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[PMID]:29232579
[Au] Autor:Wu KJ; Zhong HJ; Li G; Liu C; Wang HD; Ma DL; Leung CH
[Ad] Endereço:State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.
[Ti] Título:Structure-based identification of a NEDD8-activating enzyme inhibitor via drug repurposing.
[So] Source:Eur J Med Chem;143:1021-1027, 2018 Jan 01.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:NEDD8-activating enzyme (NAE) is an essential player of the NEDD8 conjugation pathway that regulates protein degradation. Meanwhile, drug repurposing is a cost-efficient strategy to identify new therapeutic uses for existing scaffolds. In this report, mitoxantrone (1) was repurposed as an inhibitor of NAE by virtual screening of an FDA-approved drug database. Compound 1 inhibited NAE activity in cell-free and cell-based systems with high selectivity and was competitive with ATP. Furthermore, compound 1 induced apoptosis of colorectal adenocarcinoma cancer cells through inhibiting the degradation of the neddylation substrate p53.
[Mh] Termos MeSH primário: Adenocarcinoma/tratamento farmacológico
Neoplasias Colorretais/tratamento farmacológico
Inibidores Enzimáticos/farmacologia
Mitoxantrona/farmacologia
Proteína NEDD8/antagonistas & inibidores
Enzimas Ativadoras de Ubiquitina/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adenocarcinoma/metabolismo
Adenocarcinoma/patologia
Apoptose/efeitos dos fármacos
Células CACO-2
Linhagem Celular
Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/patologia
Relação Dose-Resposta a Droga
Descoberta de Drogas
Avaliação Pré-Clínica de Medicamentos
Inibidores Enzimáticos/síntese química
Inibidores Enzimáticos/química
Seres Humanos
Mitoxantrona/síntese química
Mitoxantrona/química
Modelos Moleculares
Estrutura Molecular
Proteína NEDD8/metabolismo
Relação Estrutura-Atividade
Proteína Supressora de Tumor p53/antagonistas & inibidores
Proteína Supressora de Tumor p53/metabolismo
Enzimas Ativadoras de Ubiquitina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (NEDD8 Protein); 0 (NEDD8 protein, human); 0 (Tumor Suppressor Protein p53); BZ114NVM5P (Mitoxantrone); EC 6.2.1.45 (Ubiquitin-Activating Enzymes)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE


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[PMID]:28976984
[Au] Autor:Liu D; Hu Y; Guo Y; Zhu Z; Lu B; Wang X; Huang Y
[Ad] Endereço:Department of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
[Ti] Título:Mycoplasma-associated multidrug resistance of hepatocarcinoma cells requires the interaction of P37 and Annexin A2.
[So] Source:PLoS One;12(10):e0184578, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mycoplasma infection has been reported to be associated with cancer migration, invasion, epithelial-mesenchymal transition as well as the resistance to nucleoside analogues chemotherapeutic drugs. In this study, we found that the sensitivity of hepatocarcinoma cells to Cisplatin, Gemcitabine and Mitoxantrone was increased by mycoplasma elimination. Similar to the effect of anti-mycoplasma agent, interrupting the interaction between Mycoplasma hyorhinis membrane protein P37 and Annexin A2 of host cells using the N-terminal of ANXA2 polypeptide enhanced the sensitivity of HCC97L cells to Gemcitabine and Mitoxantrone. Meanwhile, we did not observe any changes in expression or distribution of multidrug resistance associated transporters, ATP-Binding Cassette protein B1, C1 and G2, on the removal of mycoplasma. These results suggest that mycoplasma induces a resistance to multiple drugs in hepatocarcinoma cells which required the interaction of P37 and Annexin A2. The pathway downstream this interaction needs to be explored.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Anexina A2/metabolismo
Carcinoma Hepatocelular/patologia
Neoplasias Hepáticas/patologia
Mycoplasma hyorhinis/fisiologia
[Mh] Termos MeSH secundário: Antibacterianos/farmacologia
Antineoplásicos/farmacologia
Azitromicina/farmacologia
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/microbiologia
Linhagem Celular Tumoral
Desoxicitidina/análogos & derivados
Desoxicitidina/farmacologia
Resistência a Múltiplos Medicamentos
Resistência a Medicamentos Antineoplásicos
Fluoroquinolonas/farmacologia
Seres Humanos
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/microbiologia
Mitoxantrona/farmacologia
Mycoplasma hyorhinis/efeitos dos fármacos
Mycoplasma hyorhinis/genética
Mycoplasma hyorhinis/isolamento & purificação
Ligação Proteica
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Annexin A2); 0 (Anti-Bacterial Agents); 0 (Antineoplastic Agents); 0 (Fluoroquinolones); 0 (p37 protein, human); 0W860991D6 (Deoxycytidine); 83905-01-5 (Azithromycin); B76N6SBZ8R (gemcitabine); BZ114NVM5P (Mitoxantrone); U188XYD42P (moxifloxacin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184578


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[PMID]:28820965
[Au] Autor:Arduino DM; Wettmarshausen J; Vais H; Navas-Navarro P; Cheng Y; Leimpek A; Ma Z; Delrio-Lorenzo A; Giordano A; Garcia-Perez C; Médard G; Kuster B; García-Sancho J; Mokranjac D; Foskett JK; Alonso MT; Perocchi F
[Ad] Endereço:Gene Center/Department of Biochemistry, Ludwig-Maximilians Universität München, Munich 81377, Germany; Institute for Diabetes and Obesity, Helmholtz Zentrum München, Neuherberg 85764, Germany.
[Ti] Título:Systematic Identification of MCU Modulators by Orthogonal Interspecies Chemical Screening.
[So] Source:Mol Cell;67(4):711-723.e7, 2017 Aug 17.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mitochondrial calcium uniporter complex is essential for calcium (Ca ) uptake into mitochondria of all mammalian tissues, where it regulates bioenergetics, cell death, and Ca signal transduction. Despite its involvement in several human diseases, we currently lack pharmacological agents for targeting uniporter activity. Here we introduce a high-throughput assay that selects for human MCU-specific small-molecule modulators in primary drug screens. Using isolated yeast mitochondria, reconstituted with human MCU, its essential regulator EMRE, and aequorin, and exploiting a D-lactate- and mannitol/sucrose-based bioenergetic shunt that greatly minimizes false-positive hits, we identify mitoxantrone out of more than 600 clinically approved drugs as a direct selective inhibitor of human MCU. We validate mitoxantrone in orthogonal mammalian cell-based assays, demonstrating that our screening approach is an effective and robust tool for MCU-specific drug discovery and, more generally, for the identification of compounds that target mitochondrial functions.
[Mh] Termos MeSH primário: Bloqueadores dos Canais de Cálcio/farmacologia
Canais de Cálcio/efeitos dos fármacos
Cálcio/metabolismo
Descoberta de Drogas/métodos
Ensaios de Triagem em Larga Escala
Mitocôndrias/efeitos dos fármacos
Mitoxantrona/farmacologia
Saccharomyces cerevisiae/efeitos dos fármacos
[Mh] Termos MeSH secundário: Equorina/metabolismo
Animais
Bloqueadores dos Canais de Cálcio/química
Canais de Cálcio/genética
Canais de Cálcio/metabolismo
Relação Dose-Resposta a Droga
Metabolismo Energético/efeitos dos fármacos
Células HEK293
Células HeLa
Seres Humanos
Cinética
Ácido Láctico/metabolismo
Manitol/metabolismo
Potenciais da Membrana
Camundongos Transgênicos
Mitocôndrias/metabolismo
Mitoxantrona/química
Modelos Moleculares
Estrutura Molecular
Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/metabolismo
Relação Estrutura-Atividade
Sacarose/metabolismo
Xenopus laevis
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Calcium Channels); 0 (SMDT1 protein, human); 0 (mitochondrial calcium uniporter); 33X04XA5AT (Lactic Acid); 3OWL53L36A (Mannitol); 50934-79-7 (Aequorin); 57-50-1 (Sucrose); BZ114NVM5P (Mitoxantrone); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170819
[St] Status:MEDLINE


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[PMID]:28668386
[Au] Autor:Chiappella A; Martelli M; Angelucci E; Brusamolino E; Evangelista A; Carella AM; Stelitano C; Rossi G; Balzarotti M; Merli F; Gaidano G; Pavone V; Rigacci L; Zaja F; D'Arco A; Cascavilla N; Russo E; Castellino A; Gotti M; Congiu AG; Cabras MG; Tucci A; Agostinelli C; Ciccone G; Pileri SA; Vitolo U
[Ad] Endereço:Department of Haematology, Azienda Ospedaliero Universitaria Città della Salute e della Scienza di Torino, Turin, Italy. Electronic address: achiappella@cittadellasalute.to.it.
