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[PMID]:29331379
[Au] Autor:Shinagawa-Kobayashi Y; Kamimura K; Goto R; Ogawa K; Inoue R; Yokoo T; Sakai N; Nagoya T; Sakamaki A; Abe S; Sugitani S; Yanagi M; Fujisawa K; Nozawa Y; Koyama N; Nishina H; Furutani-Seiki M; Sakaida I; Terai S
[Ad] Endereço:Division of Gastroenterology and Hepatology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Niigata, Japan.
[Ti] Título:Effect of histidine on sorafenib-induced vascular damage: Analysis using novel medaka fish model.
[So] Source:Biochem Biophys Res Commun;496(2):556-561, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Sorafenib (SFN) is an anti-angiogenic chemotherapeutic that prolongs survival of patients with hepatocellular carcinoma (HCC); its side effects, including vascular damages such as hand-foot syndrome (HFS), are a major cause of therapy discontinuation. We previously reported that maintenance of peripheral blood flow by intake of dried bonito broth (DBB) significantly prevented HFS and prolonged the administration period. The amino acids contained in DBB probably contribute to its effects, but the mechanism has not been clarified. We hypothesized that histidine, the largest component among the amino acids contained in DBB, has effects on SFN-induced vascular damage, and evaluated this possibility using a novel medaka fish model. METHODS: The fli::GFP transgenic medaka fish model has a fluorescently visible systemic vasculature. We fed the fish with SFN with and without histidine to compare blood flow and vascular structure among the differently fed models. The vascular cross-sectional area of each fish was measured to determine vascular diameter changes. RESULTS: Our results demonstrated that SFN-fed medaka developed a narrower vascular diameter. In addition, this narrowing was counteracted by addition of histidine to the medaka diet. We observed no positive effect of histidine on regeneration of cut vessels or on cell growth of endothelial cells and HCC cell lines. CONCLUSION: We proved the efficacy of the medaka model to assess vascular changes after administration of specific chemicals. And our results suggest that SFN causes vascular damage by narrowing peripheral vessel diameter, and that histidine effectively counteracts these changes to maintain blood flow.
[Mh] Termos MeSH primário: Antineoplásicos/efeitos adversos
Velocidade do Fluxo Sanguíneo/efeitos dos fármacos
Vasos Sanguíneos/efeitos dos fármacos
Vasos Sanguíneos/patologia
Histidina/farmacologia
Niacinamida/análogos & derivados
Compostos de Fenilureia/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Carcinoma Hepatocelular/tratamento farmacológico
Seres Humanos
Neoplasias Hepáticas/tratamento farmacológico
Niacinamida/efeitos adversos
Oryzias
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Phenylurea Compounds); 25X51I8RD4 (Niacinamide); 4QD397987E (Histidine); 9ZOQ3TZI87 (sorafenib)
[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:180115
[St] Status:MEDLINE


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[PMID]:29249005
[Au] Autor:Trevisani F; Brandi G; Garuti F; Barbera MA; Tortora R; Casadei Gardini A; Granito A; Tovoli F; De Lorenzo S; Inghilesi AL; Foschi FG; Bernardi M; Marra F; Sacco R; Di Costanzo GG
[Ad] Endereço:Department of Medical and Surgical Sciences, Medical Semeiotics, University of Bologna, via Albertoni 15, 40138, Bologna, Italy. franco.trevisani@unibo.it.
[Ti] Título:Metronomic capecitabine as second-line treatment for hepatocellular carcinoma after sorafenib discontinuation.
[So] Source:J Cancer Res Clin Oncol;144(2):403-414, 2018 Feb.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Metronomic capecitabine (MC) is a well-tolerated systemic treatment showing promising results in one retrospective study, as second-line therapy after sorafenib failure, in patients with hepatocellular carcinoma (HCC). METHODS: 117 patients undergoing MC were compared to 112 patients, eligible for this treatment, but undergoing best supportive care (BSC) after sorafenib discontinuation for toxicity or HCC progression. The two groups were compared for demographic and clinical features. A multivariate regression analysis was conducted to detect independent prognostic factors. To balance confounding factors between the two groups, a propensity score model based on independent prognosticators (performance status, neoplastic thrombosis, causes of sorafenib discontinuation and pre-sorafenib treatment) was performed. RESULTS: Patients undergoing MC showed better performance status, lower tumor burden, lower prevalence of portal vein thrombosis, and better cancer stage. Median (95% CI) post-sorafenib survival (PSS) was longer in MC than in BSC patients [9.5 (7.5-11.6) vs 5.0 (4.2-5.7) months (p < 0.001)]. Neoplastic thrombosis, cause of sorafenib discontinuation, pre-sorafenib treatment and MC were independent prognosticators. The benefit of capecitabine was confirmed in patients after matching with propensity score [PSS: 9.9 (6.8-12.9) vs. 5.8 (4.8-6.8) months, (p = 0.001)]. MC lowered the mortality risk by about 40%. MC achieved better results in patients who stopped sorafenib for adverse events than in those who progressed during it [PSS: 17.3 (10.5-24.1) vs. 7.8 (5.2-10.1) months, (p = 0.035)]. Treatment toxicity was low and easily manageable with dose modulation. CONCLUSIONS: MC may be an efficient and safe second-line systemic therapy for HCC patients who discontinued sorafenib for toxicity or tumor progression.
[Mh] Termos MeSH primário: Capecitabina/administração & dosagem
Carcinoma Hepatocelular/tratamento farmacológico
Neoplasias Hepáticas/tratamento farmacológico
Niacinamida/análogos & derivados
Compostos de Fenilureia/administração & dosagem
[Mh] Termos MeSH secundário: Administração Metronômica
Idoso
Antimetabólitos Antineoplásicos/administração & dosagem
Feminino
Seres Humanos
Masculino
Niacinamida/administração & dosagem
Niacinamida/efeitos adversos
Compostos de Fenilureia/efeitos adversos
Inibidores de Proteínas Quinases/administração & dosagem
Inibidores de Proteínas Quinases/efeitos adversos
Estudos Retrospectivos
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (Phenylurea Compounds); 0 (Protein Kinase Inhibitors); 25X51I8RD4 (Niacinamide); 6804DJ8Z9U (Capecitabine); 9ZOQ3TZI87 (sorafenib)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2556-6


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[PMID]:28453695
[Au] Autor:Suenaga M; Schirripa M; Cao S; Zhang W; Yang D; Murgioni S; Rossini D; Marmorino F; Mennitto A; Ning Y; Okazaki S; Berger MD; Miyamoto Y; Gopez R; Barzi A; Yamaguchi T; Loupakis F; Lenz HJ
[Ad] Endereço:Department of Medical Oncology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, USA.
[Ti] Título:Genetic variants of DNA repair-related genes predict efficacy of TAS-102 in patients with refractory metastatic colorectal cancer.
[So] Source:Ann Oncol;28(5):1015-1022, 2017 05 01.
[Is] ISSN:1569-8041
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background: Tri-phosphorylated trifluridine (FTD) incorporation into DNA is TAS-102's main anti-tumor action. We tested whether genetic polymorphisms in homologous recombination (HR) and cell cycle checkpoint pathway for DNA repair is associated with outcomes in refractory metastatic colorectal cancer (mCRC) patients treated with TAS-102. Patients and methods: We analyzed genomic DNA extracted from 233 samples of three cohorts: an evaluation cohort of 52 patients receiving TAS-102, a validation cohort of 129 patients receiving TAS-102 and a control cohort of 52 patients receiving regorafenib. Single nucleotide polymorphisms of genes involved in HR (ATM, BRCA1, BRCA2, XRCC3, FANCD2, H2AX, RAD51) and cell cycle checkpoint (ATR, CHEK1, CHEK2, CDKN1A, TP53, CHE1, PIN1, PCNA) were analyzed by PCR-based direct sequencing. Results: In univariate analysis for the evaluation cohort, patients with any G allele in ATM rs609429 had longer overall survival (OS) than those with the C/C variant (8.7 vs. 4.4 months, HR 0.37, 95% CI: 0.14-0.99, P = 0.022). Patients carrying any A allele in XRCC3 rs861539 had significantly longer progression-free survival (PFS) (3.8 vs. 2.3 months, HR 0.44, 95% CI: 0.21-0.92, P = 0.024) and OS (15.6 vs. 6.3 months, HR 0.25, 95% CI: 0.08-0.79, P = 0.012) than those with the G/G variant. In multivariable analysis, ATM rs609429 remained significant for OS (P = 0.020). In the validation cohort, patients having ATM rs609429 with any G allele showed longer OS and PFS; the G/A variant in XRCC3 rs861539 showed longer OS, though without statistical significance. Conclusion: Genetic variants in the HR pathway may predict clinical outcome in mCRC patients receiving TAS-102.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Neoplasias Colorretais/genética
Enzimas Reparadoras do DNA/genética
Neoplasias Hepáticas/genética
Trifluridina/uso terapêutico
Uracila/análogos & derivados
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Antineoplásicos/farmacologia
Neoplasias Colorretais/tratamento farmacológico
Neoplasias Colorretais/mortalidade
Neoplasias Colorretais/patologia
Intervalo Livre de Doença
Combinação de Medicamentos
Resistência a Medicamentos Antineoplásicos/genética
Feminino
Estudos de Associação Genética
Seres Humanos
Neoplasias Hepáticas/tratamento farmacológico
Neoplasias Hepáticas/mortalidade
Neoplasias Hepáticas/secundário
Masculino
Meia-Idade
Compostos de Fenilureia/farmacologia
Compostos de Fenilureia/uso terapêutico
Modelos de Riscos Proporcionais
Piridinas/farmacologia
Piridinas/uso terapêutico
Estudos Retrospectivos
Resultado do Tratamento
Trifluridina/farmacologia
Uracila/farmacologia
Uracila/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Drug Combinations); 0 (Phenylurea Compounds); 0 (Pyridines); 0 (TAS 102); 24T2A1DOYB (regorafenib); 56HH86ZVCT (Uracil); EC 6.5.1.- (DNA Repair Enzymes); RMW9V5RW38 (Trifluridine)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.1093/annonc/mdx035


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Registro de Ensaios Clínicos
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[PMID]:27771610
[Au] Autor:Agulnik M; Costa RLB; Milhem M; Rademaker AW; Prunder BC; Daniels D; Rhodes BT; Humphreys C; Abbinanti S; Nye L; Cehic R; Polish A; Vintilescu C; McFarland T; Skubitz K; Robinson S; Okuno S; Van Tine BA
[Ad] Endereço:Division of Hematology/Oncology, Northwestern University, Feinberg School of Medicine, Chicago, USA.
[Ti] Título:A phase II study of tivozanib in patients with metastatic and nonresectable soft-tissue sarcomas.
[So] Source:Ann Oncol;28(1):121-127, 2017 01 01.
[Is] ISSN:1569-8041
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background: Soft tissue sarcomas (STSs) overexpress vascular endothelial growth factors (VEGF) and VEGF-receptors (VEGFR) activation have been associated with tumor aggressiveness. Tivozanib is a potent small molecule tyrosine kinase inhibitor against VEGFR1-3, with activity against PDGFRα/ß and cKIT. The primary endpoint of this study was progression free survival (PFS) rate at 16 weeks. Secondary end points were overall survival (OS), response rate, safety and correlative studies. Patients and methods: A Simon two-stage phase II trial was performed using tivozanib given orally at 1.5 mg daily, 3 week on 1 week off on a 28 day cycle until disease progression or intolerable toxicity. Results: Fifty-eight patients were enrolled and treated with tivozanib. Leiomyosarcoma was the most common STS histological type in our cohort (47%) and 27 patients (46%) had received at least 3 lines of therapy prior to study entry. Up to 24 patients (41%) had prior VEGF targeted therapies. Partial response and stable disease were observed in 2 (3.6%) and 30 (54.5%) patients. The 16 week PFS rate was 36.4% [95% confidence interval (CI) 23.7-49.1] and a median PFS of 3.5 months (95% CI 1.8-3). Median OS observed was 12.2 months (95% CI 8.1-16.8). The most frequent all grade toxicities were fatigue (48.3%), hypertension (43.1%), nausea (31%) and diarrhea (27.6%). The most common grade three toxicity was hypertension (22.4%). Correlative studies demonstrate no correlation between the expression of VEGFR 1, 2 or 3, PDGFRα/ß or FGF, and activity of tivozanib. Conclusion: Tivozanib was well tolerated and showed antitumor activity with a promising median PFS and PFS rate at 4 months in a heavily pretreated population of metastatic STSs. Our results support further studies to assess the clinical efficacy of tivozanib in STS. Clinical Trial Number: NCT01782313.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Compostos de Fenilureia/uso terapêutico
Quinolinas/uso terapêutico
Sarcoma/tratamento farmacológico
Neoplasias de Tecidos Moles/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Intervalo Livre de Doença
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Receptores de Fatores de Crescimento do Endotélio Vascular/antagonistas & inibidores
Sarcoma/mortalidade
Neoplasias de Tecidos Moles/mortalidade
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Phenylurea Compounds); 0 (Quinolines); 172030934T (tivozanib); EC 2.7.10.1 (Receptors, Vascular Endothelial Growth Factor)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1093/annonc/mdw444


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[PMID]:27771613
[Au] Autor:Gyawali B; Shimokata T; Ando M; Honda K; Ando Y
[Ad] Endereço:Department of Clinical Oncology and Chemotherapy, Nagoya University Graduate School of Medicine, Nagoya.
[Ti] Título:Risk of serious adverse events and fatal adverse events with sorafenib in patients with solid cancer: a meta-analysis of phase 3 randomized controlled trials†.
[So] Source:Ann Oncol;28(2):246-253, 2017 02 01.
[Is] ISSN:1569-8041
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background: Sorafenib is a multikinase-tyrosine kinase inhibitor commonly used in a variety of cancers. There are concerns about the increased risk of serious adverse events (SAEs) and fatal adverse events (FAEs) with sorafenib. We performed an up-to-date meta-analysis of all phase 3 randomized controlled trials (RCTs) of sorafenib to quantify the increased risk of SAEs and FAEs. Patients and methods: We carried out a systematic search of electronic databases for studies published from inception to February 2016 without any restrictions. Eligibility criteria included phase 3 RCTs of solid tumors comparing sorafenib, alone or in combination with nontargeted chemotherapy (Sorafenib arm) versus placebo or nontargeted chemotherapy (control arm). Data on SAEs and FAEs for both the arms were extracted from each study and pooled to determine the overall incidence, relative risks (RRs) and 95% Confidence Intervals (CIs). Results: Of 471 studies identified, a total of 12 phase 3 RCTs involving 6797 solid cancer patients comparing sorafenib with control met the eligibility criteria and were included. The overall incidence of SAEs and FAEs with sorafenib were 26.4% (95% CI, 18.0-36.9%) and 1.3% (95% CI: 0.8-2.2%), respectively. Compared with control, sorafenib use significantly increased the risk of both SAEs (RR: 1.49, 95% CI: 1.18-1.89, P = 0.001) and FAEs (RR: 1.82, 95% CI: 1.05-3.14, P = 0.033). This association varied significantly with cancer types (P < 0.001) and approval status (P = 0.012) for SAEs but no evidence of heterogeneity was found for FAEs. Conclusions: This meta-analysis of phase 3 RCTs demonstrates an increased risk of both SAEs and FAEs with sorafenib use in adult patients with solid cancers. This quantification of increased risks of SAEs and FAEs will be important in considering the trade-off of sorafenib treatment during shared decision-making.
[Mh] Termos MeSH primário: Antineoplásicos/efeitos adversos
Neoplasias/tratamento farmacológico
Niacinamida/análogos & derivados
Compostos de Fenilureia/efeitos adversos
[Mh] Termos MeSH secundário: Ensaios Clínicos Fase III como Assunto
Seres Humanos
Neoplasias/mortalidade
Niacinamida/efeitos adversos
Modelos de Riscos Proporcionais
Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Phenylurea Compounds); 25X51I8RD4 (Niacinamide); 9ZOQ3TZI87 (sorafenib)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1093/annonc/mdw549


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[PMID]:29478629
[Au] Autor:Jiang L; Feng Z; Dai L; Shang B; Paoletti E
[Ad] Endereço:State Key Laboratory of Urban and Regional Ecology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China; State Key Laboratory of Soil and Sustainable Agriculture, Institute of Soil Science, Chinese Academy of Sciences, Nanjing 210008, China; College of
[Ti] Título:Large variability in ambient ozone sensitivity across 19 ethylenediurea-treated Chinese cultivars of soybean is driven by total ascorbate.
