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[PMID]: 29424453 [Au] Autor: Esenboga S; Cagdas D; Ozgur TT; Gur Cetinkaya P; Turkdemir LM; Sanal O; VanDerBurg M; Tezcan I [Ad] Endereço: Department of Pediatrics, Division of Immunology, Hacettepe University Faculty of Medicine, Ankara, Turkey. [Ti] Título: Clinical and genetic features of the patients with X-Linked agammaglobulinemia from Turkey: Single-centre experience. [So] Source: Scand J Immunol;87(3), 2018 Mar. [Is] ISSN: 1365-3083 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: X-linked agammaglobulinemia is a primary immunodeficiency disorder resulting from BTK gene mutations. There are many studies in the literature suggesting contradictory ideas about phenotype-genotype correlation. The aim of this study was to identify the mutations and clinical findings of patients with XLA in Turkey, to determine long-term complications related to the disease and to analyse the phenotype-genotype correlation. Thirty-two patients with XLA diagnosed between 1985 and 2016 in Pediatric Immunology Department of Hacettepe University Ihsan Dogramaci Children's Hospital were investigated. A clinical survey including clinical features of the patients was completed, and thirty-two patients from 26 different families were included in the study. Getting early diagnosis and regular assessment with imaging techniques seem to be the most important issues for improving the health status of the patients with XLA. Early molecular analysis gives chance for definitive diagnosis and genetic counselling, but not for predicting the clinical severity and prognosis. [Mh] Termos MeSH primário: Agamaglobulinemia/diagnóstico Agamaglobulinemia/genética Anticorpos/sangue Doenças Genéticas Ligadas ao Cromossomo X/diagnóstico Doenças Genéticas Ligadas ao Cromossomo X/genética Proteínas Tirosina Quinases/genética [Mh] Termos MeSH secundário: Adolescente Adulto Agamaglobulinemia/patologia Infecções Bacterianas/imunologia Criança Pré-Escolar Doenças Genéticas Ligadas ao Cromossomo X/patologia Seres Humanos Imunoglobulina A/sangue Imunoglobulina G/sangue Imunoglobulina M/sangue Lactente Estudos Retrospectivos Turquia Adulto Jovem [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antibodies); 0 (Immunoglobulin A); 0 (Immunoglobulin G); 0 (Immunoglobulin M); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases) [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: 180210 [St] Status: MEDLINE [do] DOI: 10.1111/sji.12647

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[PMID]: 29180487 [Au] Autor: Pierog PL; Zhao Y; Singh S; Dai J; Yap GS; Fitzgerald-Bocarsly P [Ad] Endereço: Department of Pathology and Laboratory Medicine, Rutgers New Jersey Medical School, Newark, NJ 07103. [Ti] Título: Inactivates Human Plasmacytoid Dendritic Cells by Functional Mimicry of IL-10. [So] Source: J Immunol;200(1):186-195, 2018 01 01. [Is] ISSN: 1550-6606 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Plasmacytoid dendritic cells (pDCs) are the major producers of IFN-α, an antiviral cytokine involved in immunomodulation and control of HIV type 1 replication, whereas is a life-threatening opportunistic infection in AIDS patients. During infection with HIV type 1, human pDCs decrease in circulation and remaining pDC produce lower amounts of IFN-α in response to viral stimulation. In this study, we investigated the impact of coinfection with on the innate virus-directed responses of human pDCs. Using intracellular flow cytometry and fluorescence microscopy, we determined that invaded but did not induce IFN-α or TNF-α in human pDC. However, inhibited IFN-α and TNF-α produced in response to HSV and HIV, thus functionally inactivating pDC. IFN-α production was inhibited only in cells infected by , which inhibited neither uptake of GFP-HSV nor localization of TLR9 in CD71 endosomes, directing us to investigate downstream events. Using imaging flow cytometry, we found that both and IL-10 inhibited virus-induced nuclear translocation, but not phosphorylation, of IFN