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[PMID]:29482389
[Au] Autor:Elzahabi HSA; Nossier ES; Khalifa NM; Alasfoury RA; El-Manawaty MA
[Ad] Endereço:a Department of Pharmaceutical Chemistry , Faculty of Pharmacy (Girls), Al-Azhar University , Cairo , Egypt.
[Ti] Título:Anticancer evaluation and molecular modeling of multi-targeted kinase inhibitors based pyrido[2,3-d]pyrimidine scaffold.
[So] Source:J Enzyme Inhib Med Chem;33(1):546-557, 2018 Dec.
[Is] ISSN:1475-6374
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:An efficient synthesis of substituted pyrido[2,3-d]pyrimidines was carried out and evaluated for in vitro anticancer activity against five cancer cell lines, namely hepatic cancer (HepG-2), prostate cancer (PC-3), colon cancer (HCT-116), breast cancer (MCF-7), and lung cancer (A-549) cell lines. Regarding HepG-2, PC-3, HCT-116 cancer cell lines, 7-(4-chlorophenyl)-2-(3-methyl-5-oxo-2,3-dihydro-1H-pyrazol-1-yl)-5-(p-tolyl)- pyrido[2,3-d]pyrimidin-4(3H)-one (5a) exhibited strong, more potent anticancer (IC : 0.3, 6.6 and 7 µM) relative to the standard doxorubicin (IC : 0.6, 6.8 and 12.8 µM), respectively. Kinase inhibitory assessment of 5a showed promising inhibitory activity against three kinases namely PDGFR ß, EGFR, and CDK4/cyclin D1 at two concentrations 50 and 100 µM in single measurements. Further, a molecular docking study for compound 5a was performed to verify the binding mode towards the EGFR and CDK4/cyclin D1 kinases.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Quinase 4 Dependente de Ciclina/antagonistas & inibidores
Inibidores de Proteínas Quinases/farmacologia
Piridinas/farmacologia
Pirimidinas/farmacologia
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
Receptor beta de Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Quinase 4 Dependente de Ciclina/metabolismo
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Modelos Moleculares
Estrutura Molecular
Inibidores de Proteínas Quinases/síntese química
Inibidores de Proteínas Quinases/química
Piridinas/síntese química
Piridinas/química
Pirimidinas/síntese química
Pirimidinas/química
Receptor do Fator de Crescimento Epidérmico/metabolismo
Receptor beta de Fator de Crescimento Derivado de Plaquetas/metabolismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Protein Kinase Inhibitors); 0 (Pyridines); 0 (Pyrimidines); 0 (pyrido(3,2-d)pyrimidine); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta); EC 2.7.11.22 (CDK4 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 4)
[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:180228
[St] Status:MEDLINE
[do] DOI:10.1080/14756366.2018.1437729


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[PMID]:29455234
[Au] Autor:Wang S; Wang X; Liu M; Bai O
[Ad] Endereço:Department of Hematology, The First Hospital of Jilin University, No. 71 Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, People's Republic of China.
[Ti] Título:Blastic plasmacytoid dendritic cell neoplasm: update on therapy especially novel agents.
[So] Source:Ann Hematol;97(4):563-572, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive hematopoietic malignancy mainly affecting elderly patients. Most patients present with asymptomatic skin lesions as the first symptom and has a high frequency of bone marrow involvement. BPDCN is typically characterized by CD4+ and CD 56+ co-expression without common lymphoid or myeloid lineage markers. There is no consensus on the optimal therapeutic strategy for BPDCN. It is highly responsive to chemotherapy but the median event-free survival is very short. Allogeneic stem cell transplantation may improve the prognosis of BPDCN but the rate of relapse is still high. There are no specific targeted agents approved for patients with BPDCN, but advances in the understanding of the pathobiology of BPDCN and the results of early clinical studies have revealed novel targets and potentially effective agents. Novel targeted therapies may improve outcomes for patients with BPDCN in the future.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Células Dendríticas/efeitos dos fármacos
Drogas em Investigação/uso terapêutico
Neoplasias Hematológicas/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Linhagem Celular Tumoral
Neoplasias do Sistema Nervoso Central/diagnóstico
Neoplasias do Sistema Nervoso Central/prevenção & controle
Neoplasias do Sistema Nervoso Central/secundário
Células Dendríticas/patologia
Drogas em Investigação/farmacologia
Neoplasias Hematológicas/diagnóstico
Neoplasias Hematológicas/patologia
Neoplasias Hematológicas/cirurgia
Transplante de Células-Tronco Hematopoéticas/efeitos adversos
Seres Humanos
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Drugs, Investigational)
[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:180219
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-018-3259-z


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[PMID]:29409738
[Au] Autor:Li XP; Lan JY; Liu DQ; Zhou H; Qian MM; Wang WW; Yang M
[Ad] Endereço:Department of Laboratory Medicine, The Hospital Of Hangzhou Dianzi University, Hangzhou, Zhejiang, China.
