Base de dados : MEDLINE
Pesquisa : C04 [Categoria DeCS]
Referências encontradas : 285082 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 28509 ir para página                         

  1 / 285082 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27771786
[Au] Autor:Osinski A; Vreugdenhil G; de Koning J; van der Hoeven JG
[Ad] Endereço:Department of Internal Medicine, Maxima Medical Centre, De Run 4600, 5504DB, Veldhoven, the Netherlands. aart_osinski@hotmail.com.
[Ti] Título:Do-not-resuscitate orders in cancer patients: a review of literature.
[So] Source:Support Care Cancer;25(2):677-685, 2017 02.
[Is] ISSN:1433-7339
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Discussing do-not-resuscitate (DNR) orders is part of daily hospital practice in oncology departments. Several medical factors and patient characteristics are associated with issuing DNR orders in cancer patients. DNR orders are often placed late in the disease process. This may be a cause for disagreements between doctors and between doctors and patients and may cause for unnecessary treatments and admissions. In addition, DNR orders on itself may influence the rest of the medical treatment for patients. We present recommendations for discussing DNR orders and medical futility in practice through shared decision-making. Prospective studies are needed to investigate in which a patient's cardiopulmonary resuscitation (CPR) is futile and whether or not DNR orders influence the medical care of patients.
[Mh] Termos MeSH primário: Reanimação Cardiopulmonar/ética
Tomada de Decisões/ética
Neoplasias/psicologia
Ordens quanto à Conduta (Ética Médica)/ética
[Mh] Termos MeSH secundário: Seres Humanos
Masculino
Meia-Idade
Neoplasias/terapia
Estudos Prospectivos
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180310
[Lr] Data última revisão:
180310
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1007/s00520-016-3459-9


  2 / 285082 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29408272
[Au] Autor:Saif I; Kasmi Y; Allali K; Ennaji MM
[Ad] Endereço:Team of Virology, Oncology and Medical Biotechnologies, Laboratory of Virology, Microbiology, Quality and Biotechnologies/ETB, Faculty of Science sand Technologies-Mohammedia, Hassan II University of Casablanca, Morocco.
[Ti] Título:Prediction of DNA methylation in the promoter of gene suppressor tumor.
[So] Source:Gene;651:166-173, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The epigenetics methylation of cytosine is the most common epigenetic form in DNA sequences. It is highly concentrated in the promoter regions of the genes, leading to an inactivation of tumor suppressors regardless of their initial function. In this work, we aim to identify the highly methylated regions; the cytosine-phosphate-guanine (CpG) island located on the promoters and/or the first exon gene known for their key roles in the cell cycle, hence the need to study gene-gene interactions. The Frommer and hidden Markov model algorithms are used as computational methods to identify CpG islands with specificity and sensitivity up to 76% and 80%, respectively. The results obtained show, on the one hand, that the genes studied are suspected of developing hypermethylation in the promoter region of the gene involved in the case of a cancer. We then showed that the relative richness in CG results from a high level of methylation. On the other hand, we observe that the gene-gene interaction exhibits co-expression between the chosen genes. This let us to conclude that the hidden Markov model algorithm predicts more specific and valuable information about the hypermethylation in gene as a preventive and diagnostics tools for the personalized medicine; as that the tumor-suppresser-genes have relative co-expression and complementary relations which the hypermethylation affect in the samples studied in our work.
[Mh] Termos MeSH primário: Biologia Computacional/métodos
Ilhas de CpG
Metilação de DNA
Genes Supressores de Tumor
Regiões Promotoras Genéticas
[Mh] Termos MeSH secundário: Algoritmos
DNA de Neoplasias
Conjuntos de Dados como Assunto
Epistasia Genética
Seres Humanos
Cadeias de Markov
Modelos Genéticos
Neoplasias/genética
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Neoplasm)
[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:180207
[St] Status:MEDLINE


  3 / 285082 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29381830
[Au] Autor:Sioud M
[Ad] Endereço:Department of Cancer Immunology, Oslo University Hospital, The Norwegian Radium Hospital, Montebello, Oslo, Norway.
[Ti] Título:T-cell cross-reactivity may explain the large variation in how cancer patients respond to checkpoint inhibitors.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The therapeutic use of the immune system to specifically attack tumours has been a long-standing vision among tumour immunologists. Recently, the use of checkpoint inhibitors to turn-off immunosuppressive signals has proven to be effective in enhancing T-cell reactivity against patient-specific neoantigens, resulting from somatic mutations. Several of the identified T-cell epitopes share similarity with common bacterial and viral antigens, suggesting the involvement of pre-existing microbial cross-reactive T cells in rapid and durable tumour regression seen in some patients. This notion of T-cell cross-reactivity is further supported by the findings that intestinal bacteria can influence checkpoint-blockade therapy. Moreover, early data indicate the presence of such T cells in long-term survival breast cancer patients. This review highlights the main challenges for cancer immunotherapy and discusses the potential contribution of T-cell cross-reactivity in cancer immunotherapy and whether it can be used as a biomarker to predict the responsiveness to checkpoint inhibitors.
[Mh] Termos MeSH primário: Reações Cruzadas/imunologia
Imunoterapia/métodos
Neoplasias/imunologia
Neoplasias/terapia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Antígenos de Bactérias/imunologia
Antígenos de Neoplasias/imunologia
Antígenos Virais/imunologia
Biomarcadores Tumorais/imunologia
Antígeno CTLA-4/antagonistas & inibidores
Células Dendríticas/imunologia
Epitopos de Linfócito T/imunologia
Seres Humanos
Ativação Linfocitária/imunologia
Receptor de Morte Celular Programada 1/antagonistas & inibidores
Receptores Imunológicos/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Antigens, Neoplasm); 0 (Antigens, Viral); 0 (Biomarkers, Tumor); 0 (CTLA-4 Antigen); 0 (Epitopes, T-Lymphocyte); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); 0 (Receptors, Immunologic); 0 (TIGIT protein, human)
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12643


  4 / 285082 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29357376
[Au] Autor:Li Y; Zhou C; Li J; Liu J; Lin L; Li L; Cao D; Li Q; Wang Z
[Ad] Endereço:School of Pharmaceutical Sciences, School of Pharmaceutical Sciences, Guangzhou, China.
[Ti] Título:Single domain based bispecific antibody, Muc1-Bi-1, and its humanized form, Muc1-Bi-2, induce potent cancer cell killing in muc1 positive tumor cells.
[So] Source:PLoS One;13(1):e0191024, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Muc1 is one of the most studied tumor antigens. However, antibodies or antibody-toxin conjugates against Muc1 have not shown significant efficacy for tumors with Muc1 overexpression. In this study, we employed bispecific antibody approach to target Muc1 positive tumor cells. A novel bispecific antibody, Muc1-Bi-1, was constructed by linking single domain antibodies, anti-Muc1-VHH and anti-CD16-VHH. Muc1-Bi-2, the humanized form of Muc1-Bi-1, was also constructed by grafting. Both Muc1-Bi bispecific antibodies can be efficiently expressed and purified from bacteria. In vitro, the Muc1-Bi bispecific antibodies can recruit Natural Killer (NK) cells to drive potent and specific cell killing of Muc1-overexpressing tumor cells. In xenograft model, the Muc1-Bi bispecific antibodies can suppress tumor growth in the presence of human peripheral blood mononuclear cells (PBMC). These data suggested that the single domain based Muc1-Bi may provide a valid strategy for targeting tumors with Muc1 overexpression.
[Mh] Termos MeSH primário: Anticorpos Biespecíficos/imunologia
Mucina-1/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Biespecíficos/genética
Células CHO
Linhagem Celular Tumoral
Proliferação Celular
Cricetulus
Ensaio de Imunoadsorção Enzimática
Citometria de Fluxo
Seres Humanos
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Neoplasias/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Bispecific); 0 (MUC1 protein, human); 0 (Mucin-1)
[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:180123
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191024


  5 / 285082 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[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


  6 / 285082 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[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


  7 / 285082 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[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


  8 / 285082 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29268130
[Au] Autor:Lin HY; Han HW; Sun WX; Yang YS; Tang CY; Lu GH; Qi JL; Wang XM; Yang YH
[Ad] Endereço:State Key Laboratory of Pharmaceutical Biotechnology, NJU-NJFU Institute of Plant Molecular Biology, School of Life Sciences, Nanjing University, Nanjing, 210023, China; Co-Innovation Center for Sustainable Forestry in Southern China, Nanjing Forestry University, Nanjing, 210037, China.
[Ti] Título:Design and characterization of α-lipoic acyl shikonin ester twin drugs as tubulin and PDK1 dual inhibitors.
[So] Source:Eur J Med Chem;144:137-150, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Shikonin exhibits powerful anticancer activities for various cancer cells, but its poor solubility and strong toxicity hinder its development as clinical anticancer agent. We previously confirmed that shikonin and its derivatives can disturb mitosis through targeting tubulin. In this study, α-lipoic acid, the naturally-occurring co-factor of pyruvate dehydrogenase (PDH), was introduced into shikonin to design the twin drugs against both mitosis (tubulin) and glycolysis (PDK). 18 kinds of α-lipoic acid shikonin ester derivatives were achieved through three rounds of screening process performed by computer assistant drug design method, being designated as the outstanding compounds. Among them, 1c displayed the most potent cytotoxicity towards cervical cancer cells (HeLa) with an IC value of 3.14 ± 0.58 µM and inhibited xenotransplanted tumor growth in a dose-dependent manner. Further pharmacologic study demonstrated that 1c can cause cell cycle arrest in G2/M phase as tubulin polymerization inhibitor. Moreover, it also showed good PDK1 inhibitory activity, promoting PDH activity and forced HeLa cells to process more aerobic metabolism to undergo cell apoptosis. We reported here the first dual inhibitors of tubulin and PDK1 based on shikonin. It may form a basis for shikonin optimization through twin drug design framework for the discovery of new and potent shikonin derivatives in the study of targeted cancer therapy.
[Mh] Termos MeSH primário: Antineoplásicos/química
Antineoplásicos/farmacologia
Naftoquinonas/química
Naftoquinonas/farmacologia
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Moduladores de Tubulina/química
Moduladores de Tubulina/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Desenho de Drogas
Glicólise/efeitos dos fármacos
Células HeLa
Seres Humanos
Mitose/efeitos dos fármacos
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Tubulina (Proteína)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Naphthoquinones); 0 (Tubulin); 0 (Tubulin Modulators); 3IK6592UBW (shikonin); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.2 (pyruvate dehydrogenase (acetyl-transferring) 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:171222
[St] Status:MEDLINE


  9 / 285082 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29268127
[Au] Autor:Khan I; Garikapati KR; Shaik AB; Makani VKK; Rahim A; Shareef MA; Reddy VG; Pal-Bhadra M; Kamal A; Kumar CG
[Ad] Endereço:Medicinal Chemistry and Biotechnology Division, CSIR-Indian Institute of Chemical Technology (IICT), Hyderabad 500007, India; Academy of Scientific and Innovative Research, New Delhi 110 025, India.
[Ti] Título:Design, synthesis and biological evaluation of 1, 4-dihydro indeno[1,2-c] pyrazole linked oxindole analogues as potential anticancer agents targeting tubulin and inducing p53 dependent apoptosis.
[So] Source:Eur J Med Chem;144:104-115, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:A series of 1, 4-dihydroindeno-[1,2-c] pyrazole linked oxindole conjugates have been synthesized by using Knoevenagel condensation method and further evaluated for their antiproliferative activity against HeLa, A549 and MDA-MB-231 human cancer cell lines along with HEK-293 (normal human embryonic kidney cells). Among the derivatives, compounds 12a, 12b, and 12d showed excellent cytotoxicity with IC values ranging between 1.33 to 4.33 µM. Furthermore, detailed biological assays showed that there was accumulation of mitotic cells in G2/M phase, disruption of microtubule network and increase in the G2/M checkpoint proteins (Cyclin B1 and CDK1). Moreover, compound 12d with IC value of 1.33 µM showed significant upregulation of tumor suppressor proteins like p53, p21 and pro-apoptotic Bax. The molecular docking analysis demonstrated that these congeners occupy the colchicine binding pocket of the tubulin.
[Mh] Termos MeSH primário: Antineoplásicos/química
Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Pirazóis/química
Pirazóis/farmacologia
Moduladores de Tubulina/química
Moduladores de Tubulina/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Desenho de Drogas
Ensaios de Seleção de Medicamentos Antitumorais
Pontos de Checagem da Fase G2 do Ciclo Celular/efeitos dos fármacos
Células HEK293
Células HeLa
Seres Humanos
Indóis/química
Indóis/farmacologia
Simulação de Acoplamento Molecular
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Tubulina (Proteína)/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Indoles); 0 (Pyrazoles); 0 (Tubulin); 0 (Tubulin Modulators); 0 (Tumor Suppressor Protein p53); 0S9338U62H (2-oxindole)
[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:171222
[St] Status:MEDLINE


  10 / 285082 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29238188
[Au] Autor:Zhang J; Tang H; Liu Z; Chen B
[Ad] Endereço:Department of Hematology and Oncology, Zhongda Hospital, School of Medicine, Southeast University, Nanjing.
[Ti] Título:Effects of major parameters of nanoparticles on their physical and chemical properties and recent application of nanodrug delivery system in targeted chemotherapy.
[So] Source:Int J Nanomedicine;12:8483-8493, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Chemotherapy is still one of the main cancer therapy treatments, but the curative effect of chemotherapy is relatively low, as such the development of a new cancer treatment is highly desirable. The gradual maturation of nanotechnology provides an innovative perspective not only for cancer therapy but also for many other applications. There are a diverse variety of nanoparticles available, and choosing the appropriate carriers according to the demand is the key issue. The performance of nanoparticles is affected by many parameters, mainly size, shape, surface charge, and toxicity. Using nanoparticles as the carriers to realize passive targeting and active targeting can improve the efficacy of chemotherapy drugs significantly, reduce the mortality rate of cancer patients, and improve the quality of life of patients. In recent years, there has been extensive research on nanocarriers. In this review, the effects of several major parameters of nanoparticles on their physical and chemical properties are reviewed, and then the recent progress in the application of several commonly used nanoparticles is presented.
[Mh] Termos MeSH primário: Antineoplásicos/administração & dosagem
Portadores de Fármacos/química
Sistemas de Liberação de Medicamentos/métodos
Nanopartículas/efeitos adversos
Nanopartículas/química
[Mh] Termos MeSH secundário: Dendrímeros/administração & dosagem
Dendrímeros/química
Portadores de Fármacos/farmacologia
Seres Humanos
Lipossomos/administração & dosagem
Lipossomos/química
Micelas
Nanopartículas/administração & dosagem
Nanotecnologia/métodos
Nanotubos de Carbono/química
Neoplasias/tratamento farmacológico
Tamanho da Partícula
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Dendrimers); 0 (Drug Carriers); 0 (Liposomes); 0 (Micelles); 0 (Nanotubes, Carbon)
[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:171215
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S148359



página 1 de 28509 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde