Base de dados : MEDLINE
Pesquisa : D23.050.285 [Categoria DeCS]
Referências encontradas : 41488 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 4149 ir para página                         

  1 / 41488 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29444082
[Au] Autor:Khan MI; Su YK; Zou J; Yang LW; Chou RH; Yu C
[Ad] Endereço:National Tsing Hua University, Chemistry Department, Hsinchu, Taiwan.
[Ti] Título:S100B as an antagonist to block the interaction between S100A1 and the RAGE V domain.
[So] Source:PLoS One;13(2):e0190545, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ca2+-binding human S100A1 protein is a type of S100 protein. S100A1 is a significant mediator during inflammation when Ca2+ binds to its EF-hand motifs. Receptors for advanced glycation end products (RAGE) correspond to 5 domains: the cytoplasmic, transmembrane, C2, C1, and V domains. The V domain of RAGE is one of the most important target proteins for S100A1. It binds to the hydrophobic surface and triggers signaling transduction cascades that induce cell growth, cell proliferation, and tumorigenesis. We used nuclear magnetic resonance (NMR) spectroscopy to characterize the interaction between S100A1 and the RAGE V domain. We found that S100B could interact with S100A1 via NMR 1H-15N HSQC titrations. We used the HADDOCK program to generate the following two binary complexes based on the NMR titration results: S100A1-RAGE V domain and S100A1-S100B. After overlapping these two complex structures, we found that S100B plays a crucial role in blocking the interaction site between RAGE V domain and S100A1. A cell proliferation assay WST-1 also supported our results. This report could potentially be useful for new protein development for cancer treatment.
[Mh] Termos MeSH primário: Antígenos de Neoplasias/metabolismo
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Subunidade beta da Proteína Ligante de Cálcio S100/fisiologia
Proteínas S100/metabolismo
[Mh] Termos MeSH secundário: Cálcio/metabolismo
Seres Humanos
Interações Hidrofóbicas e Hidrofílicas
Ressonância Magnética Nuclear Biomolecular
Ligação Proteica
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (S100 Calcium Binding Protein beta Subunit); 0 (S100 Proteins); 0 (S100A1 protein); 0 (S100B protein, human); EC 2.7.11.22 (MOK protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190545


  2 / 41488 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29381830
[Au] Autor:Sioud M
[Ad] Endereço:Department of Cancer Immunology, Oslo University Hospital, The Norwegian Radium Hospital, Montebello, Oslo, Norway.
[Ti] Título:T-cell cross-reactivity may explain the large variation in how cancer patients respond to checkpoint inhibitors.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The therapeutic use of the immune system to specifically attack tumours has been a long-standing vision among tumour immunologists. Recently, the use of checkpoint inhibitors to turn-off immunosuppressive signals has proven to be effective in enhancing T-cell reactivity against patient-specific neoantigens, resulting from somatic mutations. Several of the identified T-cell epitopes share similarity with common bacterial and viral antigens, suggesting the involvement of pre-existing microbial cross-reactive T cells in rapid and durable tumour regression seen in some patients. This notion of T-cell cross-reactivity is further supported by the findings that intestinal bacteria can influence checkpoint-blockade therapy. Moreover, early data indicate the presence of such T cells in long-term survival breast cancer patients. This review highlights the main challenges for cancer immunotherapy and discusses the potential contribution of T-cell cross-reactivity in cancer immunotherapy and whether it can be used as a biomarker to predict the responsiveness to checkpoint inhibitors.