[Ti] Título:Rituximab-dose-dense chemotherapy with or without high-dose chemotherapy plus autologous stem-cell transplantation in high-risk diffuse large B-cell lymphoma (DLCL04): final results of a multicentre, open-label, randomised, controlled, phase 3 study.
[So] Source:Lancet Oncol;18(8):1076-1088, 2017 Aug.
[Is] ISSN:1474-5488
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The prognosis of young patients with diffuse large B-cell lymphoma at high risk (age-adjusted International Prognostic Index [aa-IPI] score 2 or 3) treated with R-CHOP (rituximab, cyclophosphamide, vincristine, doxorubicin, and prednisone) is poor. The aim of this study was to investigate the possible benefit of intensification with high-dose chemotherapy and autologous stem-cell transplantation as part of first-line treatment in these patients. METHODS: We did a multicentre, open-label, randomised, controlled, phase 3 trial with a 2 × 2 factorial design to compare, at two different R-CHOP dose levels, a full course of rituximab-dose-dense chemotherapy (no transplantation group) versus an abbreviated course of rituximab-dose-dense chemotherapy followed by consolidation with R-MAD (rituximab plus high-dose cytarabine plus mitoxantrone plus dexamethasone) and high-dose BEAM chemotherapy (carmustine, etoposide, cytarabine, and melphalan) plus autologous stem-cell transplantation (transplantation group) in young patients (18-65 years) with untreated high-risk diffuse large B-cell lymphoma (aa-IPI score 2-3). At enrolment, patients were stratified according to aa-IPI score and randomly assigned (1:1:1:1) to receive R-CHOP (intravenous rituximab 375 mg/m , cyclophosphamide 750 mg/m , doxorubicin 50 mg/m , and vincristine 1·4 mg/m on day 1, plus oral prednisone 100 mg on days 1-5) delivered in a 14-day cycle (R-CHOP-14) for eight cycles; high-dose R-CHOP-14 (R-MegaCHOP-14; R-CHOP-14 except for cyclophosphamide 1200 mg/m and doxorubicin 70 mg/m ) for six cycles; R-CHOP-14 for four cycles followed by R-MAD (intravenous rituximab 375 mg/m on day 1 or 4 plus intravenous cytarabine 2000 mg/m and dexamethasone 4 mg/m every 12 h on days 1-3 plus intravenous mitoxantrone 8 mg/m on days 1-3) plus BEAM (intravenous carmustine 300 mg/m on day -7, intravenous cytarabine 200 mg/m twice a day on days -6 to -3, intravenous etoposide 100 mg/m twice a day on days -6 to -3, plus intravenous melphalan 140 mg/m on day -2) and autologous stem-cell transplantation (day 0); or R-MegaCHOP-14 for four cycles followed by R-MAD plus BEAM and autologous stem-cell transplantation. The primary endpoint was failure-free survival at 2 years in the intention-to-treat population. This study is registered with EudraCT (2005-002181-14; 2007-000275-42) and with ClinicalTrials.gov, number NCT00499018. FINDINGS: Between Jan 10, 2006, and Sept 8, 2010, 399 patients were randomly assigned to receive transplantation (n=199) or no transplantation (n=200); 203 patients were assigned to receive R-CHOP-14 and 196 were assigned to receive R-MegaCHOP-14. With a median follow-up of 72 months (IQR 57-88), 2-year failure-free survival was 71% (95% CI 64-77) in the transplantation group versus 62% (95% CI 55-68) in the no transplantation group (hazard ratio [HR] 0·65 [95% CI 0·47-0·91]; stratified log-rank test p=0·012). No difference in 5-year overall survival was observed between these groups (78% [95% CI 71-83] versus 77% [71-83]; HR 0·98 [0·65-1·48]; stratified log-rank test p=0·91). Grade 3 or worse haematological adverse events were reported in 183 (92%) of 199 patients in the transplantation group versus 135 (68%) of 200 patients in the no transplantation group. Grade 3 or worse non-haematological adverse events were reported in 90 (45%) versus 31 (16%); the most common grade 3 or worse non-haematological adverse event was gastrointestinal (49 [25%] vs 19 [10%]). Treatment-related deaths occurred in 13 (3%) patients; eight in the transplantation group and five in the no transplantation group. INTERPRETATION: Abbreviated rituximab-dose-dense chemotherapy plus R-MAD plus BEAM and autologous stem-cell transplantation reduced the risk of treatment failure compared with full course rituximab-dose-dense chemotherapy in young patients with diffuse large B-cell lymphoma at high risk. However, these results might not be clinically meaningful, since this improvement did not reflect an improvement in overall survival. These results do not support further consideration of the use of intensification of R-CHOP as an upfront strategy in patients with diffuse large B-cell lymphoma with poor prognosis. FUNDING: Fondazione Italiana Linfomi.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Linfoma Difuso de Grandes Células B/terapia
Rituximab/administração & dosagem
Transplante de Células-Tronco
[Mh] Termos MeSH secundário: Adulto
Anticorpos Monoclonais Murinos/administração & dosagem
Anticorpos Monoclonais Murinos/efeitos adversos
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Carmustina/administração & dosagem
Quimioterapia de Consolidação
Ciclofosfamida/administração & dosagem
Ciclofosfamida/efeitos adversos
Citarabina/administração & dosagem
Dexametasona/administração & dosagem
Intervalo Livre de Doença
Doxorrubicina/administração & dosagem
Doxorrubicina/efeitos adversos
Etoposídeo/administração & dosagem
Feminino
Seguimentos
Doenças Hematológicas/induzido quimicamente
Seres Humanos
Quimioterapia de Indução
Análise de Intenção de Tratamento
Masculino
Melfalan/administração & dosagem
Meia-Idade
Mitoxantrona/administração & dosagem
Prednisona/administração & dosagem
Prednisona/efeitos adversos
Fatores de Risco
Transplante de Células-Tronco/efeitos adversos
Taxa de Sobrevida
Transplante Autólogo
Vincristina/administração & dosagem
Vincristina/efeitos adversos
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Murine-Derived); 0 (R-CHOP protocol); 04079A1RDZ (Cytarabine); 4F4X42SYQ6 (Rituximab); 5J49Q6B70F (Vincristine); 6PLQ3CP4P3 (Etoposide); 7S5I7G3JQL (Dexamethasone); 80168379AG (Doxorubicin); 8N3DW7272P (Cyclophosphamide); BZ114NVM5P (Mitoxantrone); Q41OR9510P (Melphalan); U68WG3173Y (Carmustine); VB0R961HZT (Prednisone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170703
[St] Status:MEDLINE


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[PMID]:28572277
[Au] Autor:Stellmann JP; Krumbholz M; Friede T; Gahlen A; Borisow N; Fischer K; Hellwig K; Pache F; Ruprecht K; Havla J; Kümpfel T; Aktas O; Hartung HP; Ringelstein M; Geis C; Kleinschnitz C; Berthele A; Hemmer B; Angstwurm K; Young KL; Schuster S; Stangel M; Lauda F; Tumani H; Mayer C; Zeltner L; Ziemann U; Linker RA; Schwab M; Marziniak M; Then Bergh F; Hofstadt-van Oy U; Neuhaus O; Zettl U; Faiss J; Wildemann B; Paul F; Jarius S; Trebst C; Kleiter I; NEMOS (Neuromyelitis Optica Study Group)
[Ad] Endereço:Institut für Neuroimmunologie und Multiple Sklerose (INIMS), Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.
[Ti] Título:Immunotherapies in neuromyelitis optica spectrum disorder: efficacy and predictors of response.
[So] Source:J Neurol Neurosurg Psychiatry;88(8):639-647, 2017 Aug.
[Is] ISSN:1468-330X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To analyse predictors for relapses and number of attacks under different immunotherapies in patients with neuromyelitis optica spectrum disorder (NMOSD). DESIGN: This is a retrospective cohort study conducted in neurology departments at 21 regional and university hospitals in Germany. Eligible participants were patients with aquaporin-4-antibody-positive or aquaporin-4-antibody-negative NMOSD. Main outcome measures were HRs from Cox proportional hazard regression models adjusted for centre effects, important prognostic factors and repeated treatment episodes. RESULTS: 265 treatment episodes with a mean duration of 442 days (total of 321 treatment years) in 144 patients (mean age at first attack: 40.9 years, 82.6% female, 86.1% aquaporin-4-antibody-positive) were analysed. 191 attacks occurred during any of the treatments (annual relapse rate=0.60). The most common treatments were rituximab (n=77, 111 patient-years), azathioprine (n=52, 68 patient-years), interferon-ß (n=32, 61 patient-years), mitoxantrone (n=34, 32.1 patient-years) and glatiramer acetate (n=17, 10 patient-years). Azathioprine (HR=0.4, 95% CI 0.3 to 0.7, p=0.001) and rituximab (HR=0.6, 95% CI 0.4 to 1.0, p=0.034) reduced the attack risk compared with interferon-ß, whereas mitoxantrone and glatiramer acetate did not. Patients who were aquaporin-4-antibody-positive had a higher risk of attacks (HR=2.5, 95% CI 1.3 to 5.1, p=0.009). Every decade of age was associated with a lower risk for attacks (HR=0.8, 95% CI 0.7 to 1.0, p=0.039). A previous attack under the same treatment tended to be predictive for further attacks (HR=1.5, 95% CI 1.0 to 2.4, p=0.065). CONCLUSIONS: Age, antibody status and possibly previous attacks predict further attacks in patients treated for NMOSD. Azathioprine and rituximab are superior to interferon-ß.
[Mh] Termos MeSH primário: Imunoterapia/métodos
Neuromielite Óptica/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Aquaporina 4/imunologia
Autoanticorpos/sangue
Azatioprina/uso terapêutico
Estudos de Coortes
Feminino
Seguimentos
Alemanha
Acetato de Glatiramer/uso terapêutico
Seres Humanos
Interferon beta/uso terapêutico
Assistência de Longa Duração
Masculino
Meia-Idade
Mitoxantrona/uso terapêutico
Neuromielite Óptica/imunologia
Prognóstico
Recidiva
Sistema de Registros
Estudos Retrospectivos
Rituximab/uso terapêutico
Resultado do Tratamento
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (AQP4 protein, human); 0 (Aquaporin 4); 0 (Autoantibodies); 4F4X42SYQ6 (Rituximab); 5M691HL4BO (Glatiramer Acetate); 77238-31-4 (Interferon-beta); BZ114NVM5P (Mitoxantrone); MRK240IY2L (Azathioprine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1136/jnnp-2017-315603


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[PMID]:28556917
[Au] Autor:Alexander TB; Wang L; Inaba H; Triplett BM; Pounds S; Ribeiro RC; Pui CH; Rubnitz JE
[Ad] Endereço:Department of Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee.
[Ti] Título:Decreased relapsed rate and treatment-related mortality contribute to improved outcomes for pediatric acute myeloid leukemia in successive clinical trials.
[So] Source:Cancer;123(19):3791-3798, 2017 Oct 01.
[Is] ISSN:1097-0142
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Outcomes for children with acute myeloid leukemia (AML) have improved over the past 20 years even though the medications used for induction therapy have not changed. METHODS: This study analyzed data from patients with AML who were enrolled in successive protocols (AML97 and AML02) to determine the contributors to the improved outcomes of the latter clinical trial. RESULTS: There were significant improvements in 5-year overall survival (48.9% vs 71.2%; P < .0001) and event-free survival (43.5% vs 61.8%; P = .002) from AML97 to AML02. The 5-year cumulative incidence of early death (ED)/treatment-related mortality (TRM) was reduced for patients treated in AML02 (18.5% vs 7.9%; P = .007). Although the overall incidence of refractory disease (6.5% vs 5.6%; P = .736) and relapse (29.3% vs 21.0%; P = .12) did not differ between the 2 studies, patients with low-risk AML who were treated in AML02 had a reduced incidence of relapse (27.3% vs 8.8%; P = .036). CONCLUSIONS: The improved outcomes of the AML02 trial resulted from improved disease control for low-risk patients and overall decreased ED/TRM. These results emphasize the importance of supportive-care measures throughout chemotherapy courses and hematopoietic cell transplantation and the value of treatment intensity for patients with low-risk AML while underscoring the need for novel therapy, rather than increased therapy intensity, for children with high-risk AML. Cancer 2017;123:3791-3798. © 2017 American Cancer Society.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Quimioterapia de Indução/métodos
Leucemia Mieloide Aguda/tratamento farmacológico
Leucemia Mieloide Aguda/mortalidade
[Mh] Termos MeSH secundário: Adolescente
Aminoglicosídeos/administração & dosagem
Anticorpos Monoclonais Humanizados/administração & dosagem
Asparaginase/administração & dosagem
Criança
Pré-Escolar
Cladribina/administração & dosagem
Protocolos Clínicos
Quimioterapia de Consolidação/métodos
Citarabina/administração & dosagem
Daunorrubicina/administração & dosagem
Intervalo Livre de Doença
Etoposídeo/administração & dosagem
Feminino
Transplante de Células-Tronco Hematopoéticas
Seres Humanos
Lactente
Recém-Nascido
Masculino
Mitoxantrona/administração & dosagem
Neoplasia Residual
Recidiva
Estudos Retrospectivos
Análise de Sobrevida
Fatores de Tempo
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Aminoglycosides); 0 (Antibodies, Monoclonal, Humanized); 0 (Antineoplastic Agents); 04079A1RDZ (Cytarabine); 47M74X9YT5 (Cladribine); 6PLQ3CP4P3 (Etoposide); 93NS566KF7 (gemtuzumab); BZ114NVM5P (Mitoxantrone); EC 3.5.1.1 (Asparaginase); ZS7284E0ZP (Daunorubicin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170531
[St] Status:MEDLINE
[do] DOI:10.1002/cncr.30791


  7 / 4038 MEDLINE  
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[PMID]:28346686
[Au] Autor:Sugihara N; Kuroda N; Watanabe F; Choshi T; Kamishikiryo J; Seo M
[Ad] Endereço:Faculty of Pharmacy and Pharmaceutical Sciences, Fukuyama Univ., Sanzou 1,Gakuen-cho, Fukuyama, Hiroshima, Japan.
[Ti] Título:Effects of Catechins and Their Related Compounds on Cellular Accumulation and Efflux Transport of Mitoxantrone in Caco-2 Cell Monolayers.
[So] Source:J Food Sci;82(5):1224-1230, 2017 May.
[Is] ISSN:1750-3841
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The ability of catechins and their related compounds to inhibit breast cancer resistance protein (BCRP) function in Caco-2 cell monolayers was investigated with mitoxantrone as a BCRP substrate. The gallate or pyrogallol moiety on the catechin structure seemed to promote increased cellular accumulation and inhibit efflux transport of mitoxantrone. The ability of gallate catechins such as (-)-epigallocatechin gallate (EGCG) and (-)-epicatechin gallate (ECG) to increase cellular accumulation and inhibit efflux transport of mitoxantrone was greater than that of nongallate catechins. Gallic acid octyl ester (GAO) also increased intracellular mitoxantrone accumulation. Experiments using GAO derivatives indicated that the gallate moiety required the presence of a long carbon chain for BCRP inhibition. Cellular accumulation and reduced efflux transport of mitoxantrone were greater with epigallocatechin 3-(3″-O-butyl) gallate than with EGCG. EGCG inhibition of BCRP seemed to be restricted by hydrophobicity. The co-administration of catechins, particularly EGCG and related compounds, with greater hydrophobicity may increase the therapeutic activities of BCRP substrates such as mitoxantrone.
[Mh] Termos MeSH primário: Analgésicos/metabolismo
Catequina/análogos & derivados
Catequina/farmacologia
Mitoxantrona/metabolismo
[Mh] Termos MeSH secundário: Transporte Biológico/efeitos dos fármacos
Células CACO-2
Seres Humanos
Chá/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (Tea); 8R1V1STN48 (Catechin); BZ114NVM5P (Mitoxantrone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE
[do] DOI:10.1111/1750-3841.13680


  8 / 4038 MEDLINE  
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[PMID]:28340281
[Au] Autor:Nastoupil LJ; McLaughlin P; Feng L; Neelapu SS; Samaniego F; Hagemeister FB; Ayala A; Romaguera JE; Goy AH; Neal E; Wang M; Fayad L; Fanale MA; Oki Y; Westin JR; Rodriguez MA; Cabanillas F; Fowler NH
[Ad] Endereço:Department of Lymphoma and Myeloma, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.
[Ti] Título:High ten-year remission rates following rituximab, fludarabine, mitoxantrone and dexamethasone (R-FND) with interferon maintenance in indolent lymphoma: Results of a randomized Study.
[So] Source:Br J Haematol;177(2):263-270, 2017 Apr.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We report a single-centre, randomized study evaluating the efficacy and safety of concurrent fludarabine, mitoxantrone, dexamethasone (FND) and rituximab versus sequential FND followed by rituximab in 158 patients with advanced stage, previously untreated indolent lymphoma, enrolled between 1997 and 2002. Patients were randomized to 6-8 cycles of FND followed by 6 monthly doses of rituximab or 6 doses of rituximab given concurrently with FND. All patients who achieved at least a partial response received 12 months of interferon (IFN) maintenance. Median ages were 54 and 55 years. The two groups were comparable with the exception of a higher percentage of females (65% vs. 43%) and baseline anaemia (23% vs. 11%) in the FND followed by rituximab group. Complete response/unconfirmed complete response rates were 89% and 93%. The most frequent grade ≥ 3 toxicity was neutropenia (86% vs. 96%). Neutropenic fever occurred in 21% and 16%. Late toxicity included myelodysplastic syndrome (n = 3) and acute myeloid leukaemia (n = 5). With 12·5 years of follow-up, no significant differences based on treatment schedule were observed. 10-year overall survival estimates were 76% and 73%. 10-year progression-free survival estimates were 52% and 51%. FND with concurrent or sequential rituximab, and IFN maintenance in indolent lymphoma demonstrated high response rates and robust survival.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Interferons/uso terapêutico
Linfoma não Hodgkin/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Dexametasona/administração & dosagem
Feminino
Seres Humanos
Linfoma não Hodgkin/patologia
Quimioterapia de Manutenção
Masculino
Meia-Idade
Mitoxantrona/administração & dosagem
Indução de Remissão
Rituximab/administração & dosagem
Vidarabina/administração & dosagem
Vidarabina/análogos & derivados
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
4F4X42SYQ6 (Rituximab); 7S5I7G3JQL (Dexamethasone); 9008-11-1 (Interferons); BZ114NVM5P (Mitoxantrone); FA2DM6879K (Vidarabine); P2K93U8740 (fludarabine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170614
[Lr] Data última revisão:
170614
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14541


  9 / 4038 MEDLINE  
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[PMID]:28334948
[Au] Autor:Ikeda M; Okusaka T; Sato Y; Furuse J; Mitsunaga S; Ueno H; Morizane C; Inaba Y; Kobayashi T; Arai Y
[Ad] Endereço:Department of Hepatobiliary & Pancreatic Oncology, National Cancer Center Hospital East.
[Ti] Título:A Phase I/II trial of continuous hepatic intra-arterial infusion of 5-fluorouracil, mitoxantrone and cisplatin for advanced hepatocellular carcinoma.
[So] Source:Jpn J Clin Oncol;47(6):512-519, 2017 Jun 01.
[Is] ISSN:1465-3621
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background: The aim of this study was to investigate the dose-limiting toxicities (DLTs) and determine the recommended doses in the Phase I part of the study, and to evaluate the efficacy and toxicity in the Phase II part, of continuous hepatic intra-arterial infusion therapy with 5-fluorouracil, mitoxantrone and cisplatin (FMP therapy) in patients with advanced hepatocellular carcinoma (HCC). Methods: Forty-five patients with advanced HCC were enrolled. The therapy consisted of continuous intra-arterial infusion of 5-fluorouracil from Day 1 through Day 5, and intra-arterial administration of mitoxantrone and cisplatin on Day 1 [5-fluorouracil/mitoxantrone/cisplatin (mg/m2): Level 1; 400/4/60, Level 2; 400/6/60, Level 3; 500/6/60]. Results: In the Phase I part of the study, one of the six patients at Level 1 developed DLTs, including Grade 3 pulmonary embolism, while none of the patients at either Level 2 or Level 3 exhibited any DLTs. In the Phase II part, at Level 3, 36 patients were enrolled. Nine patients (25%) showed partial response, representing a response rate of 25% (95% confidence interval: 12-42%). The overall median survival time, 1-year survival rate and median progression-free survival time were 11.3 months, 46.9% and 7.0 months, respectively. The main Grade 3 or 4 hematological and non-hematological toxicities were leukopenia (36%), neutropenia (39%), thrombocytopenia (19%), and elevated serum aspartate aminotransferase (22%), elevated serum alanine aminotransferase (14%) and occlusion of hepatic artery (22%), respectively. Conclusion: Hepatic intra-arterial infusion therapy of FMP could not demonstrate a favorable tumor response and overall survival in patients with advanced HCC.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Carcinoma Hepatocelular/tratamento farmacológico
Cisplatino/administração & dosagem
Fluoruracila/administração & dosagem
Neoplasias Hepáticas/tratamento farmacológico
Mitoxantrona/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Idoso
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Cateteres
Cisplatino/uso terapêutico
Intervalo Livre de Doença
Relação Dose-Resposta a Droga
Feminino
Fluoruracila/uso terapêutico
Seres Humanos
Infusões Intra-Arteriais
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Mitoxantrona/uso terapêutico
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
BZ114NVM5P (Mitoxantrone); Q20Q21Q62J (Cisplatin); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1093/jjco/hyx038


  10 / 4038 MEDLINE  
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[PMID]:28323029
[Au] Autor:Hussein N; Amawi H; Karthikeyan C; Hall FS; Mittal R; Trivedi P; Ashby CR; Tiwari AK
[Ad] Endereço:Department of Pharmacology and Experimental Therapeutics, College of Pharmacy and Pharmaceutical Sciences, University of Toledo, OH 43614, USA.
