Base de dados : MEDLINE
Pesquisa : D08.811.520.241.300.150.450 [Categoria DeCS]
Referências encontradas : 937 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 94 ir para página                         

  1 / 937 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29289880
[Au] Autor:Ansari MF; Idrees D; Hassan MI; Ahmad K; Avecilla F; Azam A
[Ad] Endereço:Department of Chemistry, Jamia Millia Islamia, Jamia Nagar, 110 025, New Delhi, India.
[Ti] Título:Design, synthesis and biological evaluation of novel pyridine-thiazolidinone derivatives as anticancer agents: Targeting human carbonic anhydrase IX.
[So] Source:Eur J Med Chem;144:544-556, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:In order to obtain novel Human carbonic anhydrase IX (CAIX) inhibitors, a series of pyridine-thiazolidinone derivatives was synthesized and characterized by various spectroscopic techniques. The binding affinity of the compounds was measured by fluorescence binding studies and enzyme inhibition activity using esterase assay of CAIX. It was observed that compound 8 and 11 significantly inhibit the CAIX activity with the IC value, 1.61 µM and 1.84 µM, respectively. The binding-affinity of compound 8 and 11 for CAIX was significantly high with their K values 11.21 µM and 2.32 µM, respectively. Docking studies revealed that compound 8 and 11 efficiently binds in the active site cavity of CA IX by forming sufficient numbers of H-bonds and van der Waals interactions with active side residues. All the compounds were further screened in vitro for anticancer activity and found that compound 8 and 11 exhibit considerable anticancer activity against MCF-7 and HepG-2 cell lines. All these findings suggest that compound 8 and 11 may be further exploited as a novel pharmacophore model for the development of anticancer agents.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Anidrase Carbônica IX/antagonistas & inibidores
Inibidores da Anidrase Carbônica/farmacologia
Desenho de Drogas
Piridinas/farmacologia
Tiazolidinas/farmacologia
[Mh] Termos MeSH secundário: Antígenos de Neoplasias/metabolismo
Antineoplásicos/síntese química
Antineoplásicos/química
Anidrase Carbônica II/antagonistas & inibidores
Anidrase Carbônica II/metabolismo
Anidrase Carbônica IX/metabolismo
Inibidores da Anidrase Carbônica/síntese química
Inibidores da Anidrase Carbônica/química
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Simulação de Acoplamento Molecular
Estrutura Molecular
Piridinas/síntese química
Piridinas/química
Relação Estrutura-Atividade
Tiazolidinas/síntese química
Tiazolidinas/química
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Antineoplastic Agents); 0 (Carbonic Anhydrase Inhibitors); 0 (Pyridines); 0 (Thiazolidines); EC 4.2.1.- (Carbonic Anhydrase II); EC 4.2.1.1 (CA9 protein, human); EC 4.2.1.1 (Carbonic Anhydrase IX); NH9L3PP67S (pyridine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180101
[St] Status:MEDLINE


  2 / 937 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29251173
[Au] Autor:Lucarini L; Magnelli L; Schiavone N; Crisci A; Innocenti A; Puccetti L; Cianchi F; Peri S; Supuran CT; Papucci L; Masini E
[Ad] Endereço:a Department of Neuroscience, Psychiatry and Drug Area and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology and Section of Pharmaceutical Sciences , University of Florence , Florence , Italy.
[Ti] Título:Plasmatic carbonic anhydrase IX as a diagnostic marker for clear cell renal cell carcinoma.
[So] Source:J Enzyme Inhib Med Chem;33(1):234-240, 2018 Dec.