[So] Source:J Environ Sci (China);64:10-22, 2018 Feb.
[Is] ISSN:1001-0742
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The sensitivity of Chinese soybean cultivars to ambient ozone (O ) in the field is unknown, although soybean is a major staple food in China. Using ethylenediurea (EDU) as an O protectant, we tested the gas exchange, pigments, antioxidants and biomass of 19 cultivars exposed to 28ppm·hr AOT40 (accumulated O over an hourly concentration threshold of 40ppb) over the growing season at a field site in China. By comparing the average biomass with and without EDU, we estimated the cultivar-specific sensitivity to O and ranked the cultivars from very tolerant (<10% change) to highly sensitive (>45% change), which helps in choosing the best-suited cultivars for local cultivation. Higher lipid peroxidation and activity of the ascorbate peroxidase enzyme were major responses to O damage, which eventually translated into lower biomass production. The constitutional level of total ascorbate in the leaves was the most important parameter explaining O sensitivity among these cultivars. Surprisingly, the role of stomatal conductance was insignificant. These results will guide future breeding efforts towards more O -tolerant cultivars in China, while strategies for implementing control measures of regional O pollution are being implemented. Overall, these results suggest that present ambient O pollution is a serious concern for soybean in China, which highlights the urgent need for policy-making actions to protect this critical staple food.
[Mh] Termos MeSH primário: Poluentes Atmosféricos/toxicidade
Antioxidantes/metabolismo
Ozônio/toxicidade
Compostos de Fenilureia/metabolismo
Feijão de Soja/fisiologia
[Mh] Termos MeSH secundário: Ácido Ascórbico
China
Fotossíntese/fisiologia
Folhas de Planta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Air Pollutants); 0 (Antioxidants); 0 (Phenylurea Compounds); 54924-46-8 (ethylene diurea); 66H7ZZK23N (Ozone); PQ6CK8PD0R (Ascorbic Acid)
[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:180227
[St] Status:MEDLINE


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Texto completo SciELO Brasil
[PMID]:28746590
[Au] Autor:Campregher PV; Mattos VRP; Salvino MA; Santos FPS; Hamerschlak N
[Ad] Endereço:Hospital Israelita Albert Einstein, São Paulo, SP, Brazil.
[Ti] Título:Successful treatment of post-transplant relapsed acute myeloid leukemia with FLT3 internal tandem duplication using the combination of induction chemotherapy, donor lymphocyte infusion, sorafenib and azacitidine. Report of three cases.
[So] Source:Einstein (Sao Paulo);15(3):355-358, 2017 Jul-Sep.
[Is] ISSN:2317-6385
[Cp] País de publicação:Brazil
[La] Idioma:eng; por
[Ab] Resumo:Acute myeloid leukemia is a hematopoietic stem cell neoplastic disease associated with high morbidity and mortality. The presence of FLT3 internal tandem duplication mutations leads to high rates of relapse and decreased overall survival. Patients with FLT3 internal tandem duplication are normally treated with hematopoietic stem cell transplantation in first complete remission. Nevertheless, the incidence of post-transplant relapse is considerable in this group of patients, and the management of this clinical condition is challenging. The report describes the outcomes of patients with FLT3 internal tandem duplication positive acute myeloid leukemia who relapsed after allogeneic hematopoietic stem cell transplantation and were treated with the combination of re-induction chemotherapy, donor lymphocyte infusion, sorafenib and azacitidine. Three cases are described and all patients achieved prolonged complete remission with the combined therapy. The combination of induction chemotherapy followed by donor lymphocyte infusion, and the maintenance with azacitidine and sorafenib can be effective approaches in the treatment of post-hematopoietic stem cell transplant and relapsed FLT3 internal tandem duplication positive acute myeloid leukemia patients. This strategy should be further explored in the context of clinical trials.