[Mh] Termos MeSH primário: Reações Cruzadas/imunologia
Imunoterapia/métodos
Neoplasias/imunologia
Neoplasias/terapia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Antígenos de Bactérias/imunologia
Antígenos de Neoplasias/imunologia
Antígenos Virais/imunologia
Biomarcadores Tumorais/imunologia
Antígeno CTLA-4/antagonistas & inibidores
Células Dendríticas/imunologia
Epitopos de Linfócito T/imunologia
Seres Humanos
Ativação Linfocitária/imunologia
Receptor de Morte Celular Programada 1/antagonistas & inibidores
Receptores Imunológicos/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Antigens, Neoplasm); 0 (Antigens, Viral); 0 (Biomarkers, Tumor); 0 (CTLA-4 Antigen); 0 (Epitopes, T-Lymphocyte); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); 0 (Receptors, Immunologic); 0 (TIGIT protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12643


  3 / 41488 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28460478
[Au] Autor:Vo MC; Nguyen-Pham TN; Lee HJ; Jaya Lakshmi T; Yang S; Jung SH; Kim HJ; Lee JJ
[Ad] Endereço:Research Center for Cancer Immunotherapy, Chonnam National University Hwasun Hospital, Hwasun, Jeollanamdo, Republic of Korea.
[Ti] Título:Combination therapy with dendritic cells and lenalidomide is an effective approach to enhance antitumor immunity in a mouse colon cancer model.
[So] Source:Oncotarget;8(16):27252-27262, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, we investigated efficacy of lenalidomide in combination with tumor antigen-loaded dendritic cells (DCs) in murine colon cancer model. MC-38 cell lines were injected subcutaneously to establish colon cancer-bearing mice. After tumor growth, lenalidomide (50 mg/kg/day) was injected intraperitoneally on 3 consecutive days in combination with tumor antigen-loaded DC vaccination on days 8, 12, 16, and 20. The tumor antigen-loaded DCs plus lenalidomide combination treatment exhibited a significant inhibition of tumor growth compared with the other groups. These effects were associated with a reduction in immune suppressor cells, such as myeloid-derived suppressor cells and regulatory T cells, with the induction of immune effector cells, such as natural killer cells, CD4+ T cells and CD8+ T cells in spleen, and with the activation of cytotoxic T lymphocytes and NK cells. This study suggests that a combination of tumor antigen-loaded DC vaccination and lenalidomide synergistically enhanced antitumor immune response in the murine colon cancer model, by inhibiting the generation of immune suppressive cells and recovery of effector cells, and demonstrated superior polarization of Th1/Th2 balance in favor of Th1 immune response. This combination approach with DCs and lenalidomide may provide a new therapeutic option to improve the treatment of colon cancer.
[Mh] Termos MeSH primário: Neoplasias do Colo/imunologia
Neoplasias do Colo/patologia
Células Dendríticas/imunologia
Imunidade
Talidomida/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Antígenos de Neoplasias/imunologia
Vacinas Anticâncer/administração & dosagem
Vacinas Anticâncer/imunologia
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Neoplasias do Colo/genética
Neoplasias do Colo/terapia
Terapia Combinada
Citocinas/biossíntese
Células Dendríticas/metabolismo
Modelos Animais de Doenças
Feminino
Expressão Gênica
Imunidade/efeitos dos fármacos
Imunoterapia
Células Matadoras Naturais/imunologia
Células Matadoras Naturais/metabolismo
Camundongos
Linfócitos T Citotóxicos/efeitos dos fármacos
Linfócitos T Citotóxicos/imunologia
Linfócitos T Citotóxicos/metabolismo
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/imunologia
Linfócitos T Reguladores/metabolismo
Talidomida/farmacologia
Vacinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Cancer Vaccines); 0 (Cytokines); 4Z8R6ORS6L (Thalidomide); F0P408N6V4 (lenalidomide)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15917


  4 / 41488 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28460461
[Au] Autor:Nilofar Danishmalik S; Lee SH; Sin JI
[Ad] Endereço:BK21 Plus Graduate Program and Department of Microbiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon-do 200-701, Korea.
[Ti] Título:Tumor regression is mediated via the induction of HER263-71- specific CD8+ CTL activity in a 4T1.2/HER2 tumor model: no involvement of CD80 in tumor control.