[Is] ISSN:1475-6374
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Carbonic anhydrase (CA, EC 4.2.1.1) IX is regarded as a tumour hypoxia marker and CA inhibitors have been proposed as a new class of antitumor agents, with one such agent in Phase II clinical trials. The expression of some CAs, in particular the isoforms CA IX and CA XII, has been correlated with tumour aggressiveness and progression in several cancers. The aim of this study was to evaluate the possibility that CA IX could represent a marker related to clear cell Renal Cell Carcinoma (ccRCC). Bcl-2 and Bax, and the activity of caspase-3, evaluated in tissue biopsies from patients, were congruent with resistance to apoptosis in ccRCCs with respect to healthy controls, respectively. In the same samples, the CA IX and pro-angiogenic factor VEGF expressions revealed that both these hypoxia responsive proteins were strongly increased in ccRCC with respect to controls. CA IX plasma concentration and CA activity were assessed in healthy volunteers and patients with benign kidney tumours and ccRCCs. CA IX expression levels were found strongly increased only in plasma from ccRCC subjects, whereas, CA activity was found similarly increased both in plasma from ccRCC and benign tumour patients, compared to healthy volunteers. These results show that the plasmatic level of CA IX, but not the CA total activity, can be considered a diagnostic marker of ccRCCs. Furthermore, as many reports exist relating CA IX inhibition to a better outcome to anticancer therapy in ccRCC, plasma levels of CA IX could be also predictive for response to therapy.
[Mh] Termos MeSH primário: Biomarcadores Tumorais
Anidrase Carbônica IX/sangue
Carcinoma de Células Renais/sangue
Carcinoma de Células Renais/diagnóstico
[Mh] Termos MeSH secundário: Idoso
Western Blotting
Anidrase Carbônica IX/genética
Anidrase Carbônica IX/metabolismo
Carcinoma de Células Renais/enzimologia
Caspase 3/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
Valor Preditivo dos Testes
Reação em Cadeia da Polimerase em Tempo Real
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); EC 3.4.22.- (Caspase 3); EC 4.2.1.1 (Carbonic Anhydrase IX)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1080/14756366.2017.1411350


  3 / 937 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27777776
[Au] Autor:Chow S; Galvis V; Pillai M; Leach R; Keene E; Spencer-Shaw A; Shablak A; Shanks J; Liptrot T; Thistlethwaite F; Hawkins RE
[Ad] Endereço:The Christie NHS Foundation Trust, Manchester, UK.
[Ti] Título:High-dose interleukin2 - a 10-year single-site experience in the treatment of metastatic renal cell carcinoma: careful selection of patients gives an excellent outcome.
[So] Source:J Immunother Cancer;4:67, 2016.
[Is] ISSN:2051-1426
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: VEGF-targeted therapy has become the mainstay of treatment for majority of mRCC patients. For most patients, benefit is short-lived and therefore treatment remains palliative in intent. HD IL2 is an effective immunotherapy treatment capable of durable remission in some patients but its unselected use has been difficult due to its modest response rate and considerable adverse effects. Using set pathology criteria as a selection tool in clinical practice, we have been able to show improved outcomes in our previous report. Here, we present an updated and extended report of this treatment and seek to explore any pathological, clinical and treatment variables likely to predict better outcomes. METHODS: This is an extension of a previously reported clinical audit, which includes mRCC cases treated with HD IL2 between 2003 and 2013. Since 2006, tumour specimens of potential candidates were routinely reviewed prospectively and stratified into or categories based on constitution of histological growth pattern, namely alveolar or solid versus papillary and/or sarcomatoid architecture; clear cell versus granular cell cytoplasmic morphology. HD IL2 was preferentially offered to patients with pathology. Outcome evaluation includes response rates, survival, and treatment tolerance. Multivariate analysis was performed to explore potential prognostic and predictive factors. RESULTS: Among prospectively selected patients with pathology ( = 106), overall response rate was 48.1 % (51/106) with CR rate of 21.6 % (23/106). Median OS was 58.1 months. Factors associated with significantly better response and/or survival includes favourable pathology pattern, higher cycle 1 tolerance and lower number of metastatic organ sites (<3). CAIX (Carbonic anhydrase 9) has prognostic value but is not predictive of response. Toxicities were those expected of IL2 but were manageable on general medical wards, with no treatment-related death. Importantly most complete responses were durable with 76 % (23/30) cases remained relapse-free (median 39 months follow up) and 2 of the seven who relapsed had had long-term disease free survival after resection of oligometastatic relapse. CONCLUSIONS: Our experience shows that HD IL2 remains an effective and safe treatment in well-selected cases of mRCC. The result in this single-institution patient series confirms similar outcomes to our previously reported retrospective series. Given the prospect of long-term remission, fit patients with histology and low disease burden should be considered for HD IL2 in an experienced centre. Better understanding has been gained from this in-depth analysis especially the examination of possible response predictors and strategies that can improve treatment outcome.