response factor 7. Blockade of IFN response factor 7 nuclear translocation and inhibition of the IFN-α response was partially reversed by a deficiency in the -derived ROP16 kinase, known to directly phosphorylate STAT3, a critical mediator of IL-10's anti-inflammatory effects. Taken together, our results indicate that suppresses pDC activation by mimicking IL-10's regulatory effects through an ROP16 kinase-dependent mechanism. Our findings further imply a convergent mechanism of inhibition of TLR signaling by and IL-10 and suggest potential negative consequences of HIV/ coinfection. [Mh] Termos MeSH primário: Células Dendríticas/imunologia Infecções por HIV/imunologia HIV-1/imunologia Interleucina-10/metabolismo Infecções Oportunistas/imunologia Proteínas Tirosina Quinases/metabolismo Proteínas de Protozoários/metabolismo Toxoplasma/imunologia Toxoplasmose/imunologia [Mh] Termos MeSH secundário: Diferenciação Celular Células Cultivadas Coinfecção Células Dendríticas/parasitologia Seres Humanos Imunidade Inata Imunomodulação Fator Regulador 7 de Interferon/metabolismo Interferon-alfa/metabolismo Fator de Transcrição STAT3/metabolismo Transdução de Sinais Receptor Toll-Like 9/metabolismo Fator de Necrose Tumoral alfa/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL [Nm] Nome de substância: 0 (IRF7 protein, human); 0 (Interferon Regulatory Factor-7); 0 (Interferon-alpha); 0 (Protozoan Proteins); 0 (STAT3 Transcription Factor); 0 (Toll-Like Receptor 9); 0 (Tumor Necrosis Factor-alpha); 130068-27-8 (Interleukin-10); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (Rop16 protein, Toxoplasma gondii) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180307 [Lr] Data última revisão: 180307 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 171129 [St] Status: MEDLINE [do] DOI: 10.4049/jimmunol.1701045

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[PMID]: 29480835 [Au] Autor: Li L; Tong M; Zhao YT; He Y; Zhou HY; Zhang GF; Zhang YJ [Ad] Endereço: Department of Orthopedics, Traditional Chinese Medical Hospital of Xinjiang Uygur Autonomous Region, Urumqi. [Ti] Título: Membrane translocation of Bruton kinase in multiple myeloma cells is associated with osteoclastogenic phenotype in bone metastatic lesions. [So] Source: Medicine (Baltimore);97(2):e9482, 2018 Jan. [Is] ISSN: 1536-5964 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Using bone biopsy samples, we examined whether osteolytic cytokine profile is changed in situ in bone samples of metastatic multiple myeloma, and whether this creates an environment of lysis within the bone to which it has spread. This also produces the clinical features of increased circulating plasma calcium, and deleterious effects on the kidney.Using multiple myeloma biopsy and cell extracts from bone metastatic lesions, Bruton kinase, a tyrosine kinase, was demonstrated to be translocated to the membrane. Several transcription factors were upregulated included activin A, inflammatory transcription activator like such as nuclear factor kappa B, and specific bone lytic factor such as receptor activator of nuclear factor kappa-B ligand that is known to drive osteoclastogenesis as opposed to a osteogenic environment. The transcript for Bruton kinase was also elevated in its expression.Cytokines that support osteolytic activity such as a proliferation-inducing ligand, RANTES (regulated on activation, normal T cell expressed and secreted), interleukin-8, and activin A were upregulated. Tartrate resistant acid phosphatase (TRAP)-positive osteoclastic enzymatic activity was significantly elevated in the bone microenvironment in metastatic multiple myeloma. Several tyrosine kinase inhibitors, including inhibitors for Bruton kinase such as ibrutinib have been developed. The results of the present study provide evidence that multiple myeloma possess signal transduction mechanisms to support a bone lytic environment.The results provide a preliminary molecular basis to design specific inhibitors for management of bone metastasis of multiple