[So] Source:Oncotarget;8(16):26771-26788, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the CT26/HER2 and 4T1.2/HER2 tumor models, CT26/HER2 cells form tumors that continue to grow, whereas 4T1.2/HER2 cells form tumors that eventually regress. Here, we investigated the differences in the behaviors of these two cell lines. When immune cells from 4T1.2/HER2 tumor-bearing animals were stimulated with HER2 class I peptides, they displayed a 2-fold increase in IFN-γ levels, in response to the peptides, HER263-71 and HER2342-350. In contrast, extremely high levels of antigen-non-specific IFN-γ production were observed with immune cells and sera from CT26/HER2 tumor-bearing mice. However, IFN-γ had no effect on tumor progression in the CT26/HER2 model, as determined by an IFN-γ knockout assay. 4T1.2/HER2 tumor-bearing mice displayed CTL activity in response to HER263-71 but not to HER2342-350, whereas no such induction was observed in CT26/HER2 tumor-bearing mice. When 4T1.2/HER2 cell-challenged mice were depleted of CD8+ T cells, they lost their tumor-regressing activity, suggesting an antitumor role of HER263-71-specific CD8+ CTLs in the control of this tumor type. CT26/HER2 cells also expressed CD80. However, CD80-transfected 4T1.2/HER2 and CD80-non-expressing CT26/HER2 cells failed to alter their tumorigenicity, suggesting no role of CD80 in tumor control. Despite increased levels of myeloid-derived suppressor cells in the tumor, they were not associated with tumor progression in the CT26/HER2 model, as determined by a cell depletion assay. Overall, these data show that, contrary to CT26/HER2 tumors, 4T1.2/HER2 tumors regress via the induction of HER263-71-specific CD8+ CTLs and that CD80 is not associated with the regression of these tumors.
[Mh] Termos MeSH primário: Neoplasias/imunologia
Neoplasias/metabolismo
Receptor ErbB-2/imunologia
Especificidade do Receptor de Antígeno de Linfócitos T/imunologia
Linfócitos T Citotóxicos/imunologia
Linfócitos T Citotóxicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos de Neoplasias/imunologia
Biomarcadores
Linhagem Celular Tumoral
Desoxicitidina/análogos & derivados
Desoxicitidina/farmacologia
Modelos Animais de Doenças
Feminino
Imunoglobulina G/imunologia
Interferon gama/genética
Interferon gama/metabolismo
Camundongos
Camundongos Knockout
Neoplasias/patologia
Subpopulações de Linfócitos T/efeitos dos fármacos
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
Linfócitos T Citotóxicos/efeitos dos fármacos
Células Th1/imunologia
Células Th1/metabolismo
Carga Tumoral/efeitos dos fármacos
Carga Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Biomarkers); 0 (Immunoglobulin G); 0W860991D6 (Deoxycytidine); 82115-62-6 (Interferon-gamma); B76N6SBZ8R (gemcitabine); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15816


  5 / 41488 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:29428036
[Au] Autor:Shimizu T; Asakuma M; Tomioka A; Inoue Y; Hirokawa F; Hayashi M; Uchiyama K
[Ti] Título:Span-1 and CA19-9 as Predictors of Early Recurrence and Lymph Node Metastasis for Patients with Invasive Pancreatic Cancer after Pancreatectomy.
[So] Source:Am Surg;84(1):109-113, 2018 Jan 01.
[Is] ISSN:1555-9823
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Because pancreatic cancer is a disease with a dismal prognosis due to the high rate of early recurrence even after curative surgery, selecting the most effective treatment in an individual requires preoperative assessment of the tumor characteristics, including the potential for early recurrence. The study cohort included 84 patients undergoing surgical resection of pancreatic cancer. Univariate and multivariate analyses were conducted to identify the risk factors for early recurrence within six months after curative resection. Early recurrence was associated with a platelet-lymphocyte ratio ≥0.23 (P = 0.04), carbohydrate antigen 19-9 (CA19-9) ≥200 (P = 0.01), and S-pancreas-1 antigen (Span-1) ≥37 (P = 0.0004) by univariate analysis. Multivariate analysis identified CA19-9 ≥200 and Span-1 ≥37 as independent risk factors for early recurrence. Patients with both risk factors had a significantly higher rate of lymph node metastasis than those with no or one risk factor. Span-1 ≥ 37 and CA19-9 ≥ 200 are independent risk factors for early recurrence in patients who underwent surgical resection, and the combination of Span-1 ≥37 and CA19-9 ≥200 is a useful indicator of lymph node metastasis.
