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Alves, Luiz Carlos
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[PMID]:29366735
[Au] Autor:Mariz Gomes da Silva LM; de Oliveira JF; Silva WL; da Silva AL; de Almeida Junior ASA; Barbosa Dos Santos VH; Alves LC; Brayner Dos Santos FA; Costa VMA; Aires AL; de Lima MDCA; Albuquerque MCPA
[Ad] Endereço:Keizo Asami Immunopathology Laboratory (LIKA), Federal University of Pernambuco, 50740-465, Recife, PE, Brazil.
[Ti] Título:New 1,3-benzodioxole derivatives: Synthesis, evaluation of in vitro schistosomicidal activity and ultrastructural analysis.
[So] Source:Chem Biol Interact;283:20-29, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Schistosomiasis is considered a serious public health problem in 78 countries and territories located in Africa, Asia and America and it is estimated in more than 249 million people infected by any of the species of Schistosoma. The exclusive use of praziquantel (PZQ), effective drug against all species of Schistosoma, has been the basis of the development of a possible resistance against the strains of this parasite. In addition, PZQ is not effective against young forms of worms. Thus, there is a need for the development of new drugs with schistosomicidal activity. The objective of this work was to synthesize and to evaluate the therapeutic potential of new benzodioxole derivatives (3-14) candidates for schistosomicidal drugs. All compounds synthesized showed in vitro schistosomicidal activity. The derivative 12 was considered the best compound, since it took 100% of worms to mortality in the first 72 h of exposure at the concentration of 100 µM and 83.3% at the concentration of 50 µM. Furthermore, male and female adult worms, incubated for 24 h with the compound 12 showed tegument damages characterized by extensive desquamation and edema, tuber destruction, bubble formation and exposure of the muscle layer. This compound has a restricted structure, where the thiazolidinone is attached to the 4-position of the 1,3-benzodioxol ring. The structural conformation of derivative 12 was probably responsible for the promising schistosomicidal activity, where the presence of an electron/conformational restriction of the thiazolidine ring, as well as the action of bromine as a bulk substitute, favored an increase in biological activity. In addition, tegumentary changes caused by derivative 12 may also have been responsible for the death of adult worms of Schistosoma mansoni. Therefore, we verified that the results obtained in this study make benzodioxole derivatives possible candidates for prototypes of new schistosomicidal drugs.
[Mh] Termos MeSH primário: Dioxóis/química
Dioxóis/farmacologia
Schistosoma mansoni/efeitos dos fármacos
Esquistossomicidas/síntese química
Esquistossomicidas/farmacologia
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular/efeitos dos fármacos
Dioxóis/uso terapêutico
Células HeLa
Seres Humanos
Microscopia Eletrônica de Varredura
Praziquantel/farmacologia
Praziquantel/uso terapêutico
Schistosoma mansoni/ultraestrutura
Esquistossomose/tratamento farmacológico
Esquistossomose/patologia
Esquistossomicidas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dioxoles); 0 (Schistosomicides); 6490C9U457 (Praziquantel); F0XLL582B8 (1,3-benzodioxole)
[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:180126
[St] Status:MEDLINE


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[PMID]:28454547
[Au] Autor:Pignochino Y; Capozzi F; D'Ambrosio L; Dell'Aglio C; Basiricò M; Canta M; Lorenzato A; Vignolo Lutati F; Aliberti S; Palesandro E; Boccone P; Galizia D; Miano S; Chiabotto G; Napione L; Gammaitoni L; Sangiolo D; Benassi MS; Pasini B; Chiorino G; Aglietta M; Grignani G
[Ad] Endereço:Sarcoma Unit, Medical Oncology, Candiolo Cancer Institute - FPO, IRCCS, Candiolo, Torino, Italy. ymera.pignochino@ircc.it.
[Ti] Título:PARP1 expression drives the synergistic antitumor activity of trabectedin and PARP1 inhibitors in sarcoma preclinical models.
[So] Source:Mol Cancer;16(1):86, 2017 04 28.