myeloma. [Mh] Termos MeSH primário: Neoplasias Ósseas/enzimologia Neoplasias Ósseas/secundário Membrana Celular/enzimologia Mieloma Múltiplo/enzimologia Osteogênese/fisiologia Proteínas Tirosina Quinases/metabolismo [Mh] Termos MeSH secundário: Ativinas/metabolismo Idoso Quimiocina CCL5/metabolismo Seres Humanos Masculino Meia-Idade NF-kappa B/metabolismo RNA Mensageiro/metabolismo Fosfatase Ácida Resistente a Tartarato/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (CCL5 protein, human); 0 (Chemokine CCL5); 0 (NF-kappa B); 0 (RNA, Messenger); 0 (activin A); 104625-48-1 (Activins); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase) [Em] Mês de entrada: 1803 [Cu] Atualização por classe: 180302 [Lr] Data última revisão: 180302 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 180227 [St] Status: MEDLINE [do] DOI: 10.1097/MD.0000000000009482

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[PMID]: 29480823 [Au] Autor: Qiu HB; Zhou ZG; Feng XY; Liu XC; Guo J; Ma MZ; Chen YB; Sun XW; Zhou ZW [Ad] Endereço: Department of Gastric and Pancreatic Surgery. [Ti] Título: Advanced gastrointestinal stromal tumor patients benefit from palliative surgery after tyrosine kinase inhibitors therapy. [So] Source: Medicine (Baltimore);97(2):e9097, 2018 Jan. [Is] ISSN: 1536-5964 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: The role of palliative surgery is controversial in advanced gastrointestinal stromal tumors (GIST) after tyrosine kinase inhibitors (TKIs) therapy.We evaluated safety and clinical outcomes in a single institution series of advanced GIST patients from January 2002 to December 2008.One hundred and fifty-six patients had been recruited, including 87 patients underwent surgical resection and 69 patients kept on TKIs treatment. Four patients had major surgical complications. Median follow-up was 38.3 months, the overall survival (OS) and progression-free survival (PFS) of the patients in surgical group were longer than the nonsurgical group, PFS: 46.1 versus 33.8 months (P < .01), OS: 54.8 versus 40.4 months. In the subgroup analysis for the patients received surgery, the median PFS for patients with progression disease, stable disease, and partial response was 33.3, 51.5, and 83.0 months, respectively (P < .01). Median OS was 68.0 months in those with only liver or peritoneal metastases, and 45.3 months in those with both metastases. Median PFS of patients underwent R0/R1 resection was 73.6 months compared with 35.8 months in R2 resection patients (P < .01).Patients with advanced GISTs have prolonged OS after debulking procedures. Surgery for patients who have responsive disease after TKIs treatment should be considered. [Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico Tumores do Estroma Gastrointestinal/tratamento farmacológico Tumores do Estroma Gastrointestinal/cirurgia Cuidados Paliativos Inibidores de Proteínas Quinases/uso terapêutico [Mh] Termos MeSH secundário: Adulto Idoso Idoso de 80 Anos ou mais Intervalo Livre de Doença Feminino Seguimentos Tumores do Estroma Gastrointestinal/mortalidade Tumores do Estroma Gastrointestinal/patologia Seres Humanos Mesilato de Imatinib/uso terapêutico Neoplasias Hepáticas/mortalidade Neoplasias Hepáticas/secundário Masculino Meia-Idade Neoplasias Peritoneais/mortalidade Neoplasias Peritoneais/secundário Proteínas Tirosina Quinases/antagonistas & inibidores Estudos Retrospectivos Resultado do Tratamento [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antineoplastic Agents); 0 (Protein Kinase Inhibitors); 8A1O1M485B (Imatinib Mesylate); EC 2.7.10.1 (Protein-Tyrosine Kinases) [Em] Mês de entrada: 1803 [Cu] Atualização por classe: 180302 [Lr] Data última revisão: 180302 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 180227 [St] Status: MEDLINE [do] DOI: 10.1097/MD.0000000000009097