[Mh] Termos MeSH primário: Antígenos de Neoplasias/sangue
Biomarcadores Tumorais/sangue
Antígeno CA-19-9/sangue
Recidiva Local de Neoplasia/diagnóstico
Recidiva Local de Neoplasia/cirurgia
Pancreatectomia
Neoplasias Pancreáticas/diagnóstico
Neoplasias Pancreáticas/cirurgia
[Mh] Termos MeSH secundário: Idoso
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Índice de Massa Corporal
Quimioterapia Adjuvante/métodos
Detecção Precoce de Câncer
Feminino
Seguimentos
Seres Humanos
Japão
Estimativa de Kaplan-Meier
Metástase Linfática
Masculino
Meia-Idade
Invasividade Neoplásica
Recidiva Local de Neoplasia/sangue
Recidiva Local de Neoplasia/tratamento farmacológico
Neoplasias Pancreáticas/sangue
Neoplasias Pancreáticas/tratamento farmacológico
Valor Preditivo dos Testes
Prognóstico
Estudos Retrospectivos
Fatores de Risco
Sensibilidade e Especificidade
Resultado do Tratamento
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Biomarkers, Tumor); 0 (CA-19-9 Antigen); 0 (pancreatic associated antigen, SPan-1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180212
[St] Status:MEDLINE


  6 / 41488 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27776018
[Au] Autor:Vartanian A; Baryshnikova M; Burova O; Afanasyeva D; Misyurin V; Belyаvsky A; Shprakh Z
[Ad] Endereço:Department of Experimental Diagnosis and Therapy of Tumors, N.N. Blokhin Russian Cancer Research Center, Moscow, Russia.
[Ti] Título:Inhibitor of vasculogenic mimicry restores sensitivity of resistant melanoma cells to DNA-damaging agents.
[So] Source:Melanoma Res;27(1):8-16, 2017 Feb.
[Is] ISSN:1473-5636
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The increasing incidence of melanoma makes this cancer an important public health problem. Therapeutic resistance is still a major obstacle to the therapy of patients with metastatic melanomas. The aim of this study was to develop the melanoma cell line resistant to DNA-alkylating agents and to elucidate the mechanisms involved in acquired drug resistance. We established a unique melanoma subline Mel MeR resistant to DNA-alkylating drug aranoza by continuous stepwise selection of the Mel Me/WT cell line with increasing concentrations of this drug. Mel MeR cells were also cross-resistant to streptozotocin or cisplatin. Here, we show that aranoza-resistant melanoma cells modulate the ABC transporter activity, upregulate the expression of PRAME, adopt a vascular-related phenotype and engage in vasculogenic mimicry. LCS1269, a vasculogenic mimicry low-molecular-weight inhibitor, reverses the sensitivity of resistant melanoma cells to DNA-damaging agents. In this study, we provide experimental evidence that LCS1269 might be considered as a new potential anticancer agent capable of overcoming multidrug resistance for DNA-damaging agents in melanoma.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Carbazóis/farmacologia
Linhagem Celular Tumoral
Resistência a Medicamentos Antineoplásicos
Glicosídeos/farmacologia
Melanoma/tratamento farmacológico
Melanoma/metabolismo
Metilnitrosoureia/análogos & derivados
Neovascularização Patológica/prevenção & controle
[Mh] Termos MeSH secundário: Membro 1 da Subfamília B de Cassetes de Ligação de ATP/metabolismo
Antígenos de Neoplasias/genética
Apoptose/efeitos dos fármacos
Antígeno CD24/metabolismo
Resistência a Medicamentos Antineoplásicos/genética
Endoglina/metabolismo
Corantes Fluorescentes/metabolismo
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Receptores de Hialuronatos/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Masculino