[Is] ISSN:1476-4598
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Enhancing the antitumor activity of the DNA-damaging drugs is an attractive strategy to improve current treatment options. Trabectedin is an isoquinoline alkylating agent with a peculiar mechanism of action. It binds to minor groove of DNA inducing single- and double-strand-breaks. These kinds of damage lead to the activation of PARP1, a first-line enzyme in DNA-damage response pathways. We hypothesized that PARP1 targeting could perpetuate trabectedin-induced DNA damage in tumor cells leading finally to cell death. METHODS: We investigated trabectedin and PARP1 inhibitor synergism in several tumor histotypes both in vitro and in vivo (subcutaneous and orthotopic tumor xenografts in mice). We searched for key determinants of drug synergism by comparative genomic hybridization (aCGH) and gene expression profiling (GEP) and validated their functional role. RESULTS: Trabectedin activated PARP1 enzyme and the combination with PARP1 inhibitors potentiated DNA damage, cell cycle arrest at G2/M checkpoint and apoptosis, if compared to single agents. Olaparib was the most active PARP1 inhibitor to combine with trabectedin and we confirmed the antitumor and antimetastatic activity of trabectedin/olaparib combination in mice models. However, we observed different degree of trabectedin/olaparib synergism among different cell lines. Namely, in DMR leiomyosarcoma models the combination was significantly more active than single agents, while in SJSA-1 osteosarcoma models no further advantage was obtained if compared to trabectedin alone. aCGH and GEP revealed that key components of DNA-repair pathways were involved in trabectedin/olaparib synergism. In particular, PARP1 expression dictated the degree of the synergism. Indeed, trabectedin/olaparib synergism was increased after PARP1 overexpression and reduced after PARP1 silencing. CONCLUSIONS: PARP1 inhibition potentiated trabectedin activity in a PARP1-dependent manner and PARP1 expression in tumor cells might be a useful predictive biomarker that deserves clinical evaluation.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Dioxóis/administração & dosagem
Poli(ADP-Ribose) Polimerase-1/genética
Sarcoma/tratamento farmacológico
Tetra-Hidroisoquinolinas/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Hibridização Genômica Comparativa
Dano ao DNA/efeitos dos fármacos
Sinergismo Farmacológico
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Camundongos
Ftalazinas/administração & dosagem
Piperazinas/administração & dosagem
Poli(ADP-Ribose) Polimerase-1/antagonistas & inibidores
Sarcoma/genética
Sarcoma/patologia
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Dioxoles); 0 (Phthalazines); 0 (Piperazines); 0 (Tetrahydroisoquinolines); EC 2.4.2.30 (PARP1 protein, human); EC 2.4.2.30 (Poly (ADP-Ribose) Polymerase-1); ID0YZQ2TCP (trabectedin); WOH1JD9AR8 (olaparib)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1186/s12943-017-0652-5


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[PMID]:29237438
[Au] Autor:Khansai M; Phitak T; Klangjorhor J; Udomrak S; Fanhchaksai K; Pothacharoen P; Kongtawelert P
[Ad] Endereço:Thailand Excellence Center for Tissue Engineering and Stem Cells, Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
[Ti] Título:Effects of sesamin on primary human synovial fibroblasts and SW982 cell line induced by tumor necrosis factor-alpha as a synovitis-like model.
[So] Source:BMC Complement Altern Med;17(1):532, 2017 Dec 13.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic synovitis, cartilage degradation and bone deformities. Synovitis is the term for inflammation of the synovial membrane, an early stage of RA. The pathogenesis of the disease occurs through cytokine induction. The major cytokine that increases the severity of RA is TNF-α. Thus, inhibition of the TNF-α cascade is an effective way to diminish the progression of the disease. We are interested in investigating the difference between primary human synovial fibroblast (hSF) cells and SW982 as synovitis models induced by TNF-α and in monitoring their responses to sesamin as an anti-inflammatory phytochemical. METHOD: The designed experiments were performed in hSF cells or the SW982 cell line treated with 10 ng/ml TNF-α with or without 0.25, 0.5 or 1 µM sesamin. Subsequently, pro-inflammatory cytokine genes and proteins were measured in parallel with a study of associated signalling transduction involved in inflammatory processes, including NF-κB and MAPK pathways. RESULTS: The results demonstrated that although hSF and SW982 cells responded to TNF-α induction in the same fashion, they reacted at different levels. TNF-α could induce IL-6, IL-8 and IL-1ß in both cell types, but the levels in SW982 cells were much higher than in hSF cells. This characteristic was due to the different induction of MAPKs in each cell type. Both cell types reacted to sesamin in almost the same fashion. However, hSF cells were more sensitive to sesamin than SW982 cells in terms of the anti-RA effect. CONCLUSIONS: The responses of TNF-α-induced hSF and SW982 were different at the signal transduction level. However, the two cell types showed almost the same reaction to sesamin treatment in terms of the end point of the response.
