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[PMID]:29324340
[Au] Autor:Brandão GC; Rocha Missias FC; Arantes LM; Soares LF; Roy KK; Doerksen RJ; Braga de Oliveira A; Pereira GR
[Ad] Endereço:Departamento de Farmácia, Escola de Farmácia, UFOP, Campus Morro do Cruzeiro, s/n, Balxita, CEP 35400-000, Ouro Preto, MG, Brazil.
[Ti] Título:Antimalarial naphthoquinones. Synthesis via click chemistry, in vitro activity, docking to PfDHODH and SAR of lapachol-based compounds.
[So] Source:Eur J Med Chem;145:191-205, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Lapachol is an abundant prenyl naphthoquinone occurring in Brazilian Bignoniaceae that was clinically used, in former times, as an antimalarial drug, despite its moderate effect. Aiming to search for potentially better antimalarials, a series of 1,2,3-triazole derivatives was synthesized by chemical modification of lapachol. Alkylation of the hydroxyl group gave its propargyl ether which, via copper-catalyzed cycloaddition (CuAAC) click chemistry with different organic azides, afforded 17 naphthoquinonolyl triazole derivatives. All the synthetic compounds were evaluated for their in vitro activity against chloroquine resistant Plasmodium falciparum (W2) and for cytotoxicity to HepG2 cells. Compounds containing the naphthoquinolyl triazole moieties showed higher antimalarial activity than lapachol (IC 123.5 µM) and selectivity index (SI) values in the range of 4.5-197.7. Molecular docking simulations of lapachol, atovaquone and all the newly synthesized compounds were carried out for interactions with PfDHODH, a mitochondrial enzyme of the parasite respiratory chain that is essential for de novo pyrimidine biosynthesis. Docking of the naphthoquinonolyl triazole derivatives to PfDHODH yielded scores between -9.375 and -14.55 units, compared to -9.137 for lapachol and -12.95 for atovaquone and disclosed the derivative 17 as a lead compound. Therefore, the study results show the enhancement of DHODH binding affinity correlated with improvement of SI values and in vitro activities of the lapachol derivatives.
[Mh] Termos MeSH primário: Antimaláricos/farmacologia
Naftoquinonas/farmacologia
Plasmodium falciparum/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antimaláricos/síntese química
Antimaláricos/química
Sobrevivência Celular/efeitos dos fármacos
Cloroquina/farmacologia
Química Click
Relação Dose-Resposta a Droga
Resistência a Medicamentos/efeitos dos fármacos
Células Hep G2
Seres Humanos
Modelos Moleculares
Estrutura Molecular
Naftoquinonas/química
Testes de Sensibilidade Parasitária
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimalarials); 0 (Naphthoquinones); 886U3H6UFF (Chloroquine); B221938VB6 (lapachol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE


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[PMID]:29374705
[Au] Autor:Nakamura A; Matsunaga W; Gotoh A
[Ad] Endereço:Laboratory of Cell and Gene Therapy, Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Japan.
[Ti] Título:Autophagy Induced by Naftopidil Inhibits Apoptosis of Human Gastric Cancer Cells.
[So] Source:Anticancer Res;38(2):803-809, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:AIM: Naftopidil is used to treat benign prostate hyperplasia. Moreover, previous studies have shown that naftopidil reduced viability of many types of cancer cells. Therefore, we investigated the antitumor mechanism of naftopidil in this study. MATERIALS AND METHODS: We used the HGC27 human gastric cancer cell line. It was treated with naftopidil, pan-caspase inhibitor, and chloroquine diphosphate (CQ). Cell viability and cell death were investigated by the assay and annexin V/ propidium iodide assay. Phosphorylation of protein kinase B (AKT) (Ser473) was measured by western blotting. Alteration of light chain 3B (LC3B) was investigated by western blotting and immunofluorescence. RESULTS: Naftopidil reduced phospho-AKT (Ser473) and altered LC3B. Combination of naftopidil and CQ reduced cell viability and phospho-AKT (Ser 473). CONCLUSION: Naftopidil induces apoptosis and autophagy of HGC27 cells, however, autophagy is considered to inhibit apoptosis. We concluded naftopidil and CQ have a synergistic antitumor effect.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Naftalenos/farmacologia
Piperazinas/farmacologia
Neoplasias Gástricas/tratamento farmacológico
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Cloroquina/administração & dosagem
Cloroquina/análogos & derivados
Cloroquina/farmacologia
Sinergismo Farmacológico
Seres Humanos
Proteínas Associadas aos Microtúbulos/metabolismo
Naftalenos/administração & dosagem
Fosforilação
Piperazinas/administração & dosagem
Proteínas Proto-Oncogênicas c-akt/metabolismo
Neoplasias Gástricas/metabolismo
Neoplasias Gástricas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MAP1LC3B protein, human); 0 (Microtubule-Associated Proteins); 0 (Naphthalenes); 0 (Piperazines); 6E17K3343P (chloroquine diphosphate); 886U3H6UFF (Chloroquine); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); R9PHW59SFN (naftopidil)
[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:180129
[St] Status:MEDLINE


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[PMID]:28465453
[Au] Autor:Kaufman HL
[Ad] Endereço:Departments of Surgery and Medicine, Rutgers University, New Brunswick, New Jersey. howard.kaufman@rutgers.edu.