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[PMID]: 29390324 [Au] Autor: Harada Y; Nishiwaki S; Sugimoto T; Onodera K; Goto T; Sato T; Kamoshita S; Kawashima N; Seto A; Okuno S; Yamamoto S; Iwasaki T; Ozawa Y; Miyamura K; Akatsuka Y; Sugiura I [Ad] Endereço: Division of Hematology and Oncology, Toyohashi Municipal Hospital. [Ti] Título: Successful treatment with allogeneic stem cell transplantation followed by DLI and TKIs for e6a2 BCR-ABL-positive acute myeloid leukaemia: A case report and literature review. [So] Source: Medicine (Baltimore);96(50):e9160, 2017 Dec. [Is] ISSN: 1536-5964 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: RATIONALE: Patients with the e6a2 BCR-ABL transcript, 1 of the atypical transcripts, have been reported to have a poor prognosis, and allogeneic stem cell transplantation (ASCT) can be considered as additional therapy. However, long-term survival after ASCT for this disease is rare. PATIENT CONCERNS: This report concerns a 55-year-old female patient with e6a2 BCR-ABL-positive acute myeloid leukemia including the outcome of ASCT followed by donor lymphocyte infusion (DLI). DIAGNOSES: The breakpoint was confirmed by direct sequencing. Her minimal residual disease could be detected by nested reverse-transcription polymerase chain reaction using primers for the minor BCR-ABL (e1a2) transcript. INTERVENTIONS: Treatment with tyrosine kinase inhibitors (TKIs) and ASCT followed by DLI. OUTCOMES: Despite multiple cytogenetic and molecular relapses after ASCT, she remains in molecular remission at 46 months after ASCT. LESSONS: This case indicates the efficacy of the combination of the graft-versus-leukemia effect and TKIs for e6a2 BCR-ABL-positive acute leukemia. When the Philadelphia chromosome with an unusual chromosomal breakpoint is suggested, we should clarify the breakpoint because that information can aid molecular assessments and decisions to provide an additional or alternative therapy. [Mh] Termos MeSH primário: Transplante de Células-Tronco Hematopoéticas Leucemia Mieloide Aguda/terapia [Mh] Termos MeSH secundário: Feminino Proteínas de Fusão bcr-abl Efeito Enxerto vs Leucemia Seres Humanos Transfusão de Linfócitos Meia-Idade Neoplasia Residual Cromossomo Filadélfia Proteínas Tirosina Quinases/antagonistas & inibidores Reação em Cadeia da Polimerase Via Transcriptase Reversa [Pt] Tipo de publicação: CASE REPORTS; JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.2 (Fusion Proteins, bcr-abl) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180301 [Lr] Data última revisão: 180301 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 180203 [St] Status: MEDLINE [do] DOI: 10.1097/MD.0000000000009160

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[PMID]: 29324347 [Au] Autor: He L; Pei H; Zhang C; Shao M; Li D; Tang M; Wang T; Chen X; Xiang M; Chen L [Ad] Endereço: State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center, Chengdu, Sichuan 610041, PR China. [Ti] Título: Design, synthesis and biological evaluation of 7H-pyrrolo[2,3-d]pyrimidin-4-amine derivatives as selective Btk inhibitors with improved pharmacokinetic properties for the treatment of rheumatoid arthritis. [So] Source: Eur J Med Chem;145:96-112, 2018 Feb 10. [Is] ISSN: 1768-3254 [Cp] País de publicação: France [La] Idioma: eng [Ab] Resumo: Bruton's tyrosine kinase (Btk) is a Tec family kinase with a well-defined role in the B cell receptor (BCR) and Fcγ receptor (FcR) signaling pathways, which makes it a uniquely attractive target for the treatment of autoimmune diseases, such as rheumatoid arthritis (RA). We reported a series of compounds bearing 7H-pyrrolo [2,3-d]pyrimidin-4-amine scaffold that potently inhibited Btk in vitro. Analysis of the structure-activity relationships (SAR) and drug-like profiles led to the discovery of the optimal compound B16. B16 preferentially inhibited Btk (IC = 21.70 ±â€¯0.82 nM) over closely related kinases with moderate selectivity. Cell-based tests also confirmed that B16 significantly inhibited Btk Y223 auto-phosphorylation and PLCγ2 Y1217 phosphorylation. MTT revealed that B16 displayed weak suppression against normal LO2, HEK293 and THP-1 cell lines with IC values over 30 µM. Moreover, B16 showed very weak potential to block the