[Mh] Termos MeSH primário: Dioxóis/farmacologia
Fibroblastos/efeitos dos fármacos
Lignanas/farmacologia
Membrana Sinovial/citologia
Sinovite/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Artrite Reumatoide
Linhagem Celular
Citocinas/metabolismo
Seres Humanos
Modelos Biológicos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Dioxoles); 0 (Lignans); 0 (Tumor Necrosis Factor-alpha); S7946O4P76 (sesamin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-2035-2


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[PMID]:28977600
[Au] Autor:Bai L; Chang HM; Cheng JC; Chu G; Leung PCK; Yang G
[Ad] Endereço:College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, People's Republic of China.
[Ti] Título:ALK2/ALK3-BMPR2/ACVR2A Mediate BMP2-Induced Downregulation of Pentraxin 3 Expression in Human Granulosa-Lutein Cells.
[So] Source:Endocrinology;158(10):3501-3511, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone morphogenetic protein 2 (BMP2) belongs to the transforming growth factor-ß superfamily and plays a critical role in regulating ovarian follicle function. Currently, the role of BMP2 during cumulus expansion remains to be determined. The aim of this study was to investigate the effect of BMP2 on the regulation of pentraxin 3 (PTX3) expression (the major component of cumulus expansion) and the underlying mechanisms in human granulosa-lutein (hGL) cells. Both primary and immortalized hGL cells were used as research models. Our results showed that treatment with BMP2 significantly suppressed the basal and luteinizing hormone-induced upregulation of PTX3. In addition, BMP2 stimulated the phosphorylation of SMAD1/5/8, and this effect was abolished by the addition of BMP type I receptor inhibitors, dorsomorphin homolog 1, and dorsomorphin but not SB431542. Moreover, the knockdown of activin receptorlike kinase 2/3 or BMP receptor type II/activin receptor type IIB receptors completely reversed the BMP2-induced phosphorylation of SMAD1/5/8 and restored PTX3 expression. Similarly, the knockdown of SMAD4 completely reversed the suppressive effect of BMP2 on the expression of PTX3. These results improve our understanding of the molecular mechanisms of BMP2 signaling. Our findings suggest that BMP2 may be involved in the regulation of cumulus expansion during the periovulatory stage.
[Mh] Termos MeSH primário: Proteína Morfogenética Óssea 2/farmacologia
Proteína C-Reativa/efeitos dos fármacos
Células Lúteas/efeitos dos fármacos
Componente Amiloide P Sérico/efeitos dos fármacos
[Mh] Termos MeSH secundário: Receptores de Ativinas Tipo I/genética
Receptores de Activinas Tipo II/genética
Benzamidas/farmacologia
Western Blotting
Receptores de Proteínas Morfogenéticas Ósseas Tipo I/genética
Receptores de Proteínas Morfogenéticas Ósseas Tipo II/genética
Proteína C-Reativa/genética
Proteína C-Reativa/metabolismo
Dioxóis/farmacologia
Regulação para Baixo
Ensaio de Imunoadsorção Enzimática
Feminino
Técnicas de Silenciamento de Genes
Seres Humanos
Células Lúteas/metabolismo
Indução da Ovulação
Fosforilação/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Pirazóis/farmacologia
Pirimidinas/farmacologia
RNA Interferente Pequeno
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Componente Amiloide P Sérico/genética
Componente Amiloide P Sérico/metabolismo
Proteína Smad1/efeitos dos fármacos