[Ti] Título:The dopamine D receptor antagonists PG01037, NGB2904, SB277011A, and U99194 reverse ABCG2 transporter-mediated drug resistance in cancer cell lines.
[So] Source:Cancer Lett;396:167-180, 2017 Jun 28.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The ATP - binding cassette (ABC) family G2 (ABCG2) transporters are known to produce multidrug resistance (MDR) in cancer, thereby limiting the clinical response to chemotherapy. Molecular modeling data indicated that certain dopamine (DA) D receptor antagonists had a significant binding affinity for ABCG2 transporter. Therefore, in this in vitro study, we determined the effect of the D receptor antagonists PG01037, NGB2904, SB277011A, and U99194 on MDR resulting from the overexpression of ABCG2 transporters. The D receptor antagonists, at concentrations >100 µM, did not significantly affect the viability of H460-MX20, S1M1-80, A549-MX10 or wild type ABCG2 overexpressing (HEK293-R2) cells. However, at concentrations ranging from 0.01 to 10 µM, the D receptor antagonists PG01037, NGB2904, SB-277011A, and U99194 significantly increased the efficacy of the anticancer drugs mitoxantrone and doxorubicin in ABCG2-overexpressing MDR cells. Efflux studies indicated that both PG01037 and NGB2904, at a concentration of 5 µM, significantly decreased the efflux of rhodamine 123 from H460-MX20 cells. Interestingly, 5 µM of PG01037 or NGB2904 significantly decreased the expression levels of the ABCG2 protein, suggesting that these compounds inhibit both the function and expression of ABCG2 transporters at non-toxic concentrations.
[Mh] Termos MeSH primário: Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/antagonistas & inibidores
Proteínas de Neoplasias/antagonistas & inibidores
Receptores de Dopamina D3/antagonistas & inibidores
[Mh] Termos MeSH secundário: Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/biossíntese
Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/metabolismo
Benzamidas/farmacologia
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Linhagem Celular Tumoral
Neoplasias do Colo/tratamento farmacológico
Neoplasias do Colo/metabolismo
Regulação para Baixo/efeitos dos fármacos
Doxorrubicina/farmacologia
Resistência a Múltiplos Medicamentos
Resistência a Medicamentos Antineoplásicos
Sinergismo Farmacológico
Fluorenos/farmacologia
Células HEK293
Seres Humanos
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/metabolismo
Mitoxantrona/farmacologia
Proteínas de Neoplasias/biossíntese
Proteínas de Neoplasias/metabolismo
Nitrilos/farmacologia
Piperazinas/farmacologia
Piridinas/farmacologia
Tetra-Hidroisoquinolinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCG2 protein, human); 0 (ATP Binding Cassette Transporter, Sub-Family G, Member 2); 0 (Benzamides); 0 (Fluorenes); 0 (N-(4-(4-(2,3-dichlorophenyl)piperazin-1-yl)but-2-enyl)-4-pyridine-2-ylbenzamide); 0 (NGB 2904); 0 (Neoplasm Proteins); 0 (Nitriles); 0 (Piperazines); 0 (Pyridines); 0 (Receptors, Dopamine D3); 0 (SB 277011); 0 (Tetrahydroisoquinolines); 80168379AG (Doxorubicin); BZ114NVM5P (Mitoxantrone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE



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