[Mh] Termos MeSH primário: Antineoplásicos/administração & dosagem
Azacitidina/administração & dosagem
Quimioterapia de Indução
Leucemia Mieloide Aguda/terapia
Transfusão de Linfócitos
Niacinamida/análogos & derivados
Compostos de Fenilureia/administração & dosagem
Tirosina Quinase 3 Semelhante a fms/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Terapia Combinada/métodos
Feminino
Seres Humanos
Leucemia Mieloide Aguda/genética
Masculino
Meia-Idade
Recidiva Local de Neoplasia/terapia
Niacinamida/administração & dosagem
Recidiva
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Phenylurea Compounds); 25X51I8RD4 (Niacinamide); 9ZOQ3TZI87 (sorafenib); EC 2.7.10.1 (FLT3 protein, human); EC 2.7.10.1 (fms-Like Tyrosine Kinase 3); M801H13NRU (Azacitidine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE


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[PMID]:28923722
[Au] Autor:Agathokleous E; Paoletti E; Manning WJ; Kitao M; Saitanis CJ; Koike T
[Ad] Endereço:Silviculture & Forest Ecological Studies, Hokkaido University, Sapporo, Hokkaido 060-8589, Japan; Hokkaido Research Center, Forestry and Forest Products Research Institute (FFPRI), Forest Research and Management Organization, 7 Hitsujigaoka, Sapporo, Hokkaido 062-8516, Japan. Electronic address:
[Ti] Título:High doses of ethylenediurea (EDU) as soil drenches did not increase leaf N content or cause phytotoxicity in willow grown in fertile soil.
[So] Source:Ecotoxicol Environ Saf;147:574-584, 2018 Jan.
[Is] ISSN:1090-2414
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Ground-level ozone (O ) levels are nowadays elevated in wide regions of the Earth, causing significant effects on plants that finally lead to suppressed productivity and yield losses. Ethylenediurea (EDU) is a chemical compound which is widely used in research projects as phytoprotectant against O injury. The EDU mode of action remains still unclear, while there are indications that EDU may contribute to plants with nitrogen (N) when the soil is poor in N and the plants have relatively small leaf area. To reveal whether the N content of EDU acts as a fertilizer to plants when the soil is not poor in N and the plants have relatively large total plant leaf area, willow plants (Salix sachalinensis Fr. Schm) were exposed to low ambient O levels and treated ten times (9-day interval) with 200mL soil drench containing 0, 800 or 1600mg EDU L . Fertilizer was added to a nutrient-poor soil, and the plants had an average plant leaf area of 9.1m at the beginning of EDU treatments. Indications for EDU-induced hormesis in maximum electron transport rate (J ) and ratio of intercellular to ambient CO concentration (C :C ) were observed at the end of the experiment. No other EDU-induced effects on leaf greenness and N content, maximum quantum yield of photosystem II (F /F ), gas exchange, growth and matter production suggest that EDU did not act as N fertilizer and did not cause toxicity under these experimental conditions.
[Mh] Termos MeSH primário: Nitrogênio/metabolismo
Compostos de Fenilureia/farmacologia
Folhas de Planta/efeitos dos fármacos
Salix/efeitos dos fármacos
Solo/química
[Mh] Termos MeSH secundário: Poluentes Atmosféricos/toxicidade
Monitoramento Ambiental
Hormese
Japão
Ozônio/toxicidade
Folhas de Planta/crescimento & desenvolvimento
Folhas de Planta/metabolismo
Salix/crescimento & desenvolvimento
Salix/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Air Pollutants); 0 (Phenylurea Compounds); 0 (Soil); 54924-46-8 (ethylene diurea); 66H7ZZK23N (Ozone); N762921K75 (Nitrogen)
[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:170920
[St] Status:MEDLINE


  9 / 6926 MEDLINE  
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[PMID]:29304109
[Au] Autor:Lin CY; Lin TH; Chen CC; Chen MC; Chen CP
[Ad] Endereço:Division of Colorectal Surgery, Department of Surgery, Taichung Veterans General Hospital, Taichung, Taichung, Taiwan.
[Ti] Título:Combination chemotherapy with Regorafenib in metastatic colorectal cancer treatment: A single center, retrospective study.