[Ti] Título:OCA2 rs4778137 polymorphism predicts survival of breast cancer patients receiving neoadjuvant chemotherapy.
[So] Source:Gene;651:161-165, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Genome-wide association study (GWAS) studies have showed that single nucleotide polymorphisms (SNPs) in OCA2 gene were associated with the survival of breast cancer patients treated with adjuvant chemotherapy. To further explain the association between OCA2 SNPs and breast cancer survival, we investigated the predictive value of rs4778137 located in OCA2 in local advanced breast cancer patients receiving neoadjuvant chemotherapy. PATIENTS AND METHODS: A case-cohort with 150 breast cancer patients was performed to evaluate the effects of the OCA2 rs4778137 on breast cancer survival. The association between rs4778137 genotypes and pathological complete response (pCR, defined that the postoperative pathology indicating no residual invasive breast cancer in the breast or the axillary lymph node) were analyzed. Logistic regression analysis was performed to identify the independent predictors of pCR. Survival was assessed by Kaplan-Meier method and Cox regression analysis according to the rs4778137 genotypes. RESULTS: The differences between pCR and the rs4778137 genotypes were statistically significant (p < 0.05). The patients with genotype GG harbored a better disease-free survival (HR: 2.358, p = 0.000) and overall survival (HR: 1.578, p = 0.008) than the patients with genotype CC in rs4778137. The further Univariate and Multivariate survival analysis revealed that SNP rs4778137 was an independent predictive factor of disease-free survival (p = 0.000/p = 0.001) and overall survival (p = 0.006/p = 0.045). CONCLUSION: The OCA2 rs4778137 may be a predictor for the clinical response and survival in local advanced breast cancer patients who received neoadjuvant chemotherapy.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Neoplasias da Mama/genética
Neoplasias da Mama/terapia
Proteínas de Membrana Transportadoras/genética
Terapia Neoadjuvante
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Adulto
Neoplasias da Mama/mortalidade
Quimioterapia Adjuvante
Estudos de Coortes
Terapia Combinada
Epirubicina/uso terapêutico
Feminino
Seguimentos
Seres Humanos
Meia-Idade
Prognóstico
Análise de Sobrevida
Taxoides/uso terapêutico
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Membrane Transport Proteins); 0 (OCA2 protein, human); 0 (Taxoids); 3Z8479ZZ5X (Epirubicin)
[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:180208
[St] Status:MEDLINE


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Registro de Ensaios Clínicos
Registro de Ensaios Clínicos
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[PMID]:29396713
[Au] Autor:Kiladjian JJ; Guglielmelli P; Griesshammer M; Saydam G; Masszi T; Durrant S; Passamonti F; Jones M; Zhen H; Li J; Gadbaw B; Perez Ronco J; Khan M; Verstovsek S
[Ad] Endereço:Centre d'Investigations Cliniques (CIC1427), Hôpital Saint-Louis, AP-HP, INSERM, CLIP2 "Saint-Louis - Paris Nord," Early Phase Research Center, Université Paris Diderot, 1, Avenue Claude Vellefaux, 75010, Paris, France. jean-jacques.kiladjian@aphp.fr.
[Ti] Título:Efficacy and safety of ruxolitinib after and versus interferon use in the RESPONSE studies.