Proteína Smad1/metabolismo
Proteína Smad4/genética
Proteína Smad5/efeitos dos fármacos
Proteína Smad5/metabolismo
Proteína Smad8/efeitos dos fármacos
Proteína Smad8/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide); 0 (BMP2 protein, human); 0 (Benzamides); 0 (Bone Morphogenetic Protein 2); 0 (Dioxoles); 0 (Protein Kinase Inhibitors); 0 (Pyrazoles); 0 (Pyrimidines); 0 (RNA, Small Interfering); 0 (SMAD1 protein, human); 0 (SMAD4 protein, human); 0 (SMAD5 protein, human); 0 (SMAD8 protein, human); 0 (Serum Amyloid P-Component); 0 (Smad1 Protein); 0 (Smad4 Protein); 0 (Smad5 Protein); 0 (Smad8 Protein); 10K52CIC1Z ((6-(4-(2-piperidin-1-ylethoxy)phenyl))-3-pyridin-4-ylpyrazolo(1,5-a)pyrimidine); 148591-49-5 (PTX3 protein); 9007-41-4 (C-Reactive Protein); EC 2.7.11.30 (ACVR1 protein, human); EC 2.7.11.30 (ACVR2B protein, human); EC 2.7.11.30 (Activin Receptors, Type I); EC 2.7.11.30 (Activin Receptors, Type II); EC 2.7.11.30 (BMPR1A protein, human); EC 2.7.11.30 (BMPR2 protein, human); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors, Type I); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors, Type II); EC 2.7.11.30 (activin receptor type II-A)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00436


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[PMID]:28844238
[Au] Autor:Ono Y; Tomimori N; Hori H; Kitagawa Y; Shibata H
[Ad] Endereço:Suntory Wellness Limited, 8-1-1 Seikadai, Seika-cho, Soraku-gun, Kyoto 619-0284, Japan. Electronic address: Yoshiko_Toyoda@suntory.co.jp.
[Ti] Título:Mechanisms of chromosomal aberrations induced by sesamin metabolites in Chinese hamster lung cells.
[So] Source:Mutat Res;822:19-26, 2017 Oct.
[Is] ISSN:1873-135X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Sesamin is a major lignan in sesame seeds and oil. We previously demonstrated that sesamin induces chromosomal aberrations (CA) in Chinese hamster lung (CHL/IU) cells in the presence of a metabolic activation system (S9 mix), although no genotoxicity was detected in vivo. To clarify the mechanism of CA induction by sesamin, we identified its principal active metabolite. A mono-catechol derivative, [2-(3,4-methylenedioxyphenyl)-6-(3,4-dihydroxyphenyl)-3,7-dioxabi-cyclo[3.3.0]octane (SC-1)], was previously identified in culture medium when sesamin was incubated with S9 mix. In the present study, we show that SC-1 induces CA in CHL/IU cells but not in human hepatoblastoma (HepG2) cells. SC-1 was unstable in culture medium. Addition of glutathione (GSH) to the incubation mixture decreased the rate of decomposition and also suppressed induction of CA in CHL/IU cells. These results indicate that SC-1 itself may not contribute to the induction of CA. Two GSH adducts of SC-1 were identified when SC-1 was incubated with GSH, suggesting that SC-1 was converted to the semiquinone/quinone form and then conjugated with GSH in the culture medium. Sodium sulfite (a quinone-responsive compound) also suppressed CA induction by SC-1. These findings strongly suggest that SC-1 is oxidized to semiquinone/quinone derivatives extracellularly in culture medium, that these derivatives are responsible for the induction of CA in CHL/IU cells, and therefore that the positive results obtained with sesamin in in vitro CA tests using CHL/IU cells may not be relevant to the assessment of in vivo activity.