hERG channel (IC = 11.10 µM) in comparison to ibrutinib (IC = 0.97 µM). Owing to its favorable physicochemical properties (ClogP = 2.53, aqueous solubility ≈ 0.1 mg/mL), pharmacokinetic profiles (F = 49.15%, t = 7.02 h) and reasonable CYP450 profile, B16 exhibited potent anti-arthritis activity and similar efficacy to ibrutinib in reducing paw thickness in CIA mice. In conclusion, B16 is a potent, selective and durable inhibitor of Btk and has the potential to a safe and efficacious treatment for arthritis. [Mh] Termos MeSH primário: Artrite Reumatoide/tratamento farmacológico Desenho de Drogas Inibidores de Proteínas Quinases/farmacologia Proteínas Tirosina Quinases/antagonistas & inibidores Pirimidinas/farmacologia Pirróis/farmacologia [Mh] Termos MeSH secundário: Animais Artrite Reumatoide/metabolismo Linhagem Celular Proliferação Celular/efeitos dos fármacos Cães Relação Dose-Resposta a Droga Haplorrinos Seres Humanos Camundongos Microssomos Hepáticos/química Microssomos Hepáticos/metabolismo Modelos Moleculares Estrutura Molecular Inibidores de Proteínas Quinases/síntese química Inibidores de Proteínas Quinases/química Proteínas Tirosina Quinases/metabolismo Pirimidinas/síntese química Pirimidinas/química Pirróis/síntese química Pirróis/química Ratos Ratos Sprague-Dawley Relação Estrutura-Atividade [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (7H-pyrrolo(2,3-d)pyrimidin-4-amine); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); 0 (Pyrroles); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases) [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: 180112 [St] Status: MEDLINE

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[PMID]: 27776353 [Au] Autor: Wu J; Zhang M; Liu D [Ad] Endereço: Department of Oncology, The first Affiliated Hospital of Zhengzhou University, Zhengzhou, China. [Ti] Título: Bruton tyrosine kinase inhibitor ONO/GS-4059: from bench to bedside. [So] Source: Oncotarget;8(4):7201-7207, 2017 Jan 24. [Is] ISSN: 1949-2553 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: The Bruton tyrosine kinase (BTK) inhibitor, ibrutinib, has been approved for the treatment of chronic lymphocytic leukemia, mantle cell lymphoma, and Waldenstrom's macroglobulinemia. Acquired resistance to ibrutinib due to BTK C481S mutation has been reported. Mutations in PLCγ2 can also mediate resistance to ibrutinib. Untoward effects due to off-target effects are also disadvantages of ibrutinib. More selective and potent BTK inhibitors (ACP-196, ONO/GS-4059, BGB-3111, CC-292) are being investigated. This review summarized the preclinical research and clinical data of ONO/GS-4059. [Mh] Termos MeSH primário: Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos Imidazóis/uso terapêutico Leucemia Linfocítica Crônica de Células B/tratamento farmacológico Linfoma de Célula do Manto/tratamento farmacológico Pirimidinas/uso terapêutico Macroglobulinemia de Waldenstrom/tratamento farmacológico [Mh] Termos MeSH secundário: Ensaios Clínicos como Assunto Seres Humanos Imidazóis/farmacologia Leucemia Linfocítica Crônica de Células B/genética Linfoma de Célula do Manto/genética Mutação Fosfolipase C gama/genética Proteínas Tirosina Quinases/antagonistas & inibidores Proteínas Tirosina Quinases/genética Pirimidinas/farmacologia Resultado do Tratamento Macroglobulinemia de Waldenstrom/genética [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: 0 (GS-4059); 0 (Imidazoles); 0 (Pyrimidines); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 3.1.4.3 (Phospholipase C gamma) [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: 161025 [St] Status: MEDLINE [do] DOI: 10.18632/oncotarget.12786