[So] Source:Ann Hematol;97(4):617-627, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Ruxolitinib was well tolerated and superior to best available therapy (including interferon [IFN]) in controlling hematocrit without phlebotomy eligibility, normalizing blood counts, and improving polycythemia vera-related symptoms in the Study of Efficacy and Safety in Polycythemia Vera Subjects Who Are Resistant to or Intolerant of Hydroxyurea: JAK Inhibitor INC424 (INCB018424) Tablets Versus Best Available Care (RESPONSE) studies. This ad hoc analysis focuses on ruxolitinib in relation to IFN in the RESPONSE studies, with attention on the following: (1) safety and efficacy of ruxolitinib and best available therapy in patients who received IFN before study randomization, (2) safety and efficacy of IFN during randomized treatment in best available therapy arm, and (3) use of ruxolitinib after crossover from best available therapy in IFN-treated patients. IFN exposure before randomization had little effect on the efficacy or safety of ruxolitinib. In the randomized treatment arms, ruxolitinib was superior to IFN in efficacy [hematocrit control (RESPONSE = 60% of ruxolitinib vs 23% of IFN patients; RESPONSE-2 = 62% of ruxolitinib vs 15% of IFN patients)] and was tolerated better in hydroxyurea-resistant or hydroxyurea-intolerant patients. After crossing over to receive ruxolitinib, patients who had initially received IFN and did not respond had improved hematologic and spleen responses (62% of patients at any time after crossover) and an overall reduction in phlebotomy procedures. Rates and incidences of the most common adverse events decreased after crossover to ruxolitinib, except for infections (primarily grade 1 or 2). These data suggest that ruxolitinib is efficacious and well tolerated in patients who were previously treated with IFN. The RESPONSE (NCT01243944) and RESPONSE-2 (NCT02038036) studies were registered at clinicaltrials.gov .
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Interferons/uso terapêutico
Janus Quinases/antagonistas & inibidores
Policitemia Vera/tratamento farmacológico
Inibidores de Proteínas Quinases/uso terapêutico
Pirazóis/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Antineoplásicos/efeitos adversos
Sangria/efeitos adversos
Terapia Combinada/efeitos adversos
Estudos Cross-Over
Monitoramento de Medicamentos
Resistência a Múltiplos Medicamentos
Resistência a Medicamentos Antineoplásicos
Feminino
Seres Humanos
Hidroxiureia/efeitos adversos
Hidroxiureia/uso terapêutico
Interferons/efeitos adversos
Janus Quinases/metabolismo
Masculino
Meia-Idade
Policitemia Vera/metabolismo
Policitemia Vera/fisiopatologia
Policitemia Vera/terapia
Padrões de Prática Médica
Inibidores de Proteínas Quinases/efeitos adversos
Pirazóis/efeitos adversos
Reprodutibilidade dos Testes
Esplenomegalia/etiologia
Esplenomegalia/prevenção & controle
[Pt] Tipo de publicação:CLINICAL TRIAL; CLINICAL TRIAL, PHASE III; COMPARATIVE STUDY; EQUIVALENCE TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (INCB018424); 0 (Protein Kinase Inhibitors); 0 (Pyrazoles); 9008-11-1 (Interferons); EC 2.7.10.2 (Janus Kinases); X6Q56QN5QC (Hydroxyurea)
[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:180204
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3225-1


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[PMID]:29351887
[Au] Autor:Jin R; Chen Q; Yao S; Bai E; Fu W; Wang L; Wang J; Du X; Wei T; Xu H; Jiang C; Qiu P; Wu J; Li W; Liang G
[Ad] Endereço:Department of Digestive Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China; Chemical Biology Research Center, College of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.
[Ti] Título:Synthesis and anti-tumor activity of EF24 analogues as IKKß inhibitors.
[So] Source:Eur J Med Chem;144:218-228, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:EF24 is an IKKß inhibitor (IC : 72 µM) containing various anti-tumor activities. In this study, a series of EF24 analogs targeting IKKß were designed and synthesized. Several IKKß inhibitors with better activities than EF24 were screened out and B3 showed best IKKß inhibitory (IC : 6.6 µM). Molecular docking and dynamic simulation experiments further confirmed this inhibitory effect. B3 obviously suppressed the viability of Hela229, A549, SGC-7901 and MGC-803 cells. Then, in SGC-7901 and MGC-803 cells, B3 blocked the NF-κB signal pathway by inhibiting IKKß phosphorylation, and followed arrested the cell cycle at G2/M phase by suppressing the Cyclin B1 and Cdc2 p34 expression, induced the cell apoptosis by down-regulating Bcl-2 protein and up-regulating cleaved-caspase3. Moreover, B3 significantly reduced tumor growth and suppressed the IKKß-NF-κB signal pathway in SGC-7901 xenograft model. In total, this study present a potential IKKß inhibitor as anti-tumor precursor.