[Ti] Título:Rational Combination Immunotherapy: Understand the Biology.
[So] Source:Cancer Immunol Res;5(5):355-356, 2017 May.
[Is] ISSN:2326-6074
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Selecting rational treatment combinations remains a major challenge for improving immunotherapy outcomes. In this issue of , Zhang and colleagues reduced tumors by inhibiting CD47 in a lung carcinoma model, a treatment that inadvertently induced autophagy through inhibition of the Akt/mTOR pathway. By also targeting autophagy, the therapeutic response improved, highlighting the importance of understanding the biology beneath antitumor immunity.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/terapia
Imunoterapia
Neoplasias Pulmonares/terapia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos Imunológicos/uso terapêutico
Autofagia/efeitos dos fármacos
Antígeno CD47/antagonistas & inibidores
Antígeno CD47/imunologia
Carcinoma Pulmonar de Células não Pequenas/imunologia
Cloroquina/uso terapêutico
Quimioterapia Combinada
Seres Humanos
Neoplasias Pulmonares/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Immunological); 0 (CD47 Antigen); 886U3H6UFF (Chloroquine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1158/2326-6066.CIR-17-0128


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[PMID]:27770439
[Au] Autor:Lei Z; Sami Shaikh A; Zheng W; Yu X; Yu J; Li J
[Ad] Endereço:Department of Physiology, School of Medicine, Qilu Hospital, Shandong University, Jinan, Shandong, China.
[Ti] Título:Non-proton ligand-sensing domain of acid-sensing ion channel 3 is required for itch sensation.
[So] Source:J Neurochem;139(6):1093-1101, 2016 12.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Itch, the unpleasant sensation that evokes a desire to scratch, accompanies numerous skin and nervous system disorders. However, the molecular mechanisms of itch are unclear. Acid-sensing ion channel 3 (ASIC3) is a sensor of acidic and primary inflammatory pain. The whole-cell patch clamp technique was used to determine the effect of chloroquine (CQ) on ASICs currents in primary sensory neurons or the Chinese hamster ovary cells transfected with rat ASIC1a or ASIC3. Site-directed mutagenesis of plasmid was performed. Scratching behavior was evaluated by measuring the number of bouts during 30 min after injection. CQ, an anti-malarial drug defined as a histamine-independent pruritogen, selectively enhanced the sustained phase of ASIC3 current in a concentration-dependent manner either in ASIC3-transfected Chinese hamster ovary cells or in primary cultured rat dorsal root ganglion neurons. Further studies revealed that the effect of CQ on ASIC3 channels depends on the newly identified non-proton ligand-sensing domain. Importantly, CQ-evoked scratching behavior was largely alleviated by APETx2, a selective ASIC3 channel blocker. Like CQ, other compounds such as amiloride, 2-guanidine-4-methylquinazoline and neuropeptide FF, which have been previously reported to be non-proton ligands that activate ASIC3, undoubtedly evoked the scratching response. In conclusion, ASIC3, a proton-gated ion channel critical for pain sensation, also functions as an essential component of itch transduction.
[Mh] Termos MeSH primário: Canais Iônicos Sensíveis a Ácido/metabolismo
Prurido/metabolismo
Células Receptoras Sensoriais/metabolismo
[Mh] Termos MeSH secundário: Animais
Antimaláricos/farmacologia
Antimaláricos/toxicidade
Células CHO
Células Cultivadas
Cloroquina/farmacologia
Cloroquina/toxicidade
Cricetinae
Cricetulus
Relação Dose-Resposta a Droga
Gânglios Espinais/efeitos dos fármacos
Gânglios Espinais/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Prurido/induzido quimicamente
Ratos
Ratos Wistar
Células Receptoras Sensoriais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Accn3 protein, rat); 0 (Acid Sensing Ion Channels); 0 (Antimalarials); 886U3H6UFF (Chloroquine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.13869


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[PMID]:29064360
[Au] Autor:Lemoine JF; Boncy J; Filler S; Kachur SP; Fitter D; Chang MA
[Ad] Endereço:Programme National de la Contrôle de la Malaria, Ministère de la Santé Publique et de la Population, Port-au-Prince, Haiti.
[Ti] Título:Haiti's Commitment to Malaria Elimination: Progress in the Face of Challenges, 2010-2016.
[So] Source:Am J Trop Med Hyg;97(4_Suppl):43-48, 2017 Oct.
[Is] ISSN:1476-1645
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Haiti is committed to malaria elimination by 2020. Following a 2010 earthquake and cholera epidemic, Haiti capitalized on investments in its health system to refocus on malaria elimination. Efforts, including expanding diagnostics, ensuring efficacy of standard treatments, building institutional capacity, and strengthening surveillance were undertaken to complement the broad health system strengthening activities. These efforts led to the adoption and scale-up of malaria rapid diagnostic tests as a diagnostic modality. In addition, drug-resistant monitoring has been established in the country, along with the development of molecular testing capacity for the parasite at the National Public Health Laboratory. The development and piloting of surveillance activities to include an enhanced community-based approach for testing and treatment of patients has increased the ability of the Ministry of Health to map foci of transmission and respond promptly to outbreaks. The reinforcement of evidence-based approaches coupled with strong collaboration among the Ministry of Health and partners has demonstrated that malaria elimination by 2020 is a realistic prospect.
[Mh] Termos MeSH primário: Erradicação de Doenças
Malária Falciparum/prevenção & controle
[Mh] Termos MeSH secundário: Antimaláricos/uso terapêutico
Cloroquina/uso terapêutico
Cólera/epidemiologia
Desastres
Surtos de Doenças
Terremotos
Monitoramento Epidemiológico
Haiti/epidemiologia
Prioridades em Saúde
Seres Humanos
Malária Falciparum/diagnóstico
Malária Falciparum/tratamento farmacológico
Técnicas de Diagnóstico Molecular
Vigilância em Saúde Pública
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimalarials); 886U3H6UFF (Chloroquine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE
[do] DOI:10.4269/ajtmh.16-0902


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[PMID]:28978341
[Au] Autor:Zheng Y; Su C; Zhao L; Shi Y
[Ad] Endereço:School of Pharmacy, Jinzhou Medical University, Jinzhou, 121000, People's Republic of China.
[Ti] Título:mAb MDR1-modified chitosan nanoparticles overcome acquired EGFR-TKI resistance through two potential therapeutic targets modulation of MDR1 and autophagy.
[So] Source:J Nanobiotechnology;15(1):66, 2017 Oct 04.
[Is] ISSN:1477-3155
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Tyrosine kinase inhibitors (TKIs) that act against the epithelial growth factor receptor (EGFR) were once widely used in chemotherapy for many human cancers. However, acquired chemoresistance occurred in almost all patients, limiting the clinical application of EGFR-TKI. Thus far, no effective methods existing can resolve this problem. Designing a therapeutic treatment with a specific multi-target profile has been regarded as a possible strategy to overcome acquired EGFR-TKI resistance. METHODS: MDR1 antibody-modified chitosan nanoparticles loading gefitinib and autophagy inhibitor chloroquine were prepared by ionic crosslinking and electrostatic attracting method. MTT assay, flow cytometry analysis and western blot assay were all performed to confirm the effect of different formulations of gefitinib on the proliferation of SMMC-7721/gefitinib cells. The preparations demonstrated their multi-target potential to achieve both tumor-targeting selectivity and the desired antitumor effects by blocking cell-surface MDR1 and inhibiting autophagy. RESULTS: mAb MDR1-modified CS NPs, when combined with the co-delivery of gefitinib and chloroquine, showed targeting and therapeutic potential on enhancing the delivery of anticancer drugs and inducing significant cell apoptosis against acquired EGFR-TKI resistance through the modulation of autophagy and while blocking the activity of the MDR1 receptor. CONCLUSIONS: A new approach to design an excellent nanoparticle drug-delivery system can overcome acquired EGFR-TKI resistance against various multiple antitumor targets.
[Mh] Termos MeSH primário: Membro 1 da Subfamília B de Cassetes de Ligação de ATP/metabolismo
Antineoplásicos/administração & dosagem
Cloroquina/administração & dosagem
Resistência a Medicamentos Antineoplásicos
Neoplasias/tratamento farmacológico
Quinazolinas/administração & dosagem
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/química
Anticorpos Monoclonais/metabolismo
Antineoplásicos/farmacologia
Autofagia/efeitos dos fármacos
Linhagem Celular Tumoral
Quitosana/análogos & derivados
Quitosana/metabolismo
Cloroquina/farmacologia
Sistemas de Liberação de Medicamentos
Seres Humanos
Nanopartículas/química
Nanopartículas/metabolismo
Neoplasias/metabolismo
Inibidores de Proteínas Quinases/administração & dosagem
Inibidores de Proteínas Quinases/farmacologia
Quinazolinas/farmacologia
Receptor do Fator de Crescimento Epidérmico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATP-Binding Cassette, Sub-Family B, Member 1); 0 (Antibodies, Monoclonal); 0 (Antineoplastic Agents); 0 (Protein Kinase Inhibitors); 0 (Quinazolines); 886U3H6UFF (Chloroquine); 9012-76-4 (Chitosan); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); S65743JHBS (gefitinib)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1186/s12951-017-0302-5


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[PMID]:28973192
[Au] Autor:Lin SJ; Wu ZR; Cao L; Zhang Y; Leng ZG; Guo YH; Shang HB; Zhao WG; Zhang X; Wu ZB
[Ad] Endereço:Department of Neurosurgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
[Ti] Título:Pituitary Tumor Suppression by Combination of Cabergoline and Chloroquine.
[So] Source:J Clin Endocrinol Metab;102(10):3692-3703, 2017 Oct 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: The dopamine agonist cabergoline (CAB) has been used widely in the treatment of prolactinomas and other types of pituitary adenomas, but its clinical use is hampered by intolerance in some patients with prolactinoma and lack of effectiveness in other pituitary tumor types. Chloroquine (CQ) is an old drug widely used to treat malaria. Recent studies, including our own, have revealed that CAB and CQ are involved in induction of autophagy and activation of autophagic cell death. Objective: To test whether CAB and CQ can function cooperatively to suppress growth of pituitary adenomas as well as other cancers. Results: In vitro studies using the rat pituitary tumor cell lines MMQ and GH3, human pituitary tumor cell primary cultures, and several human cancer cell lines showed that CQ enhanced suppression of cell proliferation by CAB. These results were confirmed in in vivo xenograft models in nude mice and estrogen-induced rat prolactinomas. To understand the mechanism of combined CAB and CQ action, we established a low-CAB-dose condition in which CAB was able to induce autophagy but failed to suppress cell growth. Addition of CQ to low-dose CAB blocked normal autophagic cycles and induced apoptosis, evidenced by the further accumulation of p62/caspase-8/LC3-II. Conclusion: The data suggest that combined use of CAB and CQ may increase clinical effectiveness in treatment of human pituitary adenomas, as well as other cancers, making it an attractive option in tumor and cancer therapies.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Cloroquina/administração & dosagem
Ergolinas/administração & dosagem
Neoplasias Hipofisárias/tratamento farmacológico
Prolactinoma/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Morte Celular/efeitos dos fármacos
Células Cultivadas
Feminino
Células Hep G2
Seres Humanos
Camundongos
Camundongos Nus
Neoplasias Hipofisárias/patologia
Prolactinoma/patologia
Ratos
Ratos Endogâmicos F344
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ergolines); 886U3H6UFF (Chloroquine); LL60K9J05T (cabergoline)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-00627


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[PMID]:28945807
[Au] Autor:Circu M; Cardelli J; Barr M; O'Byrne K; Mills G; El-Osta H
[Ad] Endereço:Feist-Weiller Cancer Center, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana, United States of America.
[Ti] Título:Modulating lysosomal function through lysosome membrane permeabilization or autophagy suppression restores sensitivity to cisplatin in refractory non-small-cell lung cancer cells.
[So] Source:PLoS One;12(9):e0184922, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lung cancer is the leading cause of cancer-related deaths. Most patients develop resistance to platinum within several months of treatment. We investigated whether triggering lysosomal membrane permeabilization (LMP) or suppressing autophagy can restore cisplatin susceptibility in lung cancer with acquired chemoresistance. Cisplatin IC50 in A549Pt (parental) and A549cisR (cisplatin resistant) cells was 13 µM and 47 µM, respectively. Following cisplatin exposure, A549cisR cells failed to elicit an apoptotic response. This was manifested by diminished Annexin-V staining, caspase 3 and 9, BAX and BAK activation in resistant but not in parental cells. Chloroquine preferentially promoted LMP in A549cisR cells, revealed by leakage of FITC-dextran into the cytosol as detected by immunofluorescence microscopy. This was confirmed by increased cytosolic cathepsin D signal on Immunoblot. Cell viability of cisplatin-treated A549cisR cells was decreased when co-treated with chloroquine, corresponding to a combination index below 0.8, suggesting synergism between the two drugs. Notably, chloroquine activated the mitochondrial cell death pathway as indicated by increase in caspase 9 activity. Interestingly, inhibition of lysosomal proteases using E64 conferred cytoprotection against cisplatin and chloroquine co-treatment, suggesting that chloroquine-induced cell death occurred in a cathepsin-mediated mechanism. Likewise, blockage of caspases partially rescued A549cisR cells against the cytotoxicity of cisplatin and chloroquine combination. Cisplatin promoted a dose-dependent autophagic flux induction preferentially in A549cisR cells, as evidenced by a surge in LC3-II/α-tubulin following pre-treatment with E64 and increase in p62 degradation. Compared to untreated cells, cisplatin induced an increase in cyto-ID-loaded autophagosomes in A549cisR cells that was further amplified by chloroquine, pointing toward autophagic flux activation by cisplatin. Interestingly, this effect was less pronounced in A549Pt cells. Blocking autophagy by ATG5 depletion using siRNA markedly enhances susceptibility to cisplatin in A549cisR cells. Taken together, our results underscore the utility of targeting lysosomal function in overcoming acquired cisplatin refractoriness in lung cancer.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Autofagia/fisiologia
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Cisplatino/uso terapêutico
Neoplasias Pulmonares/tratamento farmacológico
Lisossomos/fisiologia
[Mh] Termos MeSH secundário: Células A549
Apoptose/efeitos dos fármacos
Apoptose/fisiologia
Autofagia/efeitos dos fármacos
Cloroquina/farmacologia
Resistência a Medicamentos Antineoplásicos
Seres Humanos
Membranas Intracelulares/efeitos dos fármacos
Membranas Intracelulares/fisiologia
Lisossomos/efeitos dos fármacos
Microscopia de Fluorescência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 886U3H6UFF (Chloroquine); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184922


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[PMID]:28934438
[Au] Autor:Boudová S; Divala T; Mungwira R; Mawindo P; Tomoka T; Laufer MK
[Ad] Endereço:Division of Malaria Research, Institute for Global Health, University of Maryland School of Medicine, Baltimore.
[Ti] Título:Placental but Not Peripheral Plasmodium falciparum Infection During Pregnancy Is Associated With Increased Risk of Malaria in Infancy.
[So] Source:J Infect Dis;216(6):732-735, 2017 Sep 15.
[Is] ISSN:1537-6613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pregnancy-associated Plasmodium falciparum infection impacts the health of mothers and newborns, but little is known about the effects of these infections on infant susceptibility to malaria. We followed 473 mother-infant pairs during pregnancy and through 2 years of age. We observed that children born to mothers with placental malaria, but not those born to mothers with peripheral infection without evidence of placental sequestration, had increased risk of malaria during the first year of life compared with children born to mothers with no malaria during pregnancy. Malaria infections with placental sequestration have long-lasting impact on infant susceptibility to malaria infection.
[Mh] Termos MeSH primário: Malária Falciparum/diagnóstico
Doenças Placentárias/diagnóstico
Doenças Placentárias/parasitologia
Placenta/parasitologia
Plasmodium falciparum/isolamento & purificação
Complicações Parasitárias na Gravidez/diagnóstico
[Mh] Termos MeSH secundário: Cloroquina/uso terapêutico
Combinação de Medicamentos
Feminino
Seguimentos
Seres Humanos
Lactente
Modelos Logísticos
Estudos Longitudinais
Malária Falciparum/sangue
Análise Multivariada
Doenças Placentárias/sangue
Gravidez
Complicações Parasitárias na Gravidez/sangue
Pirimetamina/uso terapêutico
Fatores de Risco
Sulfadoxina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Drug Combinations); 37338-39-9 (fanasil, pyrimethamine drug combination); 88463U4SM5 (Sulfadoxine); 886U3H6UFF (Chloroquine); Z3614QOX8W (Pyrimethamine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1093/infdis/jix372


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[PMID]:28898049
[Au] Autor:Hassett MR; Riegel BE; Callaghan PS; Roepe PD
[Ad] Endereço:Departments of Chemistry and of Biochemistry & Cellular & Molecular Biology, Georgetown University , 37th and O Streets NW, Washington, D.C. 20057, United States.
[Ti] Título:Analysis of Plasmodium vivax Chloroquine Resistance Transporter Mutant Isoforms.
[So] Source:Biochemistry;56(41):5615-5622, 2017 Oct 17.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chloroquine (CQ) resistance (CQR) in Plasmodium falciparum malaria is widespread and has limited the use of CQ in many regions of the globe. Malaria caused by the related human parasite P. vivax is as widespread as is P. falciparum malaria and has been treated with CQ as extensively as has P. falciparum, suggesting that P. vivax parasites have been selected with CQ as profoundly as have P. falciparum parasites. Indeed, a growing number of clinical reports have presented data suggesting increased P. vivax CQR. Cytostatic (growth inhibitory) CQR for P. falciparum is caused by Plasmodium falciparum chloroquine resistance transporter (PfCRT) mutations, and it has been proposed that mutations in the PvCRT orthologue may simliarly cause P. vivax CQR via increasing CQ transport from the P. vivax digestive vacuole. Here we report the first quantitative analysis of drug transport mediated by all known mutant isoforms of Plasmodium vivax chloroquine resistance transporter (PvCRT) in order to test the protein's potential link to growing P. vivax CQR phenomena. Small, but statistically significant, differences in the transport of CQ and other quinoline antimalarial drugs were found for multiple PvCRT isoforms, relative to wild type PvCRT, suggesting that mutations in PvCRT can contribute to P. vivax CQR and other examples of quinoline antimalarial drug resistance.
[Mh] Termos MeSH primário: Antimaláricos/metabolismo
Cloroquina/metabolismo
Proteínas de Membrana Transportadoras/metabolismo
Modelos Moleculares
Mutação
Plasmodium vivax/metabolismo
Proteínas de Protozoários/metabolismo
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Antimaláricos/farmacologia
Transporte Biológico
Membrana Celular/efeitos dos fármacos
Membrana Celular/metabolismo
Cloroquina/farmacologia
Contagem de Colônia Microbiana
Resistência a Medicamentos
Seres Humanos
Malária Vivax/tratamento farmacológico
Malária Vivax/parasitologia
Proteínas de Membrana Transportadoras/química
Proteínas de Membrana Transportadoras/genética
Mutagênese Sítio-Dirigida
Plasmodium vivax/efeitos dos fármacos
Plasmodium vivax/crescimento & desenvolvimento
Plasmodium vivax/isolamento & purificação
Primaquina/metabolismo
Primaquina/farmacologia
Conformação Proteica
Isoformas de Proteínas/química
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Proteínas de Protozoários/química
Proteínas de Protozoários/genética
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
Saccharomyces cerevisiae/efeitos dos fármacos
Saccharomyces cerevisiae/crescimento & desenvolvimento
Saccharomyces cerevisiae/metabolismo
Trítio
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimalarials); 0 (Crt-o protein, Plasmodium vivax); 0 (Membrane Transport Proteins); 0 (Protein Isoforms); 0 (Protozoan Proteins); 0 (Recombinant Proteins); 10028-17-8 (Tritium); 886U3H6UFF (Chloroquine); MVR3634GX1 (Primaquine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.7b00749



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