[Mh] Termos MeSH primário: Compostos Bicíclicos Heterocíclicos com Pontes/toxicidade
Aberrações Cromossômicas/induzido quimicamente
Ciclo-Octanos/toxicidade
Dioxóis/toxicidade
Lignanas/toxicidade
[Mh] Termos MeSH secundário: Animais
Compostos Bicíclicos Heterocíclicos com Pontes/metabolismo
Técnicas de Cultura de Células
Cricetinae
Ciclo-Octanos/metabolismo
Dioxóis/metabolismo
Relação Dose-Resposta a Droga
Glutationa/metabolismo
Células Hep G2
Seres Humanos
Lignanas/metabolismo
Fígado/metabolismo
Extratos Hepáticos
Pulmão/citologia
Pulmão/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(3,4-methylenedioxyphenyl)-6-(3,4-dihydroxyphenyl)-3,7-dioxabicyclo(3.3.0)octane); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Cyclooctanes); 0 (Dioxoles); 0 (Lignans); 0 (Liver Extracts); GAN16C9B8O (Glutathione); S7946O4P76 (sesamin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE


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[PMID]:28825853
[Au] Autor:Pignata S; Scambia G; Bologna A; Signoriello S; Vergote IB; Wagner U; Lorusso D; Murgia V; Sorio R; Ferrandina G; Sacco C; Cormio G; Breda E; Cinieri S; Natale D; Mangili G; Pisano C; Cecere SC; Di Napoli M; Salutari V; Raspagliesi F; Arenare L; Bergamini A; Bryce J; Daniele G; Piccirillo MC; Gallo C; Perrone F
[Ad] Endereço:Sandro Pignata, Carmela Pisano, Sabrina Chiara Cecere, Marilena Di Napoli, Laura Arenare, Alice Bergamini, Jane Bryce, Gennaro Daniele, Maria Carmela Piccirillo, and Francesco Perrone, Istituto Nazionale per lo Studio e la Cura dei Tumori-Fondazione G. Pascale, IRCCS; Simona Signoriello and Ciro Gal
[Ti] Título:Randomized Controlled Trial Testing the Efficacy of Platinum-Free Interval Prolongation in Advanced Ovarian Cancer: The MITO-8, MaNGO, BGOG-Ov1, AGO-Ovar2.16, ENGOT-Ov1, GCIG Study.
[So] Source:J Clin Oncol;35(29):3347-3353, 2017 Oct 10.
[Is] ISSN:1527-7755
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose Platinum-based chemotherapy (PBC) for patients with progressing ovarian cancer (OC) is more effective with a longer time interval from previous platinum treatment (platinum-free interval [PFI]). In 1999, it was hypothesized that prolonging PFI with single-agent non-PBC (NPBC) may offer a strategy to improve overall outcome. MITO-8 aimed to verify this hypothesis commonly used in clinical practice although it has not been prospectively tested. Methods MITO-8 is an open-label, prospective, randomized, superiority trial. Patients with OC who experienced disease progression 6 to 12 months after their last platinum treatment were randomly assigned 1:1 to the experimental sequence of NPBC followed by PBC at subsequent relapse or the standard reverse treatment sequence. Overall survival (OS) was the primary end point. Results Two hundred fifteen patients were enrolled (standard arm [n = 108]; experimental arm [n = 107]). The trial ended before planned because of slow enrollment. PFI was prolonged in the experimental arm (median, 7.8 v 0.01 months). There was no OS benefit in the experimental arm (median, 21.8 v 24.5 months; hazard ratio, 1.38; 95% CI, 0.99 to 1.94; P = .06). Progression-free survival after the sequence was significantly shorter in the experimental arm (median, 12.8 v 16.4 months; hazard ratio, 1.41; 95% CI, 1.04 to 1.92; P = .025). Global quality-of-life change after three cycles was worse in the experimental arm. Slight differences were observed in the incidence of adverse effects. Conclusion MITO-8 supports the recommendation that PBC not be delayed in favor of an NPBC in patients with partially platinum-sensitive OC. PBC should be used as a control arm in future trials of new drugs in this setting.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Neoplasias Ovarianas/tratamento farmacológico
[Mh] Termos MeSH secundário: Idoso
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Carboplatina/administração & dosagem
Desoxicitidina/administração & dosagem
Desoxicitidina/análogos & derivados
Dioxóis/administração & dosagem
Progressão da Doença
Intervalo Livre de Doença
Doxorrubicina/administração & dosagem
Doxorrubicina/análogos & derivados
Esquema de Medicação
Término Precoce de Ensaios Clínicos
Europa (Continente)
Feminino
Seres Humanos
Estimativa de Kaplan-Meier
Meia-Idade
Recidiva Local de Neoplasia
Neoplasias Ovarianas/mortalidade
Neoplasias Ovarianas/patologia
Paclitaxel/administração & dosagem
Polietilenoglicóis/administração & dosagem
Estudos Prospectivos
Tetra-Hidroisoquinolinas/administração & dosagem
Fatores de Tempo
Topotecan/administração & dosagem
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Dioxoles); 0 (Tetrahydroisoquinolines); 0 (liposomal doxorubicin); 0W860991D6 (Deoxycytidine); 30IQX730WE (Polyethylene Glycols); 7M7YKX2N15 (Topotecan); 80168379AG (Doxorubicin); B76N6SBZ8R (gemcitabine); BG3F62OND5 (Carboplatin); ID0YZQ2TCP (trabectedin); P88XT4IS4D (Paclitaxel)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170822
[St] Status:MEDLINE
[do] DOI:10.1200/JCO.2017.73.4293


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[PMID]:28818768
[Au] Autor:Poornima B; Siva B; Venkanna A; Shankaraiah G; Jain N; Yadav DK; Misra S; Babu KS
[Ad] Endereço:Division of Natural Products Chemistry, CSIR-Indian Institute of Chemical Technology, Hyderabad, 500 007, India.