[Mh] Termos MeSH primário: Antineoplásicos/química
Antineoplásicos/farmacologia
Compostos de Benzilideno/química
Compostos de Benzilideno/farmacologia
Quinase I-kappa B/antagonistas & inibidores
Piperidonas/química
Piperidonas/farmacologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/síntese química
Antineoplásicos/uso terapêutico
Apoptose/efeitos dos fármacos
Compostos de Benzilideno/síntese química
Compostos de Benzilideno/uso terapêutico
Linhagem Celular Tumoral
Pontos de Checagem da Fase G2 do Ciclo Celular/efeitos dos fármacos
Seres Humanos
Quinase I-kappa B/metabolismo
Camundongos Nus
Simulação de Acoplamento Molecular
NF-kappa B/metabolismo
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Neoplasias/patologia
Fosforilação/efeitos dos fármacos
Piperidonas/síntese química
Piperidonas/uso terapêutico
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3,5-bis(2-fluorobenzylidene)piperidin-4-one); 0 (Antineoplastic Agents); 0 (Benzylidene Compounds); 0 (NF-kappa B); 0 (Piperidones); EC 2.7.11.10 (I-kappa B Kinase)
[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:180121
[St] Status:MEDLINE


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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]:29322203
[Au] Autor:Dada R
[Ad] Endereço:Department of Oncology MBC J-64, King Faisal Specialist Hospital and Research Center, P.O. Box 40047, Jeddah, 21499, Kingdom of Saudi Arabia. rdada@kfshrc.edu.sa.
[Ti] Título:Program death inhibitors in classical Hodgkin's lymphoma: a comprehensive review.
[So] Source:Ann Hematol;97(4):555-561, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Cancer cells are able to induce immune system tolerance through different mechanisms. Recent achievements in the understanding of tumor microenvironment, invasion, and metastasizing have contributed to accelerated drug developments and approvals. Hodgkin lymphoma (HL) cells are the minority in a lymphocyte-rich microenvironment of HL tissue. The program death-1 (PD-1)/PD-ligand-1 checkpoint is one of the known effective pathways in classical HL to escape the immune system cells. The approval of PD-1 inhibitors in different cancer types with exciting response rates is truly revolutionizing our treatment armamentarium against cancer in general and classical HL in specific. Although the disease is one of the most curable tumors, we still need better outcome with more gentle treatment, especially for relapsed and refractory (r/r) patients. In this article, we review the current literature on immune checkpoint inhibitors and currently ongoing studies with nivolumab and pembrolizumab in r/r classical HL.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Antígeno B7-H1/antagonistas & inibidores
Doença de Hodgkin/tratamento farmacológico
Proteínas de Neoplasias/antagonistas & inibidores
Receptor de Morte Celular Programada 1/antagonistas & inibidores
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/efeitos adversos
Anticorpos Monoclonais/uso terapêutico
Anticorpos Monoclonais Humanizados/efeitos adversos
Anticorpos Monoclonais Humanizados/uso terapêutico
Antineoplásicos/efeitos adversos
Antineoplásicos Imunológicos/efeitos adversos
Antineoplásicos Imunológicos/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Antígeno B7-H1/metabolismo
Aprovação de Drogas
Resistência a Múltiplos Medicamentos
Resistência a Medicamentos Antineoplásicos
Doença de Hodgkin/metabolismo
Seres Humanos
Terapia de Alvo Molecular/efeitos adversos
Proteínas de Neoplasias/metabolismo
Receptor de Morte Celular Programada 1/metabolismo
Qualidade de Vida
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antibodies, Monoclonal, Humanized); 0 (Antineoplastic Agents); 0 (Antineoplastic Agents, Immunological); 0 (B7-H1 Antigen); 0 (CD274 protein, human); 0 (Neoplasm Proteins); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); 31YO63LBSN (nivolumab); DPT0O3T46P (pembrolizumab)
[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:180112
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3226-0


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[PMID]:29305630
[Au] Autor:Ben Lakhal R; Ghedira H; Bellaaj H; Ben Youssef Y; Menif S; Manai Z; Bedoui M; Lakhal A; M'Sadek F; Elloumi M; Khélif A; Ben Romdhane N; Laatiri MA; Ben Othmen T; Meddeb B
[Ad] Endereço:Hematology Department, Aziza Othmana University Hospital, Tunis, Tunisia. raihane.benlakhal@gmail.com.
[Ti] Título:Chronic myeloid leukemia patients in Tunisia: epidemiology and outcome in the imatinib era (a multicentric experience).
[So] Source:Ann Hematol;97(4):597-604, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Data are limited in developing countries regarding the clinicopathologic features and response to therapy of chronic myeloid leukemia (CML) in the era of imatinib (IM). The objective of this study is to report on the clinicoepidemiologic features of CML in Tunisia, to evaluate the long-term outcome of patients in chronic (CP) or accelerated phase (AP) treated with IM 400 mg daily as frontline therapy, and to determine imatinib's efficacy and safety. From October 2002 to December 2014, 410 CML patients were treated with IM in six Tunisian departments of hematology. Response (hematologic, cytogenetic, and molecular responses) and outcome-overall survival (OS), event-free survival (EFS), and progression-free survival (PFS)-were evaluated. The following prognostic factors were analyzed for their impact on the European leukemia net (ELN) response, OS, EFS, and PFS at 5 years: age, sex, leukocyte count, Sokal score, European Treatment and Outcome Study (EUTOS) score, CML phase, time to starting IM, and impact of adverse events. The median age was 45 years (3-85 years). Two hundred ten (51.2%) patients were male. Splenomegaly was present in 322 of the 410 (79%). Additional cytogenetic abnormalities were encountered in 25 (6.3%) patients. At diagnosis, 379 (92.4%) patients were in CP, 31 (7.6%) were in AP. The Sokal risk was low in 87 (22.5%), intermediate in 138 (35.7%), and high in 164 patients (41.9%). The EUTOS risk was low in 217 (74%), and high in 77 (26%) patients. The rates of cumulative complete cytogenetic response (CCyR), major molecular response (MMR), and molecular response 4/5 log (MR4.5) in CP/AP-CML patients were 72, 68.4, and 46.4%, respectively. The median time to reach CCyR, MMR, and MR4.5 was 6 months (3-51), 18 months (3-72), and 24 months (3-100), respectively. According to the ELN criteria, optimal, suboptimal response, and failure were noted in 206 (51.8%), 61 (15.3%), and 125 (31.4%) patients, respectively. Five-year event-free survival (EFS), progression-free survival (PFS), and overall survival (OS) were 81, 90, and 90%, respectively. By multivariate analysis, AP, high EUTOS risk, and baseline WBC ≥ 150G/l remained independent predictive factors of non-optimal response to IM. The adverse events (AE) of IM were moderate and tolerable. With the caveats that the monitoring of the disease was not optimal, response rates were similar to those reported in previous studies. It is clear to us that improvements should be made in treatment of AP-CML and high Sokal risk group of CP-CML. The frontline use of second-generation tyrosine kinase inhibitor (TKI) is expected to improve the results of the first-line treatment of these high-risk Tunisian patients, but cost and accessibility of this therapy remain the problems in developing countries.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Mesilato de Imatinib/uso terapêutico
Leucemia Mieloide de Fase Acelerada/tratamento farmacológico
Leucemia Mieloide de Fase Crônica/tratamento farmacológico
Inibidores de Proteínas Quinases/uso terapêutico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Antineoplásicos/efeitos adversos
Criança
Pré-Escolar
Feminino
Seguimentos
Seres Humanos
Mesilato de Imatinib/efeitos adversos
Leucemia Mieloide de Fase Acelerada/diagnóstico
Leucemia Mieloide de Fase Acelerada/epidemiologia
Leucemia Mieloide de Fase Acelerada/patologia
Leucemia Mieloide de Fase Crônica/diagnóstico
Leucemia Mieloide de Fase Crônica/epidemiologia
Leucemia Mieloide de Fase Crônica/patologia
Masculino
Meia-Idade
Padrões de Prática Médica
Prognóstico
Inibidores de Proteínas Quinases/efeitos adversos
Estudos Retrospectivos
Esplenomegalia/etiologia
Esplenomegalia/patologia
Esplenomegalia/prevenção & controle
Análise de Sobrevida
Carga Tumoral/efeitos dos fármacos
Tunísia/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Protein Kinase Inhibitors); 8A1O1M485B (Imatinib Mesylate)
[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:180107
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3224-2


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[PMID]:29274491
[Au] Autor:Srivastava P; Singh K; Verma M; Sivakumar S; Patra AK
[Ad] Endereço:Department of Chemistry, Indian Institute of Technology Kanpur, Kanpur 208016, Uttar Pradesh, India.