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[PMID]: 29381963 [Au] Autor: Liang L; Wang L; Zhu P; Xia Y; Qiao Y; Hui K; Hu C; Ren Y; Jiang X [Ad] Endereço: Department of Radiation Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University. [Ti] Título: Apatinib concurrent gemcitabine for controlling malignant ascites in advanced pancreatic cancer patient: A case report. [So] Source: Medicine (Baltimore);96(47):e8725, 2017 Nov. [Is] ISSN: 1536-5964 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: RATIONALE: Malignant ascites (MA) is one of the poor prognostic factors for advanced pancreatic cancer and can bring about serious symptoms. The improvement of quality of life for patients is priority. However, there is no standard method for the treatment for pancreatic cancer-mediated MA. Apatinib is a novel and highly selective tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor-2. There are no reports of concurrent apatinib with gemcitabine in patients with pancreatic cancer-mediated MA. PATIENT CONCERNS: Herein, we presented a 64-year-old man patient who visited hospital due to abdominal pain for 1 month. DIAGNOSES: He was initially diagnosed with pancreatic cancer and his first symptom was MA. INTERVENTIONS: After failing in tube drainage and gemcitabine therapy, the patient received gemcitabine combined apatinib orally and after administrated 1 month, the MA was evaluated as nearly clear response according to the RECIST 1.1 standard, and without further need of paracentesis. The CEA and CA199 reached the lowest level after administrating for 2.5 months during the treatment process. OUTCOMES: 10.5 months following apatinib administration, the patient achieved a progression-free survival for more than 11 months. Hypertension (grade IV), hand-foot syndrome (grade I) and proteinuria (grade II) were observed. LESSONS: It indicated that apatinib concurrent gemcitabine may be a superior choice for pancreatic cancer-mediated MA. Further clinical trials required to confirm its efficacy and safety. [Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico Ascite/tratamento farmacológico Ascite/etiologia Desoxicitidina/análogos & derivados Neoplasias Pancreáticas/complicações Piridinas/uso terapêutico [Mh] Termos MeSH secundário: Antineoplásicos/administração & dosagem Desoxicitidina/administração & dosagem Desoxicitidina/uso terapêutico Quimioterapia Combinada Seres Humanos Masculino Meia-Idade Proteínas Tirosina Quinases/antagonistas & inibidores Piridinas/administração & dosagem Receptor 2 de Fatores de Crescimento do Endotélio Vascular/antagonistas & inibidores [Pt] Tipo de publicação: CASE REPORTS; JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antineoplastic Agents); 0 (Pyridines); 0W860991D6 (Deoxycytidine); 5S371K6132 (apatinib); B76N6SBZ8R (gemcitabine); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180220 [Lr] Data última revisão: 180220 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 180201 [St] Status: MEDLINE [do] DOI: 10.1097/MD.0000000000008725

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[PMID]: 29233870 [Au] Autor: Zachari M; Ganley IG [Ad] Endereço: MRC Protein Phosphorylation and Ubiquitylation Unit, School of Life Sciences, University of Dundee, Dundee DD1 5EH, U.K. [Ti] Título: The mammalian ULK1 complex and autophagy initiation. [So] Source: Essays Biochem;61(6):585-596, 2017 12 12. [Is] ISSN: 1744-1358 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Autophagy is a vital lysosomal degradation pathway that serves as a quality control mechanism. It rids the cell of damaged, toxic or excess cellular components, which if left to persist could be detrimental to the cell. It also serves as a recycling pathway to maintain protein synthesis under starvation conditions. A key initial event in autophagy is formation of the autophagosome, a unique double-membrane organelle that engulfs the cytosolic cargo destined for degradation. This step is mediated by the serine/threonine protein kinase ULK1 (unc-51-like kinase 1), which functions in a complex with at least three protein partners: FIP200 (focal adhesion kinase family interacting protein of 200 kDa), ATG (autophagy-related protein) 13 (ATG13), and ATG101. In this artcile, we focus on the regulation of the ULK1 complex during autophagy initiation. The complex pattern of upstream pathways that converge on ULK1 suggests that this complex acts as a