia
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Histerectomia
Estimativa de Kaplan-Meier
Meia-Idade
Molécula L1 de Adesão de Célula Nervosa/sangue
Período Pré-Operatório
Prognóstico
Estatísticas não Paramétricas
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Neural Cell Adhesion Molecule L1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2017.235


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[PMID]:28710714
[Au] Autor:Kommoss S; Hartkopf AD; Krämer B; Bunz AK; Grevenkamp F; Kommoss F; Pasternak J; Arbabi SM; Wallwiener M; Staebler A; Lax SF; Brucker SY; Taran FA
[Ad] Endereço:Department of Women's Health, Tübingen University Hospital, Calwerstr. 7, 72076, Tübingen, Germany. stefan.kommoss@med.uni-tuebingen.de.
[Ti] Título:Disseminated tumor cells are not associated with established risk factors, L1CAM immunoreactivity and outcome in endometrial carcinoma.
[So] Source:J Cancer Res Clin Oncol;143(11):2183-2188, 2017 Nov.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: The presence of disseminated tumor cells (DTC) in the bone marrow of endometrial carcinoma patients has been demonstrated previously. In contrast to breast cancer, no prognostic significance or association with clinicopathological features was revealed for endometrial carcinoma so far. The aim of this study was to investigate DTC in a large patient cohort with in-depth pathology review data available and to study DTC occurrence in the context of L1CAM and long-term disease specific follow-up. METHODS: Patients treated for endometrial carcinoma at the Tuebingen University Women's hospital between 2003 and 2013 were identified. Cases with previous expert central pathology review including L1CAM immunohistochemistry and bone marrow aspirates available were selected. The presence of DTC and L1CAM expression was studied immunohistochemically. RESULTS: In 395 cases with a confirmed diagnosis of endometrial carcinoma, bone marrow aspirates were available. DTC were detected in 17.2%. The presence of DTC was independent from tumor histology, grade, lymphovascular space involvement (LVSI), FIGO stage, myoinvasion, L1CAM immunoreactivity, and nodal metastasis. DTC occurred less frequently in cases with a microcystic elongated and fragmented (MELF) pattern of invasion (2.2 vs. 21.8%, p = 0.0003). Disease progression was distributed equally among patients with and without DTC present. CONCLUSIONS: We were able to confirm previous findings of DTC presence in a large well-characterized cohort of endometrial carcinoma patients. DTC are detectable in almost one-fifth of endometrial carcinoma and occur less frequently with a MELF pattern of invasion. Further studies investigating the role of DTC in endometrial carcinoma are warranted.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Neoplasias do Endométrio/patologia
Células Neoplásicas Circulantes/patologia
Molécula L1 de Adesão de Célula Nervosa/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Medula Óssea/imunologia
Medula Óssea/patologia
Progressão da Doença
Neoplasias do Endométrio/imunologia
Neoplasias do Endométrio/metabolismo
Feminino
Seguimentos
Seres Humanos
Técnicas Imunoenzimáticas
Metástase Linfática
Meia-Idade
Gradação de Tumores
Invasividade Neoplásica
Estadiamento de Neoplasias
Células Neoplásicas Circulantes/metabolismo
Molécula L1 de Adesão de Célula Nervosa/imunologia
Prognóstico
Fatores de Risco
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Neural Cell Adhesion Molecule L1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170716
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2474-7


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[PMID]:28625395
[Au] Autor:Soovares P; Pasanen A; Bützow R; Lassus H
[Ad] Endereço:Department of Obstetrics and Gynecology, University of Helsinki, Helsinki University Hospital, Haartmaninkatu 2, PO Box 140, 00290 Helsinki, Finland. Electronic address: piret.soovares@hus.fi.
[Ti] Título:L1CAM expression associates with poor outcome in endometrioid, but not in clear cell ovarian carcinoma.
[So] Source:Gynecol Oncol;146(3):615-622, 2017 Sep.