Melanoma/irrigação sanguínea
Melanoma/genética
Metilnitrosoureia/farmacologia
Meia-Idade
Proteínas de Neoplasias/genética
Células-Tronco Neoplásicas/metabolismo
Proteínas Nucleares/genética
Fenótipo
Fosfoproteínas Fosfatases/genética
Proteínas Proto-Oncogênicas c-kit/metabolismo
Rodamina 123/metabolismo
Tetraspanina 30/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCB5 protein, human); 0 (ATP-Binding Cassette, Sub-Family B, Member 1); 0 (Antigens, Neoplasm); 0 (Antineoplastic Agents, Alkylating); 0 (CD24 Antigen); 0 (CD24 protein, human); 0 (CD44 protein, human); 0 (CD63 protein, human); 0 (Carbazoles); 0 (ENG protein, human); 0 (Endoglin); 0 (Fluorescent Dyes); 0 (GAGE1 protein, human); 0 (Glycosides); 0 (Hyaluronan Receptors); 0 (LCS1269); 0 (Neoplasm Proteins); 0 (Nuclear Proteins); 0 (PRAME protein, human); 0 (Tetraspanin 30); 0 (aranoza); 126547-89-5 (Intercellular Adhesion Molecule-1); 1N3CZ14C5O (Rhodamine 123); 684-93-5 (Methylnitrosourea); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 3.1.3.16 (CTDSP1 protein, human); EC 3.1.3.16 (Phosphoprotein Phosphatases)
[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:161025
[St] Status:MEDLINE
[do] DOI:10.1097/CMR.0000000000000308


  7 / 41488 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29463190
[Au] Autor:Shirasu H; Ono A; Omae K; Nakashima K; Omori S; Wakuda K; Kenmotsu H; Naito T; Murakami H; Endo M; Nakajima T; Takahashi T
[Ad] Endereço:1 Division of Thoracic Oncology, Shizuoka Cancer Center, Sunto-gun, Nagaizumi-cho, Shizuoka, Japan.
[Ti] Título:CYFRA 21-1 predicts the efficacy of nivolumab in patients with advanced lung adenocarcinoma.
[So] Source:Tumour Biol;40(2):1010428318760420, 2018 Feb.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CYFRA 21-1 is a prognostic marker for non-small cell lung cancer. The serum CYFRA 21-1 level is also known as an adjunct for the diagnosis of lung squamous cell carcinoma. This study aimed to examine whether CYFRA 21-1 has predictive implications for nivolumab therapy in patients with advanced lung adenocarcinoma. Of the 79 patients who were treated with nivolumab therapy at the Shizuoka Cancer Center between December 2015 and September 2016, we retrospectively reviewed the data of 50 patients. The patient characteristics were as follows: age <70/≥70 years: 43 (86%)/7; male/female: 31 (62.0%)/19; Eastern Cooperative Oncology Group performance status 0-1/2: 43 (86%)/7; smoking status: no/yes: 18 (36%)/32; epidermal growth factor receptor mutation status negative/positive: 36 (72%)/14; CYFRA 21-1 ≥2.2/<2.2 ng/mL: 28 (56%)/22; carcinoembryonic antigen ≥5/<5 ng/mL: 29 (58%)/21; and number of prior regimens 2-3/≥4: 16 (32%)/34. With a median follow-up of 263.5 (range, 64-352) days, the median progression-free survival was 70 days. The clinical variables investigated using univariate analysis were as follows: age (p = 0.423), carcinoembryonic antigen (p = 0.888), epidermal growth factor receptor mutation status (p = 0.105), performance status (p = 0.968), sex (p = 0.210), number of prior regimens (p = 0.146), CYFRA 21-1 (p = 0.026), and smoking status (p = 0.041). A multivariate analysis identified a serum CYFRA 21-1 level ≥2.2 ng/mL as an independent predictor of a favorable outcome (hazard ratio, 0.44; 95% confidence interval, 0.23-0.85; p = 0.015; median progression-free survival, 155 vs 51.5 days). In conclusion, CYFRA 21-1 might be an independent predictor of outcome for patients with advanced lung adenocarcinoma treated with nivolumab.
[Mh] Termos MeSH primário: Adenocarcinoma/tratamento farmacológico
Adenocarcinoma/metabolismo
Anticorpos Monoclonais/uso terapêutico
Antígenos de Neoplasias/metabolismo
Queratina-19/metabolismo
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores Tumorais/metabolismo
Antígeno Carcinoembrionário/metabolismo
Intervalo Livre de Doença
Feminino
Seguimentos
Seres Humanos
Masculino
Meia-Idade
Receptor do Fator de Crescimento Epidérmico/metabolismo
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antigens, Neoplasm); 0 (Biomarkers, Tumor); 0 (Carcinoembryonic Antigen); 0 (Keratin-19); 0 (antigen CYFRA21.1); 31YO63LBSN (nivolumab); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180222
[St] Status:MEDLINE
[do] DOI:10.1177/1010428318760420


  8 / 41488 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29289880
[Au] Autor:Ansari MF; Idrees D; Hassan MI; Ahmad K; Avecilla F; Azam A
[Ad] Endereço:Department of Chemistry, Jamia Millia Islamia, Jamia Nagar, 110 025, New Delhi, India.
[Ti] Título:Design, synthesis and biological evaluation of novel pyridine-thiazolidinone derivatives as anticancer agents: Targeting human carbonic anhydrase IX.
[So] Source:Eur J Med Chem;144:544-556, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:In order to obtain novel Human carbonic anhydrase IX (CAIX) inhibitors, a series of pyridine-thiazolidinone derivatives was synthesized and characterized by various spectroscopic techniques. The binding affinity of the compounds was measured by fluorescence binding studies and enzyme inhibition activity using esterase assay of CAIX. It was observed that compound 8 and 11 significantly inhibit the CAIX activity with the IC value, 1.61 µM and 1.84 µM, respectively. The binding-affinity of compound 8 and 11 for CAIX was significantly high with their K values 11.21 µM and 2.32 µM, respectively. Docking studies revealed that compound 8 and 11 efficiently binds in the active site cavity of CA IX by forming sufficient numbers of H-bonds and van der Waals interactions with active side residues. All the compounds were further screened in vitro for anticancer activity and found that compound 8 and 11 exhibit considerable anticancer activity against MCF-7 and HepG-2 cell lines. All these findings suggest that compound 8 and 11 may be further exploited as a novel pharmacophore model for the development of anticancer agents.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Anidrase Carbônica IX/antagonistas & inibidores
Inibidores da Anidrase Carbônica/farmacologia
Desenho de Drogas
Piridinas/farmacologia
Tiazolidinas/farmacologia
[Mh] Termos MeSH secundário: Antígenos de Neoplasias/metabolismo
Antineoplásicos/síntese química
Antineoplásicos/química
Anidrase Carbônica II/antagonistas & inibidores
Anidrase Carbônica II/metabolismo
Anidrase Carbônica IX/metabolismo
Inibidores da Anidrase Carbônica/síntese química
Inibidores da Anidrase Carbônica/química
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Simulação de Acoplamento Molecular
Estrutura Molecular
Piridinas/síntese química
Piridinas/química
Relação Estrutura-Atividade
Tiazolidinas/síntese química
Tiazolidinas/química
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Antineoplastic Agents); 0 (Carbonic Anhydrase Inhibitors); 0 (Pyridines); 0 (Thiazolidines); EC 4.2.1.- (Carbonic Anhydrase II); EC 4.2.1.1 (CA9 protein, human); EC 4.2.1.1 (Carbonic Anhydrase IX); NH9L3PP67S (pyridine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180101
[St] Status:MEDLINE


  9 / 41488 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29323537
[Au] Autor:Witkowska M; Smolewski P; Robak T
[Ad] Endereço:a Department of Experimental Hematology , Medical University of Lodz , Lodz , Poland.