[Ti] Título:Photoactive platinum(II) complexes of nonsteroidal anti-inflammatory drug naproxen: Interaction with biological targets, antioxidant activity and cytotoxicity.
[So] Source:Eur J Med Chem;144:243-254, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:The effect on the therapeutic efficacy of Pt(II) complexes on combining non-steroidal anti-inflammatory drugs (NSAIDs) is an attractive strategy to circumvent chronic inflammation mediated by cancer and metastasis. Two square-planar platinum(II) complexes: [Pt(dach)(nap)Cl] (1) and [Pt(dach)(nap) ] (2), where dach = (1R,2R)-dichloro(cyclohexane-1,2-diamine) and NSAID drug naproxen (nap), have been designed for studying their biological activity. The naproxen bound to the Pt(II) centre get released upon photoirradiation with low-power UV-A light as confirmed by the significant enhancement in emission intensities of the complexes. The compounds were evaluated for their photophysical properties, photostability, reactivity with 5'-guanosine monophophosphate (5'-GMP), interactions with CT-DNA and BSA, antioxidant activity and reactive oxygen species mediated photo-induced DNA damage properties. ESI-MS studies demonstrated the formation of bis-adduct with 5'-GMP and the formation of Pt -DNA crosslinks by gel electrophoretic mobility shift assay and ITC studies. The interaction of the complexes 1 and 2 with the CT-DNA exhibits potential binding affinity (K âˆ¼ 10 M , K ∼ 10 M ), implying intercalation to CT-DNA through planar naphthyl ring of the complexes. Both the complexes also exhibit strong binding affinity towards BSA (K ∼ 10 M ). The complexes exhibit efficient DNA damage activity on irradiation at 365 nm via formation of singlet oxygen ( O ) and hydroxyl radical ( OH) under physiological conditions. Both the complexes were cytotoxic in dark and exhibit significant enhancement of cytotoxicity upon photo-exposure against HeLa and HepG2 cancer cells giving IC values ranging from 8 to 12 µM for 1 and 2. The cellular internalization data showed cytosolic and nuclear localization of the complexes in the HeLa cells.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/química
Antineoplásicos/química
Antioxidantes/química
Naproxeno/análogos & derivados
Compostos Organoplatínicos/química
[Mh] Termos MeSH secundário: Anti-Inflamatórios não Esteroides/farmacologia
Antineoplásicos/farmacologia
Antioxidantes/farmacologia
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos da radiação
Dano ao DNA/efeitos dos fármacos
Dano ao DNA/efeitos da radiação
Células HeLa
Células Hep G2
Seres Humanos
Naproxeno/farmacologia
Neoplasias/tratamento farmacológico
Neoplasias/genética
Compostos Organoplatínicos/farmacologia
Fármacos Fotossensibilizantes/química
Fármacos Fotossensibilizantes/farmacologia
Raios Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Antineoplastic Agents); 0 (Antioxidants); 0 (Organoplatinum Compounds); 0 (Photosensitizing Agents); 57Y76R9ATQ (Naproxen)
[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:171224
[St] Status:MEDLINE


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[PMID]:29274489
[Au] Autor:Salikov RF; Trainov KP; Belousova IK; Belyy AY; Fatkullina US; Mulyukova RV; Zainullina LF; Vakhitova YV; Tomilov YV
[Ad] Endereço:N. D. Zelinsky Institute of Organic Chemistry, Russian Academy of Sciences, 47 Leninsky Prospect, 119991 Moscow, Russian Federation.
[Ti] Título:Branching tryptamines as a tool to tune their antiproliferative activity.
[So] Source:Eur J Med Chem;144:211-217, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:The influence of a series of tryptamine derivatives on the viability of normal (HEK293) and tumor (HepG2, Jurkat and SH-SY5Y) cells has been evaluated. All tryptamines tested were three different substitution types: C- and N-branching, and indole benzylation. All the derivations enhance the activity of compounds separately, although the effects of different substitutions were not additive. Thus, combinations of C- and N-branchings as well as C-branching and indole benzylation gave little or no increase in activity.
[Mh] Termos MeSH primário: Antineoplásicos/química
Antineoplásicos/farmacologia
Proliferação Celular/efeitos dos fármacos
Triptaminas/química
Triptaminas/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Células HEK293
Seres Humanos
Indóis/química
Indóis/farmacologia
Neoplasias/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Indoles); 0 (Tryptamines)
[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:171224
[St] Status:MEDLINE



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