[Ti] Título:Novel Gomisin B analogues as potential cytotoxic agents: Design, synthesis, biological evaluation and docking studies.
[So] Source:Eur J Med Chem;139:441-453, 2017 Oct 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:As part of pharmacological-phytochemical integrated studies on medicinal flora, Gomisin B (1) was isolated as major phytochemical lead from schisandra grandiflora, a plant traditionally used in different Asian systems of medicine. A series of 1,2,3-triazoles derivatives were synthesized at the C-7' position of the gomisin B core through diastereoselective Michael addition followed by regioselective Huisgen 1,3-dipolar cycloaddition reactions. All these triazolyl derivatives (5a-5q) were well characterized using modern spectroscopic techniques and evaluated for their anti-cancer activity against a panel of five human cancerous cell-lines. Among them, compound 5b exhibited the best cytotoxicity against SIHA cell (IC 0.24 µM) which was more than the standard drug doxorubicin, while the other derivatives were exhibited moderate to low activities in tested cell lines. The cell cycle analysis indicated that compound 5b stalled HeLa cells at G2/M phase. 5b promoted tubulin polymerization and this was supported by the docking studies, wherein 5b showed significant binding affinity at the colchicine binding pocket of tubulin. Overall, we identified a novel small molecule that demonstrated anticancer activity by promoting in vitro tubulin assembly.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Citotoxinas/farmacologia
Dioxóis/farmacologia
Desenho de Drogas
Lignanas/farmacologia
Simulação de Acoplamento Molecular
Compostos Policíclicos/farmacologia
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Ciclo-Octanos/síntese química
Ciclo-Octanos/química
Ciclo-Octanos/farmacologia
Citotoxinas/síntese química
Citotoxinas/química
Dioxóis/síntese química
Dioxóis/química
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Lignanas/síntese química
Lignanas/química
Estrutura Molecular
Compostos Policíclicos/síntese química
Compostos Policíclicos/química
Schisandra/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cyclooctanes); 0 (Cytotoxins); 0 (Dioxoles); 0 (Lignans); 0 (Polycyclic Compounds); 58546-55-7 (schisantherin B)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170819
[St] Status:MEDLINE


  8 / 3063 MEDLINE  
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[PMID]:28782526
[Au] Autor:Erba E; Romano M; Gobbi M; Zucchetti M; Ferrari M; Matteo C; Panini N; Colmegna B; Caratti G; Porcu L; Fruscio R; Perlangeli MV; Mezzanzanica D; Lorusso D; Raspagliesi F; D'Incalci M
[Ad] Endereço:Department of Oncology, IRCCS - Istituto di Ricerche Farmacologiche Mario Negri, Via La Masa 19, Milan, Italy.
[Ti] Título:Ascites interferes with the activity of lurbinectedin and trabectedin: Potential role of their binding to alpha 1-acid glycoprotein.
[So] Source:Biochem Pharmacol;144:52-62, 2017 Nov 15.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Trabectedin and its analogue lurbinectedin are effective drugs used in the treatment of ovarian cancer. Since the presence of ascites is a frequent event in advanced ovarian cancer we asked the question whether ascites could modify the activity of these compounds against ovarian cancer cells. The cytotoxicity induced by trabectedin or lurbinectedin against A2780, OVCAR-5 cell lines or primary culture of human ovarian cancer cells was compared by performing treatment in regular medium or in ascites taken from either nude mice or ovarian cancer patients. Ascites completely abolished the activity of lurbinectedin at up to 10nM (in regular medium corresponds to the IC90), strongly reduced that of trabectedin, inhibited the cellular uptake of lurbinectedin and, to a lesser extent, that of trabectedin. Since α1-acid glycoprotein (AGP) is present in ascites at relatively high concentrations, we tested if the binding of the drugs to this protein could be responsible for the reduction of their activity. Adding AGP to the medium at concentration range of those found in ascites, we reproduced the anticytotoxic effect of ascites. Erythromycin partially restored the activity of the drugs, presumably by displacing them from AGP. Equilibrium dialysis experiments showed that both drugs bind AGP, but the affinity of binding of lurbinectedin was much greater than that of trabectedin. KD values are 8±1.7 and 87±14nM for lurbinectedin and trabectedin, respectively. The studies intimate the possibility that AGP present in ascites might reduce the activity of lurbinectedin and to a lesser extent of trabectedin against ovarian cancer cells present in ascites. AGP plasma levels could influence the distribution of these drugs and thus they should be monitored in patients receiving these compounds.
[Mh] Termos MeSH primário: Ascite/metabolismo
Carbolinas/metabolismo
Dioxóis/metabolismo
Compostos Heterocíclicos de 4 ou mais Anéis/metabolismo
Orosomucoide/metabolismo
Neoplasias Ovarianas/metabolismo
Tetra-Hidroisoquinolinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Antineoplásicos Alquilantes/metabolismo
Antineoplásicos Alquilantes/farmacologia
Antineoplásicos Alquilantes/uso terapêutico
Carbolinas/farmacologia
Carbolinas/uso terapêutico
Linhagem Celular Tumoral
Dioxóis/farmacologia
Dioxóis/uso terapêutico
Relação Dose-Resposta a Droga
Feminino
Compostos Heterocíclicos de 4 ou mais Anéis/farmacologia
Compostos Heterocíclicos de 4 ou mais Anéis/uso terapêutico
Seres Humanos
Camundongos
Camundongos Nus
Neoplasias Ovarianas/tratamento farmacológico
Neoplasias Ovarianas/cirurgia
Ligação Proteica/fisiologia
Tetra-Hidroisoquinolinas/farmacologia
Tetra-Hidroisoquinolinas/uso terapêutico
Células Tumorais Cultivadas
Ensaios Antitumorais Modelo de Xenoenxerto/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (Carbolines); 0 (Dioxoles); 0 (Heterocyclic Compounds, 4 or More Rings); 0 (Orosomucoid); 0 (PM 01183); 0 (Tetrahydroisoquinolines); ID0YZQ2TCP (trabectedin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE


  9 / 3063 MEDLINE  
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[PMID]:28759311
[Au] Autor:Ibrahim I; Serrano MJ; Ruest LB; Svoboda KKH
[Ad] Endereço:1 Department of Biomedical Sciences, Texas A&M University College of Dentistry, Dallas, TX, USA.
[Ti] Título:Biglycan and Decorin Expression and Distribution in Palatal Adhesion.
[So] Source:J Dent Res;96(12):1445-1450, 2017 Nov.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous studies demonstrated that chondroitin sulfate proteoglycans (CSPGs) on apical surfaces of palatal medial edge epithelial (MEE) cells were necessary for palatal adhesion. In this study, we identified 2 proteoglycans, biglycan and decorin, that were expressed in the palatal shelves prior to adhesion. In addition, we established that these proteoglycans were dependent on transforming growth factor ß (TGFß) signaling. Laser capture microdissection was used to collect selected palatal epithelial cells from embryonic mouse embryos at various palate development stages. The expression of specific messenger RNA (mRNA) for biglycan and decorin was determined with quantitative real-time polymerase chain reaction. The TGFßrI kinase inhibitor (SB431542) was used in palatal organ cultures to determine if blocking TFGß signaling changed biglycan and decorin distribution. Immunohistochemistry of both biglycan and decorin revealed expression on the apical and lateral surfaces of MEE cells. Biglycan protein and mRNA levels peaked as the palatal shelves adhered. Decorin was less abundant on the apical epithelial surface and also had reduced mRNA levels compared to biglycan. Their proteins were not expressed on MEE cells of palates treated with SB431542, an inhibitor of TGFß signaling. The temporal expression of biglycan and decorin on the apical surface of MEE, combined with the evidence that these proteins were regulated through the TGFß pathway, indicated that they may be important for adhesion.
[Mh] Termos MeSH primário: Biglicano/metabolismo
Adesão Celular/fisiologia
Decorina/metabolismo
Palato/citologia
[Mh] Termos MeSH secundário: Animais
Benzamidas/farmacologia
Dioxóis/farmacologia
Imuno-Histoquímica
Microdissecção e Captura a Laser
Camundongos
Palato/embriologia
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Transdução de Sinais
Fator de Crescimento Transformador beta/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide); 0 (Benzamides); 0 (Biglycan); 0 (Decorin); 0 (Dioxoles); 0 (RNA, Messenger); 0 (Transforming Growth Factor beta)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE
[do] DOI:10.1177/0022034517722783


  10 / 3063 MEDLINE  
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[PMID]:28751117
[Au] Autor:Adam JP; Boumedien F; Letarte N; Provencher D
[Ad] Endereço:Pharmacy Department, Centre Hospitalier de l'Université de Montréal (CHUM), Montreal, Quebec, Canada; Centre de Recherche du CHUM, Montreal, Quebec, Canada. Electronic address: jean-philippe.adam.chum@ssss.gouv.qc.ca.
[Ti] Título:Single agent trabectedin in heavily pretreated patients with recurrent ovarian cancer.
[So] Source:Gynecol Oncol;147(1):47-53, 2017 Oct.
[Is] ISSN:1095-6859
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: In 2012, due to a shortage of pegylated liposomal doxorubicin, single agent trabectedin was proposed as an alternative of treatment to our patients with recurrent ovarian cancer (ROC) at our center. The aim of this retrospective study was to evaluate efficacy and tolerability of trabectedin in this context. PATIENTS AND METHODS: This retrospective study included all patients who received intravenous trabectedin 1.3mg/m over 3h every 3weeks for ROC between January 2012 and December 2015 at the Centre hospitalier de l'Université de Montreal. The primary outcome was the progression-free survival (PFS) based on CA-125 levels, clinical exam and/or Response Evaluation Criteria in Solid Tumors criteria. We also evaluated overall survival (OS), response rate and toxicities. RESULTS: A total of 42 patients with a median age of 59years received trabectedin in 2nd or 3rd line (12% of patients), 4th or 5th line (43%), and ≥6 lines (45%) and 45% were platinum-resistant. The median number of cycles received was 6 (range 1-19cycles). Complete response (CR), partial response (PR), stable disease (SD) and progression occurred in 19%, 29%, 33% and 19% of patients, respectively. The median PFS and OS was 4.3months (95% CI, 3.4-5.1) and 16.2months (95% CI, 9.0-23.5), respectively. In patients with a clinical benefit (CR, PR, SD), the median PFS was 4.6months. Trabectedin was well tolerated with few adverse events. CONCLUSION: Our results demonstrate that trabectedin has an interesting efficacy as a single agent in heavily treated ROC patients.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/uso terapêutico
Carcinoma/tratamento farmacológico
Dioxóis/uso terapêutico
Recidiva Local de Neoplasia/tratamento farmacológico
Neoplasias Ovarianas/tratamento farmacológico
Tetra-Hidroisoquinolinas/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Antineoplásicos Alquilantes/efeitos adversos
Dioxóis/efeitos adversos
Intervalo Livre de Doença
Feminino
Seres Humanos
Meia-Idade
Estudos Retrospectivos
Tetra-Hidroisoquinolinas/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (Dioxoles); 0 (Tetrahydroisoquinolines); ID0YZQ2TCP (trabectedin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE



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