[Ti] Título:Investigational therapies targeting CD37 for the treatment of B-cell lymphoid malignancies.
[So] Source:Expert Opin Investig Drugs;27(2):171-177, 2018 Feb.
[Is] ISSN:1744-7658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: While chemotherapy still remains a cornerstone of oncologic therapy, immunotherapy with monoclonal antibodies has steadily improved the treatment strategy for several hematologic malignancies. New treatment options need to be developed for relapsed and refractory non-Hodgkin lymphoma (NHL) patients. Currently, novel agents targeting specific molecules on the surface of lymphoma cells, such as anti-CD37 antibodies, are under considerable investigation. Here we report on anti-CD37 targeting for the treatment of patients with B-cell NHL. Areas covered: CD37 seems to be the perfect therapeutic target in patients with NHL. The CD37 antigen is abundantly expressed in B-cells, but is absent on normal stem cells and plasma cells. It is hoped that anti-CD37 monoclonal antibodies will increase the efficacy and reduce toxicity in patients with both newly diagnosed and relapsed and refractory disease. Recent clinical trials have shown promising outcomes for these agents, administered both as monotherapy and in combination with standard chemotherapeutics. Expert opinion: The development of new therapeutic options might help to avoid cytotoxic chemotherapy entirely in some clinical settings. This article presents the latest state of the art on the new treatment strategies in NHL patients. It also discusses recently approved agents and available clinical trial data.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/administração & dosagem
Antígenos de Neoplasias/imunologia
Linfoma de Células B/terapia
Tetraspaninas/imunologia
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/farmacologia
Seres Humanos
Imunoterapia/métodos
Linfoma de Células B/imunologia
Terapia de Alvo Molecular
Terapias em Estudo/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antigens, Neoplasm); 0 (CD37 protein, human); 0 (Tetraspanins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1080/13543784.2018.1427730


  10 / 41488 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28465452
[Au] Autor:Finn OJ
[Ad] Endereço:Department of Immunology, University of Pittsburgh School of Medicine and the University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania. ojfinn@pitt.edu.
[Ti] Título:Human Tumor Antigens Yesterday, Today, and Tomorrow.
[So] Source:Cancer Immunol Res;5(5):347-354, 2017 May.
[Is] ISSN:2326-6074
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The question of whether human tumors express antigens that can be recognized by the immune system has been answered with a resounding YES. Most were identified through spontaneous antitumor humoral and cellular immune responses found in cancer patients and include peptides, glycopeptides, phosphopeptides, viral peptides, and peptides resulting from common mutations in oncogenes and tumor-suppressor genes, or common gene fusion events. Many have been extensively tested as candidates for anticancer vaccines. More recently, attention has been focused on the potentially large number of unique tumor antigens, mutated neoantigens, that are the predicted products of the numerous mutations revealed by exome sequencing of primary tumors. Only a few have been confirmed as targets of spontaneous immunity and immunosurveillance, and even fewer have been tested in preclinical and clinical settings. The field has been divided for a long time on the relative importance of shared versus mutated antigens in tumor surveillance and as candidates for vaccines. This question will eventually need to be answered in a head to head comparison in well-designed clinical trials. One advantage that shared antigens have over mutated antigens is their potential to be used in vaccines for primary cancer prevention. .
[Mh] Termos MeSH primário: Antígenos de Neoplasias/imunologia
[Mh] Termos MeSH secundário: Animais
Vacinas Anticâncer
Seres Humanos
Neoplasias/imunologia
Neoplasias/prevenção & controle
Neoplasias/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Cancer Vaccines)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1158/2326-6066.CIR-17-0112



página 1 de 4149 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde