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Pesquisa : D23.050.285.050.050 [Categoria DeCS]
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  1 / 1954 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


  2 / 1954 MEDLINE  
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[PMID]:29352318
[Au] Autor:William D; Walther M; Schneider B; Linnebacher M; Classen CF
[Ad] Endereço:University Children's and Adolescents' Hospital, University Medicine of Rostock, Rostock, Germany.
[Ti] Título:Temozolomide-induced increase of tumorigenicity can be diminished by targeting of mitochondria in in vitro models of patient individual glioblastoma.
[So] Source:PLoS One;13(1):e0191511, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastoma multiforme (GBM) is a highly heterogeneous and aggressive brain tumor with a dismal prognosis. Development of resistance towards cytostatic drugs like the GBM standard drug temozolomide is a severe problem in GBM treatment. One potential source of GBM relapse could be so called cancer stem like cells (CSCs). These represent an undifferentiated subpopulation of cells with high potential for tumor initiation. Furthermore, it has been shown that differentiated GBM cells can regain CSC properties when exposed to continuous temozolomide treatment in vitro. In this study, treatment of several primary GBM cell lines with clinically relevant doses of temozolomide increased their tumorigenicity as determined by colony formation assays in soft agar. Increased tumorigenicity is a known property of CSCs. Hence, therapy options that specifically target CSCs are under investigation. CSCs appear to be particularly dependent on mitochondria biogenesis which may represent a useful target for CSC elimination. Toxicity towards mitochondria is a known side effect of several antibiotics. Thus, addition of antibiotics like doxycycline may represent a useful tool to inhibit CSCs in GBM. Here, we show that combining temozolomide treatment of primary GBM cells with doxycycline could counteract the increase of tumorigenicity induced by temozolomide treatment.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/efeitos adversos
Neoplasias Encefálicas/tratamento farmacológico
Neoplasias Encefálicas/patologia
Dacarbazina/análogos & derivados
Glioblastoma/tratamento farmacológico
Glioblastoma/patologia
[Mh] Termos MeSH secundário: Antibacterianos/administração & dosagem
Antineoplásicos Alquilantes/administração & dosagem
Biomarcadores Tumorais/metabolismo
Neoplasias Encefálicas/metabolismo
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Metilases de Modificação do DNA/genética
Enzimas Reparadoras do DNA/genética
Dacarbazina/administração & dosagem
Dacarbazina/efeitos adversos
Doxiciclina/administração & dosagem
Resistência a Medicamentos Antineoplásicos
Fucosiltransferases/metabolismo
Glioblastoma/metabolismo
Seres Humanos
Antígeno Lewis X/metabolismo
Mitocôndrias/efeitos dos fármacos
Células-Tronco Neoplásicas/efeitos dos fármacos
Células-Tronco Neoplásicas/metabolismo
Células-Tronco Neoplásicas/patologia
Nestina/metabolismo
Ensaio Tumoral de Célula-Tronco
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Antineoplastic Agents, Alkylating); 0 (Biomarkers, Tumor); 0 (Lewis X Antigen); 0 (NES protein, human); 0 (Nestin); 0 (Tumor Suppressor Proteins); 7GR28W0FJI (Dacarbazine); EC 2.1.1.- (DNA Modification Methylases); EC 2.1.1.63 (MGMT protein, human); EC 2.4.1.- (FUT4 protein, human); EC 2.4.1.- (Fucosyltransferases); EC 6.5.1.- (DNA Repair Enzymes); N12000U13O (Doxycycline); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180121
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191511


  3 / 1954 MEDLINE  
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[PMID]:29183942
[Au] Autor:Urbanska M; Winzi M; Neumann K; Abuhattum S; Rosendahl P; Müller P; Taubenberger A; Anastassiadis K; Guck J
[Ad] Endereço:Cellular Machines, Biotechnology Center, Center for Molecular and Cellular Bioengineering, Technische Universität Dresden, Tatzberg 47-49, Dresden 01307, Germany marta.urbanska@tu-dresden.de jochen.guck@tu-dresden.de.
[Ti] Título:Single-cell mechanical phenotype is an intrinsic marker of reprogramming and differentiation along the mouse neural lineage.
[So] Source:Development;144(23):4313-4321, 2017 Dec 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cellular reprogramming is a dedifferentiation process during which cells continuously undergo phenotypical remodeling. Although the genetic and biochemical details of this remodeling are fairly well understood, little is known about the change in cell mechanical properties during the process. In this study, we investigated changes in the mechanical phenotype of murine fetal neural progenitor cells (fNPCs) during reprogramming to induced pluripotent stem cells (iPSCs). We find that fNPCs become progressively stiffer en route to pluripotency, and that this stiffening is mirrored by iPSCs becoming more compliant during differentiation towards the neural lineage. Furthermore, we show that the mechanical phenotype of iPSCs is comparable with that of embryonic stem cells. These results suggest that mechanical properties of cells are inherent to their developmental stage. They also reveal that pluripotent cells can differentiate towards a more compliant phenotype, which challenges the view that pluripotent stem cells are less stiff than any cells more advanced developmentally. Finally, our study indicates that the cell mechanical phenotype might be utilized as an inherent biophysical marker of pluripotent stem cells.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Reprogramação Celular/fisiologia
Células-Tronco Neurais/citologia
Células-Tronco Neurais/fisiologia
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Fenômenos Biomecânicos
Antígeno CD24/metabolismo
Diferenciação Celular/genética
Linhagem da Célula/genética
Linhagem da Célula/fisiologia
Reprogramação Celular/genética
Células-Tronco Pluripotentes Induzidas/classificação
Células-Tronco Pluripotentes Induzidas/citologia
Células-Tronco Pluripotentes Induzidas/fisiologia
Antígeno Lewis X/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Células-Tronco Neurais/classificação
Fenótipo
Análise de Célula Única
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CD24 Antigen); 0 (Cd24a protein, mouse); 0 (Lewis X Antigen)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1242/dev.155218


  4 / 1954 MEDLINE  
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[PMID]:28718379
[Au] Autor:Picot T; Aanei CM; Fayard A; Flandrin-Gresta P; Tondeur S; Gouttenoire M; Tavernier-Tardy E; Wattel E; Guyotat D; Campos L
[Ad] Endereço:1 Laboratoire d'Hématologie, CHU de Saint-Etienne, Saint-Etienne, France.
[Ti] Título:Expression of embryonic stem cell markers in acute myeloid leukemia.
[So] Source:Tumour Biol;39(7):1010428317716629, 2017 Jul.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute myeloid leukemia is driven by leukemic stem cells which can be identified by cross lineage expression or arrest of differentiation compared to normal hematopoietic stem cells. Self-renewal and lack of differentiation are also features of stem cells and have been associated with the expression of embryonic genes. The aim of our study was to evaluate the expression of embryonic antigens (OCT4, NANOG, SOX2, SSEA1, SSEA3) in hematopoietic stem cell subsets (CD34 CD38 and CD34 CD38 ) from normal bone marrows and in samples from acute myeloid leukemia patients. We observed an upregulation of the transcription factors OCT4 and SOX2 in leukemic cells as compared to normal cells. Conversely, SSEA1 protein was downregulated in leukemic cells. The expression of OCT4, SOX2, and SSEA3 was higher in CD34 CD38 than in CD34 CD38 subsets in leukemic cells. There was no correlation with biological characteristics of the leukemia. We evaluated the prognostic value of marker expression in 69 patients who received an intensive treatment. The rate of complete remission was not influenced by the level of expression of markers. Overall survival was significantly better for patients with high SOX2 levels, which was unexpected because of the inverse correlation with favorable genetic subtypes. These results prompt us to evaluate the potential role of these markers in leukemogenesis and to test their relevance for better leukemic stem cell identification.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/biossíntese
Fucosiltransferases/biossíntese
Leucemia Mieloide Aguda/tratamento farmacológico
Antígeno Lewis X/biossíntese
Fator 3 de Transcrição de Octâmero/biossíntese
Fatores de Transcrição SOXB1/biossíntese
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/genética
Adulto
Idoso
Antígenos CD34/genética
Células da Medula Óssea/metabolismo
Diferenciação Celular/genética
Células-Tronco Embrionárias/metabolismo
Células-Tronco Embrionárias/patologia
Feminino
Citometria de Fluxo
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Células-Tronco Hematopoéticas/efeitos dos fármacos
Células-Tronco Hematopoéticas/patologia
Seres Humanos
Imunofenotipagem
Leucemia Mieloide Aguda/genética
Leucemia Mieloide Aguda/patologia
Masculino
Meia-Idade
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (Biomarkers, Tumor); 0 (Lewis X Antigen); 0 (Octamer Transcription Factor-3); 0 (POU5F1 protein, human); 0 (SOX2 protein, human); 0 (SOXB1 Transcription Factors); EC 2.4.1.- (FUT4 protein, human); EC 2.4.1.- (Fucosyltransferases); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317716629


  5 / 1954 MEDLINE  
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[PMID]:28666020
[Au] Autor:Kumar R; de Mooij T; Peterson TE; Kaptzan T; Johnson AJ; Daniels DJ; Parney IF
[Ad] Endereço:Department of Neurological Surgery, Mayo Clinic, Rochester, Minnesota, United States of America.
[Ti] Título:Modulating glioma-mediated myeloid-derived suppressor cell development with sulforaphane.
[So] Source:PLoS One;12(6):e0179012, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastoma is the most common primary tumor of the brain and has few long-term survivors. The local and systemic immunosuppressive environment created by glioblastoma allows it to evade immunosurveillance. Myeloid-derived suppressor cells (MDSCs) are a critical component of this immunosuppression. Understanding mechanisms of MDSC formation and function are key to developing effective immunotherapies. In this study, we developed a novel model to reliably generate human MDSCs from healthy-donor CD14+ monocytes by culture in human glioma-conditioned media. Monocytic MDSC frequency was assessed by flow cytometry and confocal microscopy. The resulting MDSCs robustly inhibited T cell proliferation. A cytokine array identified multiple components of the GCM potentially contributing to MDSC generation, including Monocyte Chemoattractive Protein-1, interleukin-6, interleukin-8, and Macrophage Migration Inhibitory Factor (MIF). Of these, Macrophage Migration Inhibitory Factor is a particularly attractive therapeutic target as sulforaphane, a naturally occurring MIF inhibitor derived from broccoli sprouts, has excellent oral bioavailability. Sulforaphane inhibits the transformation of normal monocytes to MDSCs by glioma-conditioned media in vitro at pharmacologically relevant concentrations that are non-toxic to normal leukocytes. This is associated with a corresponding increase in mature dendritic cells. Interestingly, sulforaphane treatment had similar pro-inflammatory effects on normal monocytes in fresh media but specifically increased immature dendritic cells. Thus, we have used a simple in vitro model system to identify a novel contributor to glioblastoma immunosuppression for which a natural inhibitor exists that increases mature dendritic cell development at the expense of myeloid-derived suppressor cells when normal monocytes are exposed to glioma conditioned media.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/patologia
Glioblastoma/patologia
Isotiocianatos/farmacologia
Células Supressoras Mieloides/efeitos dos fármacos
[Mh] Termos MeSH secundário: Neoplasias Encefálicas/imunologia
Antígeno CD11b/imunologia
Hipóxia Celular
Linhagem Celular Tumoral
Meios de Cultivo Condicionados
Fucosiltransferases/imunologia
Glioblastoma/imunologia
Seres Humanos
Antígeno Lewis X/imunologia
Células Supressoras Mieloides/imunologia
Células Supressoras Mieloides/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11b Antigen); 0 (Culture Media, Conditioned); 0 (ITGAM protein, human); 0 (Isothiocyanates); 0 (Lewis X Antigen); EC 2.4.1.- (FUT4 protein, human); EC 2.4.1.- (Fucosyltransferases); GA49J4310U (sulforafan)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179012


  6 / 1954 MEDLINE  
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[PMID]:28475011
[Au] Autor:Alexiou GA; Lazari D; Markopoulos G; Vartholomatos E; Hodaj E; Galani V; Kyritsis AP
[Ad] Endereço:1 Neurosurgical Institute, School of Medicine, University of Ioannina, Ioannina, Greece.
[Ti] Título:Moschamine inhibits proliferation of glioblastoma cells via cell cycle arrest and apoptosis.
[So] Source:Tumour Biol;39(5):1010428317705744, 2017 May.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastoma is the most common and most malignant primary brain tumor with a median survival of 15 months. Moschamine is an indole alkaloid that has a serotoninergic and cyclooxygenase inhibitory effect. In this study, we sought to determine whether moschamine could exert cytotoxic and cytostatic effects on glioma cells in vitro. Moschamine was tested for toxicity in zebrafish. We investigated the effect of moschamine on U251MG and T98G glioblastoma cell lines. Viability and proliferation of the cells were examined with trypan blue exclusion assay, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and the xCELLigence system. Apoptosis (annexin-propidium iodide), cell cycle, and CD24/CD44/CD56/CD15 expression were tested with flow cytometry. Treatment with moschamine significantly reduced cell viability in both cell lines tested. Induction of cell death and cell cycle arrest was confirmed with flow cytometry in both cell lines. After treatment with moschamine, there was a dose-dependent decrease in CD24 and CD44 expression, whereas there was no change in CD56 and CD15 expression in T98G cell line. The zebrafish mortality on the fifth post-fertilization day was zero even for 1 mM of moschamine concentration. The treatment of glioblastoma cell lines with moschamine may represent a novel strategy for targeting glioblastoma.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Glioblastoma/tratamento farmacológico
Proteínas de Neoplasias/biossíntese
[Mh] Termos MeSH secundário: Animais
Antígeno CD24/biossíntese
Antígeno CD56/biossíntese
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Modelos Animais de Doenças
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Glioblastoma/patologia
Seres Humanos
Receptores de Hialuronatos/biossíntese
Antígeno Lewis X/biossíntese
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD24 Antigen); 0 (CD56 Antigen); 0 (Hyaluronan Receptors); 0 (Lewis X Antigen); 0 (Neoplasm Proteins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317705744


  7 / 1954 MEDLINE  
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[PMID]:28341903
[Au] Autor:Gillum T; Kuennen M; McKenna Z; Castillo M; Jordan-Patterson A; Bohnert C
[Ad] Endereço:Department of Kinesiology, California Baptist University, 8432 Magnolia Ave., Riverside, CA, 92504, USA. tgillum@calbaptist.edu.
[Ti] Título:Exercise increases lactoferrin, but decreases lysozyme in salivary granulocytes.
[So] Source:Eur J Appl Physiol;117(5):1047-1051, 2017 May.
[Is] ISSN:1439-6327
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Intracellular lactoferrin (Lac) and lysozyme (Lys) content play an important role in regulating inflammation and promoting host protection. While exercise has demonstrated an increase in Lac and Lys concentration in exocrine solutions, little is known regarding intracellular concentration changes in response to exercise. PURPOSE: To quantify intracellular Lac and Lys concentration before and after exercise in salivary CD45 CD15 cells. METHODS: 11 males (20.3 ± 0.8 years, 57.2 ± 7.6 mL/kg/min V̇O , 11.1 ± 3.9% body fat) ran for 45 min at 75% of VO . 12 mL of stimulated saliva were collected pre and immediately post exercise. Saliva was filtered through a 30-µm filter before analysis of leukocytes (CD45 ) and granulocytes (CD45 CD15 ) using flow cytometry. RESULTS: Median fluorescent intensity (MFI) of Lac increased from pre (64,268 ± 46,036 MFI) to post (117,134 ± 88,115 MFI) exercise (p <0.05). Lys MFI decreased with exercise (pre: 16,933 ± 8249; post: 11,616 ± 6875) (p <0.05). CONCLUSION: Acute running resulted in an increased Lac concentration which could lead to a decrease in inflammation, adding further evidence of the anti-inflammatory effects of exercise. Conversely, the exercise-associated decrease of intracellular Lys content could be the cause of increased Lys in exocrine solutions.
[Mh] Termos MeSH primário: Exercício
Granulócitos/metabolismo
Lactoferrina/metabolismo
Muramidase/metabolismo
Saliva/metabolismo
[Mh] Termos MeSH secundário: Seres Humanos
Antígenos Comuns de Leucócito/metabolismo
Antígeno Lewis X/metabolismo
Masculino
Saliva/citologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lewis X Antigen); EC 3.1.3.48 (Leukocyte Common Antigens); EC 3.2.1.17 (Muramidase); EC 3.4.21.- (Lactoferrin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170326
[St] Status:MEDLINE
[do] DOI:10.1007/s00421-017-3594-0


  8 / 1954 MEDLINE  
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[PMID]:27840089
[Au] Autor:Luo G; Liu C; Guo M; Long J; Liu Z; Xiao Z; Jin K; Cheng H; Lu Y; Ni Q; Yu X
[Ad] Endereço:Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China; Pancreatic Cancer Institute, Fudan University, Shanghai, 200032, China.
[Ti] Título:CA19-9-Low&Lewis (+) pancreatic cancer: A unique subtype.
[So] Source:Cancer Lett;385:46-50, 2017 01 28.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The study was performed to identify unique subtype from the long-term survival (>24 months) patients with advanced pancreatic cancer (1039 cases). Long-term survival patients had higher proportion of low secretion of carbohydrate antigen 19-9 (CA19-9) than that of patients with non long-term survival (P < 0.001). Considering the impact of Lewis status on CA19-9 secretion, Lewis genotypes were further determined by Sanger sequencing. The prognosis of CA19-9-Low&Lewis (-) patients was worse than that of CA19-9-Low&Lewis (+) (hazard ratio (HR) = 0.37, P < 0.001). The proportion of epidermal growth factor receptor (EGFR) (-) cases was lower in the CA19-9-Low&Lewis (+) subgroup than that in other patients (P = 0.047). For the CA19-9-Low&Lewis (+) subgroup, chemotherapy plus radiotherapy but not chemotherapy was found to be an independent prognostic factor (versus best supportive care, chemotherapy, HR = 0.71, P = 0.267; chemotherapy plus radiotherapy, HR = 0.33, P = 0.022). We conclude that CA19-9-Low&Lewis (+) pancreatic cancer is a unique subtype with special biological properties.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Adenocarcinoma/imunologia
Antígeno CA-19-9/sangue
Fucosiltransferases/genética
Antígeno Lewis X/genética
Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/imunologia
[Mh] Termos MeSH secundário: Adenocarcinoma/mortalidade
Adenocarcinoma/terapia
Antineoplásicos/uso terapêutico
Quimiorradioterapia
Distribuição de Qui-Quadrado
Bases de Dados Factuais
Feminino
Predisposição Genética para Doença
Seres Humanos
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Estadiamento de Neoplasias
Neoplasias Pancreáticas/mortalidade
Neoplasias Pancreáticas/terapia
Fenótipo
Modelos de Riscos Proporcionais
Fatores de Risco
Sobreviventes
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (CA-19-9 Antigen); 0 (Lewis X Antigen); EC 2.4.1.- (FUT4 protein, human); EC 2.4.1.- (Fucosyltransferases)
[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:161115
[St] Status:MEDLINE


  9 / 1954 MEDLINE  
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[PMID]:27757838
[Au] Autor:Aziz F; Gao W; Yan Q
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Liaoning Provincial Core Laboratory of Glycobiology and Glycoengineering, Dalian Medical University, Dalian, People's Republic of China.
[Ti] Título:Fucosyltransferase-4 and Oligosaccharide Lewis Y Antigen as potentially Correlative Biomarkers of Helicobacter pylori CagA Associated Gastric Cancer.
[So] Source:Pathol Oncol Res;23(1):173-179, 2017 Jan.
[Is] ISSN:1532-2807
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:H. pylori cytotoxin associated antigen A (CagA) plays a significant role in the progression of gastric cancer but their effect on fucosylation to develop gastric cancer is unknown. Fucosyltransferase IV (FUT4) is the key enzyme for synthesis of LewisY (LeY) carried by glycoproteins and glycolipids on the cell membrane. Herein, we compare the expression of CagA, p-EGFR, FUT4 and LeY in gastritis (n = 128, 176), gastric ulcer (n = 174, 213), and gastric cancer (n = 323, 261) tissue and serum samples, respectively by IHC and ELISA. Moreover, we investigated the potential correlation of CagA with FUT4 and LeY overexpression through EGFR activation. IHC and ELISA results showed higher positive cases of H. pylori CagA (83, 86 %), p-EGFR (81, 72 %), FUT4 (91, 97 %) and LeY (93, 92 %) in gastric cancer, compared to gastritis and gastric ulcer, H. pylori CagA (58, 67 & 59, 73 %), p-EGFR (52, 63 & 35, 47 %), FUT4 (68, 78 & 67, 82 %) and LeY (62,76 & 65, 85 %), respectively. We found a significant high expression (H-Value) of CagA (1.79, 1.66), p-EGFR (1.53, 1.58), FUT4 (2.14, 1.66) and LeY (1.69, 1.61) in gastric cancer tissues and serum, respectively as compared to chronic gastritis and gastric ulcers, CagA (0.64,1.14), p-EGFR (0.856, 0.678), FUT4 (0.949,1.197) and LeY (0.68,1.008) (P < 0.0001), respectively. Furthermore, H. pylori CagA showed significant correlation with p-EGFR (R-0.62, -0.74), FUT4 (R-0.81, -0.76) and LeY (R-0.82, -0.70) in gastric tissues and serum (P < 0.0001). H. pylori CagA plays key role in the development of gastric cancer with overexpression of FUT4/LeY, serve as potentially correlative biomarkers of H. pylori CagA associated gastric cancer.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Fucosiltransferases/metabolismo
Helicobacter pylori/patogenicidade
Sistema do Grupo Sanguíneo de Lewis/metabolismo
Antígeno Lewis X/metabolismo
Oligossacarídeos/metabolismo
Neoplasias Gástricas/metabolismo
Neoplasias Gástricas/microbiologia
[Mh] Termos MeSH secundário: Feminino
Gastrite/metabolismo
Gastrite/microbiologia
Infecções por Helicobacter/metabolismo
Infecções por Helicobacter/microbiologia
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Lewis Blood-Group System); 0 (Lewis X Antigen); 0 (Lewis Y antigen); 0 (Oligosaccharides); EC 2.4.1.- (FUT4 protein, human); EC 2.4.1.- (Fucosyltransferases)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE
[do] DOI:10.1007/s12253-016-0122-1


  10 / 1954 MEDLINE  
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[PMID]:27698250
[Au] Autor:Chuang SS
[Ad] Endereço:Department of Pathology, Chi-Mei Medical Center, Tainan, Taiwan.
[Ti] Título:Infrequent expression of CD15 by classical Hodgkin's lymphomas in Taiwan.
[So] Source:J Clin Pathol;70(2):183-184, 2017 Feb.
[Is] ISSN:1472-4146
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Doença de Hodgkin/patologia
Antígeno Lewis X/metabolismo
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/metabolismo
Doença de Hodgkin/metabolismo
Seres Humanos
Imuno-Histoquímica
Taiwan
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Lewis X Antigen)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161005
[St] Status:MEDLINE
[do] DOI:10.1136/jclinpath-2016-204074



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