node, converting multiple signals into autophagosome formation. Here, we review our current understanding of this regulation and in turn discuss what happens downstream, once the ULK1 complex becomes activated. [Mh] Termos MeSH primário: Proteína Homóloga à Proteína-1 Relacionada à Autofagia/metabolismo Proteínas Relacionadas à Autofagia/metabolismo Autofagia/fisiologia [Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética Proteínas Adaptadoras de Transdução de Sinal/metabolismo Animais Autofagia/genética Proteína Homóloga à Proteína-1 Relacionada à Autofagia/genética Proteínas Relacionadas à Autofagia/genética Seres Humanos Proteínas Tirosina Quinases/genética Proteínas Tirosina Quinases/metabolismo Proteínas de Transporte Vesicular/genética Proteínas de Transporte Vesicular/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Adaptor Proteins, Signal Transducing); 0 (Autophagy-Related Proteins); 0 (Vesicular Transport Proteins); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.11.1 (Autophagy-Related Protein-1 Homolog) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180220 [Lr] Data última revisão: 180220 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171214 [St] Status: MEDLINE [do] DOI: 10.1042/EBC20170021

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[PMID]: 28449809 [Au] Autor: Rossing M; Yde CW; Sehested A; Østrup O; Scheie D; Dangouloff-Ros V; Geoerger B; Vassal G; Nysom K [Ad] Endereço: Center for Genomic Medicine, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark. Electronic address: caroline.maria.rossing@regionh.dk. [Ti] Título: Genomic diagnostics leading to the identification of a TFG-ROS1 fusion in a child with possible atypical meningioma. [So] Source: Cancer Genet;212-213:32-37, 2017 Apr. [Is] ISSN: 2210-7762 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Meningiomas are rare in children. They are highly complex, harboring unique clinical and pathological characteristics, and many occur in patients with neurofibromatosis type 2. Hereby, we present a case of a two-year-old boy presented with a diagnostically challenging intraventricular tumor. It was incompletely resected 6 times over 14 months but kept progressing and was ultimately deemed unresectable. Histologically, the tumor was initially classified as schwannoma, but extensive international review concluded it was most likely an atypical meningioma, WHO grade II. Comprehensive genomic profiling revealed a TFG-ROS1 fusion, suggesting that ROS1-signaling pathway alterations were driving the tumor growth. In light of this new information, the possibility of a diagnosis of inflammatory myofibroblastic tumor was considered; however the histopathological results were not conclusive. This specific molecular finding allowed the potential use of precision medicine and the patient was enrolled in the AcSé phase 2 trial with crizotinib (NCT02034981), leading to a prolonged partial tumor response which is persisting since 14 months. This case highlights the value of precision cancer medicine in children. [Mh] Termos MeSH primário: Fusão Gênica Neoplasias Meníngeas/diagnóstico Meningioma/diagnóstico Fatores de Crescimento Transformadores/genética [Mh] Termos MeSH secundário: Pré-Escolar Diagnóstico Diferencial Seres Humanos Masculino Neoplasias Meníngeas/tratamento farmacológico Neoplasias Meníngeas/genética Meningioma/tratamento farmacológico Meningioma/genética Proteínas Tirosina Quinases/genética Proteínas Proto-Oncogênicas/genética Pirazóis/uso terapêutico Piridinas/uso terapêutico [Pt] Tipo de publicação: CASE REPORTS; JOURNAL ARTICLE [Nm] Nome de substância: 0 (Proto-Oncogene Proteins); 0 (Pyrazoles); 0 (Pyridines); 53AH36668S (crizotinib); 76057-06-2 (Transforming Growth Factors); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (ROS1 protein, human) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 180221 [Lr] Data última revisão: 180221 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170429 [St] Status: MEDLINE

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