[Is] ISSN:1095-6859
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Our aim was to study the expression of L1CAM in endometrioid and clear cell ovarian carcinomas and to evaluate its correlation with clinical parameters and patient prognosis. METHODS: Tissue microarray -based immunohistochemical analysis of L1CAM expression was performed in 249 endometrioid and 140 clear cell ovarian carcinomas. Concurrent endometrial carcinoma was found in 57 of these patients. RESULTS: L1CAM expression was found in 15% of endometrioid and 23% of clear cell ovarian carcinomas. L1CAM expression was strongly associated with poor disease-specific overall survival and poor disease-free survival in endometrioid (p<0.0001, p=0.0005), but not in clear cell ovarian carcinomas. Significant association of L1CAM expression with poor overall survival was observed in grade 1-2 carcinomas (p<0.0001), but not in grade 3 tumors. In endometrioid ovarian carcinomas, L1CAM expression was associated with aggressive tumor characteristics, such as higher grade and stage, and incomplete response to primary therapy. However, L1CAM expression was not an independent prognostic factor for overall or disease-free survival. Of the 57 patients with concurrent endometrial carcinoma L1CAM positivity was found in 4 cases both in the ovarian and endometrial tumors, and in 3 cases only in the endometrial tumor. All these seven patients with L1CAM positive tumors had poor outcome. CONCLUSIONS: L1CAM expression could serve as a biomarker for predicting clinical outcome and response to therapy in patients with endometrioid ovarian carcinoma, but not in clear cell carcinomas. L1CAM positivity also predicts poor outcome in patients with concurrent endometrioid ovarian and endometrial carcinomas.
[Mh] Termos MeSH primário: Adenocarcinoma de Células Claras/química
Carcinoma Endometrioide/química
Neoplasias do Endométrio/química
Neoplasias Primárias Múltiplas/química
Molécula L1 de Adesão de Célula Nervosa/análise
Neoplasias Ovarianas/química
[Mh] Termos MeSH secundário: Adenocarcinoma de Células Claras/patologia
Adenocarcinoma de Células Claras/terapia
Biomarcadores Tumorais/análise
Carcinoma Endometrioide/patologia
Carcinoma Endometrioide/terapia
Intervalo Livre de Doença
Neoplasias do Endométrio/patologia
Neoplasias do Endométrio/terapia
Feminino
Seguimentos
Seres Humanos
Meia-Idade
Gradação de Tumores
Estadiamento de Neoplasias
Neoplasias Primárias Múltiplas/patologia
Neoplasias Primárias Múltiplas/terapia
Neoplasias Ovarianas/patologia
Neoplasias Ovarianas/terapia
Taxa de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Neural Cell Adhesion Molecule L1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE


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[PMID]:28443372
[Au] Autor:Garbuzova-Davis S; Ehrhart J; Sanberg PR
[Ad] Endereço:a Center of Excellence for Aging & Brain Repair , University of South Florida, Morsani College of Medicine , Tampa , FL , USA.
[Ti] Título:Cord blood as a potential therapeutic for amyotrophic lateral sclerosis.
[So] Source:Expert Opin Biol Ther;17(7):837-851, 2017 Jul.
[Is] ISSN:1744-7682
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive motor neuron degeneration in the brain and spinal cord. Treatment options are limited due to the complexity of underlying disease factors. Cell therapy, using human umbilical cord blood (hUCB) cells may be a promising new treatment for ALS, mainly by providing a protective microenvironment for motor neuron survival. Areas covered: Composition, in vitro and in vivo differentiation of hUCB cells, and the advantages of cord blood as a source of transplant cells are discussed. A brief history of hUCB in treatment of an ALS animal model and the feasibility of these cells in therapy for ALS patients is provided. Current ALS clinical trials are also deliberated. Expert opinion: Among multiple advantages, hUCB cells' production of various anti-inflammatory/growth/trophic factors makes them an attractive cell source for ALS therapy. Biodistribution and optimal hUCB cell dose for transplantation have been determined in preclinical studies. Repeated intravenous cell doses during disease progression may be the best approach for cell-based ALS treatment. Accumulated evidence shows the efficacy of naïve or genetically modified MNC hUCB cells in the treatment of ALS and provide a superior basis for the development of clinical trials in the near future.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/terapia
Sangue Fetal/transplante
[Mh] Termos MeSH secundário: Esclerose Amiotrófica Lateral/metabolismo
Esclerose Amiotrófica Lateral/patologia
Animais
Diferenciação Celular
Terapia Baseada em Transplante de Células e Tecidos
Ensaios Clínicos como Assunto
Modelos Animais de Doenças
Sangue Fetal/citologia
Sangue Fetal/metabolismo
Seres Humanos
Molécula L1 de Adesão de Célula Nervosa/genética
Molécula L1 de Adesão de Célula Nervosa/metabolismo
Distribuição Tecidual
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Neural Cell Adhesion Molecule L1); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1080/14712598.2017.1323862


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[PMID]:28239515
[Au] Autor:Gilabert-Juan J; Bueno-Fernandez C; Castillo-Gomez E; Nacher J
[Ad] Endereço:Neurobiology UnitProgram in Neurosciences and Interdisciplinary Research Structure for Biotechnology and Biomedicine (BIOTECMED)Universitat de ValènciaBurjassotSpain; Genetics DepartmentUniversitat de ValènciaBurjassotSpain; CIBERSAM: Spanish National Network for Research in Mental HealthBurjassotSp
[Ti] Título:Reduced interneuronal dendritic arborization in CA1 but not in CA3 region of mice subjected to chronic mild stress.
[So] Source:Brain Behav;7(2):e00534, 2017 Feb.
[Is] ISSN:2162-3279
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Chronic stress induces dendritic atrophy and decreases spine density in excitatory hippocampal neurons, although there is also ample evidence indicating that the GABAergic system is altered in the hippocampus after this aversive experience. Chronic stress causes dendritic remodeling both in excitatory neurons and interneurons in the medial prefrontal cortex and the amygdala. METHODS: In order to know whether it also has an impact on the structure and neurotransmission of hippocampal interneurons, we have analyzed the dendritic arborization, spine density, and the expression of markers of inhibitory synapses and plasticity in the hippocampus of mice submitted to 21 days of mild restrain stress. The analyses were performed in GIN mice, a strain that displays EGFP-labeled interneurons. RESULTS: We observed a significant decrease in the dendritic arborization of interneurons in the CA1 region, which did not occur in those in CA3. We found neither changes in dendritic spine density in these regions nor alterations in the number of EGFP-positive interneurons. Nevertheless, the expression of glutamic acid decarboxylase 67 was reduced in different layers of CA1 and CA3 regions of the hippocampus. No significant changes were found in the expression of the polysialylated form of the neural cell adhesion molecule (PSA-NCAM) or synaptophysin. CONCLUSIONS: Chronic stress reduces the interneuronal dendritic arborization in CA1 region of the hippocampus but not in CA3.
[Mh] Termos MeSH primário: Região CA1 Hipocampal
Região CA3 Hipocampal
Espinhas Dendríticas/fisiologia
Glutamato Descarboxilase/metabolismo
Interneurônios/fisiologia
Plasticidade Neuronal/fisiologia
Estresse Psicológico
[Mh] Termos MeSH secundário: Animais
Região CA1 Hipocampal/citologia
Região CA1 Hipocampal/enzimologia
Região CA1 Hipocampal/fisiopatologia
Região CA3 Hipocampal/citologia
Região CA3 Hipocampal/enzimologia
Região CA3 Hipocampal/fisiopatologia
Contagem de Células
Espinhas Dendríticas/enzimologia
Interneurônios/citologia
Interneurônios/enzimologia
Masculino
Camundongos
Molécula L1 de Adesão de Célula Nervosa/metabolismo
Ácidos Siálicos/metabolismo
Estresse Psicológico/enzimologia
Estresse Psicológico/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neural Cell Adhesion Molecule L1); 0 (Sialic Acids); 0 (polysialyl neural cell adhesion molecule); EC 4.1.1.15 (Glutamate Decarboxylase); EC 4.1.1.15 (glutamate decarboxylase 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170228
[St] Status:MEDLINE
[do] DOI:10.1002/brb3.534


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[PMID]:28166242
[Au] Autor:Cho S; Lee TS; Song IH; Kim AR; Lee YJ; Kim H; Hwang H; Jeong MS; Kang SG; Hong HJ
[Ad] Endereço:Department of Functional Genomics, University of Science & Technology, Daejeon, Republic of Korea.
[Ti] Título:Combination of anti-L1 cell adhesion molecule antibody and gemcitabine or cisplatin improves the therapeutic response of intrahepatic cholangiocarcinoma.
[So] Source:PLoS One;12(2):e0170078, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cholangiocarcinoma has a poor prognosis and is refractory to conventional chemotherapy and radiation therapy. Improving survival of patients with advanced cholangiocarcinoma urgently requires the development of new effective targeted therapies in combination with chemotherapy. We previously developed a human monoclonal antibody (mAb) Ab417 that binds to both the human and mouse L1 cell adhesion molecule (L1CAM) with high affinities. In the present study, we observed that Ab417 exhibited tumor targeting ability in biodistribution studies and dose-dependent tumor growth inhibition in an intrahepatic cholangiocarcinoma (Choi-CK) xenograft mouse model. Regarding the mechanism of action, Ab417 was internalized into the tumor cells and thereby down-regulated membrane L1CAM, and inhibited tumor growth by reducing tumor cell proliferation in vivo. Gemcitabine inhibited the tumor growth in a dose-dependent manner in the Choi-CK xenograft model. However, cisplatin inhibited the tumor growth moderately and not in a dose-dependent way, suggesting that the tumors may have developed resistance to apoptosis induced by cisplatin. Combined treatment with Ab417 and gemcitabine or cisplatin exerted enhanced tumor growth inhibition compared to treatment with antibody or drug alone. The results suggest that Ab417 in combination with chemotherapy may have potential as a new therapeutic regimen for cholangiocarcinoma. Our study is the first to show an enhanced therapeutic effect of a therapeutic antibody targeting L1CAM in combination with chemotherapy in cholangiocarcinoma models.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Neoplasias dos Ductos Biliares/metabolismo
Colangiocarcinoma/metabolismo
Cisplatino/farmacologia
Desoxicitidina/análogos & derivados
Molécula L1 de Adesão de Célula Nervosa/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Neoplasias dos Ductos Biliares/tratamento farmacológico
Neoplasias dos Ductos Biliares/patologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Colangiocarcinoma/tratamento farmacológico
Colangiocarcinoma/patologia
Desoxicitidina/farmacologia
Modelos Animais de Doenças
Seres Humanos
Camundongos
Terapia de Alvo Molecular
Distribuição Tecidual
Carga Tumoral/efeitos dos fármacos
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Neural Cell Adhesion Molecule L1); 0W860991D6 (Deoxycytidine); B76N6SBZ8R (gemcitabine); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170207
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0170078


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[PMID]:28134764
[Au] Autor:Angiolini F; Cavallaro U
[Ad] Endereço:Unit of Gynecological Oncology Research, European Institute of Oncology, Via G. Ripamonti 435, I-20141 Milan, Italy. francesca.angiolini@ieo.it.
[Ti] Título:The Pleiotropic Role of L1CAM in Tumor Vasculature.
[So] Source:Int J Mol Sci;18(2), 2017 Jan 26.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Angiogenesis, the formation of new vessels, is a key step in the development, invasion, and dissemination of solid tumors and, therefore, represents a viable target in the context of antitumor therapy. Indeed, antiangiogenic approaches have given promising results in preclinical models and entered the clinical practice. However, in patients, the results obtained so far with antiangiogenic drugs have not completely fulfilled expectations, especially because their effect has been transient with tumors developing resistance and evasion mechanisms. A better understanding of the mechanisms that underlie tumor vascularization and the functional regulation of cancer vessels is a prerequisite for the development of novel and alternative antiangiogenic treatments. The L1 cell adhesion molecule (L1CAM), a cell surface glycoprotein previously implicated in the development and plasticity of the nervous system, is aberrantly expressed in the vasculature of various cancer types. L1CAM plays multiple pro-angiogenic roles in the endothelial cells of tumor-associated vessels, thus emerging as a potential therapeutic target. In addition, L1CAM prevents the maturation of cancer vasculature and its inhibition promotes vessel normalization, a process that is thought to improve the therapeutic response of tumors to cytotoxic drugs. We here provide an overview on tumor angiogenesis and antiangiogenic therapies and summarize the current knowledge on the biological role of L1CAM in cancer vasculature. Finally, we highlight the clinical implications of targeting L1CAM as a novel antiangiogenic and vessel-normalizing approach.
[Mh] Termos MeSH primário: Pleiotropia Genética
Neoplasias/irrigação sanguínea
Neoplasias/metabolismo
Neovascularização Patológica/metabolismo
Molécula L1 de Adesão de Célula Nervosa/metabolismo
[Mh] Termos MeSH secundário: Inibidores da Angiogênese/uso terapêutico
Animais
Seres Humanos
Neovascularização Patológica/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Neural Cell Adhesion Molecule L1)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170131
[St] Status:MEDLINE


  9 / 1185 MEDLINE  
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[PMID]:28068836
[Au] Autor:Wei Z; Wang Y; Zhao W; Schachner M
[Ad] Endereço:1 Center for Neuroscience, Shantou University Medical College, 22 Xin Ling Road, Shantou, Guangdong 515041, P.R. China.
[Ti] Título:Electro-Acupuncture Modulates L1 Adhesion Molecule Expression After Mouse Spinal Cord Injury.
[So] Source:Am J Chin Med;45(1):37-52, 2017.
[Is] ISSN:0192-415X
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Ab] Resumo:Spinal cord injury is a devastating neurological disease in desperate need of a cure. We have previously shown that overexpression of the adhesion molecule L1 contributes to locomotor recovery after injury and were therefore interested in how electro-acupuncture would influence the expression of this molecule. Here, we investigated the effects of electro-acupuncture at "Jiaji" points (EX-B2), newly established by us, in young adult mice to determine whether improved recovery via electro-acupuncture could be due to enhanced L1 expression. Locomotor function, as evaluated by the Basso Mouse Scale score and by catwalk gait parameters, was improved by electro-acupuncture at different time points after injury in parallel with enhanced levels of L1 expression. Interestingly, the levels of the astrocytic marker glial fibrillary acidic protein (GFAP) were also increased, but only in the early phase after injury, being reduced at later stages during recovery. Acupuncture alone showed less pronounced changes in expression of these molecules. We propose that electro-acupuncture improves regeneration in part by promoting the L1 expression and beneficial activation of stem cells, and by differentially modulating the expression of GFAP by promoting regeneration-conductive astrocytic responses at initial stages and reducing regeneration-adversive activation in the secondary stages. Expression of the stem cell marker nestin was upregulated by electro-acupuncture in the acute stage. The combined observations show for the first time in mice the beneficial functions of electro-acupuncture at Jiaji points in the spinal cord injury mouse model and provide novel insights into some molecular mechanisms underlying electro-acupuncture in spinal cord injury.
[Mh] Termos MeSH primário: Eletroacupuntura
Proteína Glial Fibrilar Ácida/metabolismo
Locomoção
Nestina/metabolismo
Molécula L1 de Adesão de Célula Nervosa/metabolismo
Traumatismos da Medula Espinal/metabolismo
Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Modelos Animais de Doenças
Ensaio de Imunoadsorção Enzimática
Feminino
Camundongos
Camundongos Endogâmicos C57BL
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glial Fibrillary Acidic Protein); 0 (Nes protein, mouse); 0 (Nestin); 0 (Neural Cell Adhesion Molecule L1); 0 (glial fibrillary astrocytic protein, mouse)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170214
[Lr] Data última revisão:
170214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170111
[St] Status:MEDLINE
[do] DOI:10.1142/S0192415X17500045


  10 / 1185 MEDLINE  
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[PMID]:28061460
[Au] Autor:Jo DH; Lee K; Kim JH; Jun HO; Kim Y; Cho YL; Yu YS; Min JK; Kim JH
[Ad] Endereço:Fight against Angiogenesis-Related Blindness (FARB) Laboratory, Clinical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea.
[Ti] Título:L1 increases adhesion-mediated proliferation and chemoresistance of retinoblastoma.
[So] Source:Oncotarget;8(9):15441-15452, 2017 Feb 28.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Retinoblastoma is the most common intraocular cancer in children, affecting 1/20,000 live births. Currently, children with retinoblastoma were treated with chemotherapy using drugs such as carboplatin, vincristine, and etoposide. Unfortunately, if conventional treatment fails, the affected eyes should be removed to prevent extension into adjacent tissues and metastasis. This study is to investigate the roles of L1 in adhesion-mediated proliferation and chemoresistance of retinoblastoma. L1 was differentially expressed in 30 retinoblastoma tissues and 2 retinoblastoma cell lines. Furthermore, the proportions of L1-positive cells in retinoblastoma tumors were negatively linked with the number of Flexner-Wintersteiner rosettes, a characteristic of differentiated retinoblastoma tumors, in each tumor sample. Following in vitro experiments using L1-deleted and -overexpressing cells showed that L1 increased adhesion-mediated proliferation of retinoblastoma cells via regulation of cell cycle-associated proteins with modulation of Akt, extracellular signal-regulated kinase, and p38 pathways. In addition, L1 increased resistance against carboplatin, vincristine, and esoposide through up-regulation of apoptosis- and multidrug resistance-related genes. In vivo tumor formation and chemoresistance were also positively linked with the levels of L1 in an orthotopic transplantation model in mice. In this manner, L1 increases adhesion-mediated proliferation and chemoresistance of retinoblastoma. Targeted therapy to L1 might be effective in the treatment of retinoblastoma tumors, especially which rapidly proliferate and demonstrate resistance to conventional chemotherapeutic drugs.
[Mh] Termos MeSH primário: Proliferação Celular/genética
Resistência a Medicamentos Antineoplásicos/genética
Molécula L1 de Adesão de Célula Nervosa/genética
Neoplasias da Retina/genética
Retinoblastoma/genética
[Mh] Termos MeSH secundário: Membro 1 da Subfamília B de Cassetes de Ligação de ATP/genética
Membro 1 da Subfamília B de Cassetes de Ligação de ATP/metabolismo
Adolescente
Adulto
Animais
Antineoplásicos/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Apoptose/efeitos dos fármacos
Apoptose/genética
Western Blotting
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Criança
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Camundongos Endogâmicos BALB C
Camundongos Nus
Molécula L1 de Adesão de Célula Nervosa/metabolismo
Interferência de RNA
Neoplasias da Retina/tratamento farmacológico
Neoplasias da Retina/metabolismo
Retinoblastoma/tratamento farmacológico
Retinoblastoma/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Ensaios Antitumorais Modelo de Xenoenxerto
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATP-Binding Cassette, Sub-Family B, Member 1); 0 (Antineoplastic Agents); 0 (Neural Cell Adhesion Molecule L1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170107
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.14487



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