[So] Source:PLoS One;13(1):e0190497, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Regorafenib has been demonstrated as effective in refractory metastatic colorectal cancer. Combination use with chemotherapy has not been reported. We examined the efficacy and safety of adding chemotherapy to Regorafenib for the treatment of metastatic colorectal cancer(mCRC) patients. METHODS: We recruited mCRC patients at our institute who received either regorafenib monotherapy or regorafenib in combination with other chemotherapies. All patients had received chemo and target therapies and presented with disease progression before regorafenib treatment. The primary end point was overall survival. FINDINGS: Between September1, 2015 and May 31, 2017, 100 mCRC patients at our institute received regorafenib treatment. 39 patients were excluded due to poor performance, lack of timely treatment, or inadequate clinical data. A total of 34 patients received regorafenib combined with other chemotherapies, and 27 patients received regorafenib alone. Median follow up time was 10.4 and 6.1 months, respectively. The primary end point of median OS was higher in the combination group than in the single use group (20.9m vs 10.3m, p = 0.015). The most frequent adverse events were hand-foot skin reactions(16[47.1%]vs 12[44.4%]), fatigue(6[17.6%] vs 7[25.9%]), gastrointestinal discomfort (7[20.6%] vs 6[22.2%]), neutropenia (4[11.8%] vs 1[3.7%]), diarrhea(4[11.8%] vs 1[3.7%]), and mucositis(5[14.7%] vs 1[3.7%]). CONCLUSION: The present study showed the efficacy and side effects of regorafenib combination treatment. Superiority in median OS and median PFS was noted in the combination group. The sampling difference between the study and observation groups effects justifies the comparison. Further clinical evidence of combination therapy efficacy is pending future studies.
[Mh] Termos MeSH primário: Neoplasias Colorretais/tratamento farmacológico
Metástase Neoplásica/tratamento farmacológico
Compostos de Fenilureia/uso terapêutico
Piridinas/uso terapêutico
[Mh] Termos MeSH secundário: Neoplasias Colorretais/patologia
Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phenylurea Compounds); 0 (Pyridines); 24T2A1DOYB (regorafenib)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190497


  10 / 6926 MEDLINE  
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[PMID]:28470518
[Au] Autor:Chen D; Eyupoglu IY; Savaskan N
[Ad] Endereço:Translational Cell Biology and Neurooncology Laboratory of the Universitätsklinikum Erlangen (UKER), Friedrich-Alexander University of Erlangen - Nürnberg (FAU), and Department of Neurosurgery of the Universitätsklinikum Erlangen, Universitätsklinikum Erlangen (UKER), Friedrich-Alexander University
[Ti] Título:Ferroptosis and Cell Death Analysis by Flow Cytometry.
[So] Source:Methods Mol Biol;1601:71-77, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell death and its recently discovered regulated form ferroptosis are characterized by distinct morphological, electrophysiological, and pharmacological features. In particular ferroptosis can be induced by experimental compounds and clinical drugs (i.e., erastin, sulfasalazine, sorafenib, and artesunate) in various cell types and cancer cells. Pharmacologically, this cell death process can be inhibited by iron chelators and lipid peroxidation inhibitors. Relevance of this specific cell death form has been found in different pathological conditions such as cancer, neurotoxicity, neurodegeneration, and ischemia. Distinguishing cell viability and cell death is essential for experimental and clinical applications and a key component in flow cytometry experiments. Dead cells can compromise the integrity of the data by nonspecific binding of antibodies and dyes. Therefore it is essential that dead cells are robustly and reproducibly identified and characterized by means of cytometry application. Here we describe a procedure to detect and quantify cell death and its specific form ferroptosis based on standard flow cytometry techniques.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Citometria de Fluxo/métodos
Ferro/metabolismo
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Dactinomicina/análogos & derivados
Dactinomicina/química
Seres Humanos
Indicadores e Reagentes/química
Necrose
Niacinamida/análogos & derivados
Niacinamida/farmacologia
Compostos de Fenilureia/farmacologia
Piperazinas/farmacologia
Propídio/química
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Indicators and Reagents); 0 (Phenylurea Compounds); 0 (Piperazines); 0 (erastin); 1CC1JFE158 (Dactinomycin); 25X51I8RD4 (Niacinamide); 36015-30-2 (Propidium); 7240-37-1 (7-aminoactinomycin D); 9ZOQ3TZI87 (sorafenib); E1UOL152H7 (Iron)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6960-9_6



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