[Mh] Termos MeSH primário: Antineoplásicos Imunológicos/administração & dosagem
Carcinoma de Células Renais/tratamento farmacológico
Carcinoma de Células Renais/patologia
Fatores Imunológicos/administração & dosagem
Interleucina-2/administração & dosagem
Neoplasias Renais/tratamento farmacológico
Neoplasias Renais/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores Tumorais
Anidrase Carbônica IX/genética
Anidrase Carbônica IX/metabolismo
Carcinoma de Células Renais/mortalidade
Membrana Celular/metabolismo
Terapia Combinada
Feminino
Seres Humanos
Estimativa de Kaplan-Meier
Neoplasias Renais/mortalidade
Masculino
Meia-Idade
Metástase Neoplásica
Estadiamento de Neoplasias
Seleção de Pacientes
Modelos de Riscos Proporcionais
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Immunological); 0 (Biomarkers, Tumor); 0 (Immunologic Factors); 0 (Interleukin-2); EC 4.2.1.1 (Carbonic Anhydrase IX)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  4 / 937 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:29277801
[Au] Autor:Kashiwagi S; Asano Y; Goto W; Takada K; Takahashi K; Hatano T; Tanaka S; Takashima T; Tomita S; Motomura H; Ohsawa M; Hirakawa K; Ohira M
[Ad] Endereço:Department of Surgical Oncology, Osaka City University Graduate School of Medicine, Osaka, Japan spqv9ke9@view.ocn.ne.jp.
[Ti] Título:Mesenchymal-epithelial Transition and Tumor Vascular Remodeling in Eribulin Chemotherapy for Breast Cancer.
[So] Source:Anticancer Res;38(1):401-410, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Eribulin mesylate (eribulin) is currently used for the treatment of locally advanced or metastatic breast cancer (MBC). It is a cytotoxic agent with unique mechanisms that suppress the epithelial-mesenchymal transition (EMT) of cancer cells and promote tumor vascular remodeling. In this study, we investigated the expression of markers for EMT and hypoxia in sets of clinical specimens collected before and after eribulin treatment to verify its unique mechanisms. PATIENTS AND METHODS: The expression of markers for EMT and cellular hypoxia [E-cadherin, N-cadherin, vimentin, and carbonic anhydrase 9 (CA9)] was examined immunohistochemically in MBC tissues collected from 20 patients before and after chemotherapy with either eribulin (n=10) or paclitaxel (n=10). RESULTS: An increase of E-cadherin and decrease of CA9 expression were observed in MBC tissues from patients with objective clinical responses to eribulin treatment. Patients with E-cadherin-positive conversion and CA9-negative conversion had significantly higher response rates (p=0.004 and p=0.024, respectively) and prolonged time to treatment failure (p=0.018 and p=0.038, respectively) than patients without changes in marker expression. CONCLUSION: Expression of EMT and hypoxia markers in clinical samples from patients with MBC was suppressed by eribulin treatment. The results provide additional clinical data on improved survival of patients treated with eribulin and the mechanism of response.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Furanos/uso terapêutico
Cetonas/uso terapêutico
Paclitaxel/uso terapêutico
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
Remodelação Vascular/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antígenos de Neoplasias/metabolismo
Biomarcadores Tumorais/metabolismo
Caderinas/metabolismo
Anidrase Carbônica IX/metabolismo
Hipóxia Celular/efeitos dos fármacos
Feminino
Seres Humanos
Meia-Idade
Estudos Retrospectivos
Neoplasias de Mama Triplo Negativas/patologia
Vimentina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Antineoplastic Agents); 0 (Biomarkers, Tumor); 0 (Cadherins); 0 (Furans); 0 (Ketones); 0 (Vimentin); EC 4.2.1.1 (CA9 protein, human); EC 4.2.1.1 (Carbonic Anhydrase IX); LR24G6354G (eribulin); P88XT4IS4D (Paclitaxel)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


  5 / 937 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29197732
[Au] Autor:De Luca L; Mancuso F; Ferro S; Buemi MR; Angeli A; Del Prete S; Capasso C; Supuran CT; Gitto R
[Ad] Endereço:Dipartimento di Scienze Chimiche, Biologiche, Farmaceutiche ed Ambientali (CHIBIOFARAM), Università degli Studi di Messina, Viale Annunziata, I-98168 Messina, Italy. Electronic address: ldeluca@unime.it.
[Ti] Título:Inhibitory effects and structural insights for a novel series of coumarin-based compounds that selectively target human CA IX and CA XII carbonic anhydrases.
[So] Source:Eur J Med Chem;143:276-282, 2018 Jan 01.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Coumarin derivatives are a peculiar class of inhibitors of the family of metalloenzymes carbonic anhydrases (CA, EC 4.2.1.1). Several coumarins display higher affinity and selectivity toward most relevant and druggable CA isoforms. By decorating the natural compound umbelliferone (1) we have identified a new series of coumarin-based compounds demonstrating high CA inhibitory effects with nanomolar affinity for hCA IX and hCA XII isoforms that were considered a target amenable to develop antitumor agents. The most active tested compounds proved to be potent inhibitors with K values equal to that of the well-known inhibitor acetazolamide (AAZ), that lacks selectivity over ubiquitous hCA I and hCA II. As suggested by docking studies the coumarins, that are lacking of the canonical metal binding groups, do not interact with Zinc ion within the catalytic site as found for classical sulfonamide type inhibitors of CAs. Thus, the studied inhibitors might possess a non-classical inhibitory mode of action preventing the carbon dioxide to entry into catalytic cavity and its conversion into bicarbonate ion. Specifically, the most active inhibitor of hCA XII compound 18i (K value of 5.5 nM) and its supposed hydrolytic products could establish a web of H-bond interactions within the enzymatic cavity.
[Mh] Termos MeSH primário: Anidrase Carbônica IX/antagonistas & inibidores
Inibidores da Anidrase Carbônica/farmacologia
Anidrases Carbônicas/metabolismo
Cumarínicos/farmacologia
[Mh] Termos MeSH secundário: Antígenos de Neoplasias/metabolismo
Anidrase Carbônica IX/metabolismo
Inibidores da Anidrase Carbônica/síntese química
Inibidores da Anidrase Carbônica/química
Cumarínicos/síntese química
Cumarínicos/química
Relação Dose-Resposta a Droga
Seres Humanos
Simulação de Acoplamento Molecular
Estrutura Molecular
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Carbonic Anhydrase Inhibitors); 0 (Coumarins); EC 4.2.1.1 (CA9 protein, human); EC 4.2.1.1 (Carbonic Anhydrase IX); EC 4.2.1.1 (Carbonic Anhydrases); EC 4.2.1.1 (carbonic anhydrase XII)
[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:171204
[St] Status:MEDLINE


  6 / 937 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28905987
[Au] Autor:Bryant JL; Gieling RG; Meredith SL; Allen TJ; Walker L; Telfer BA; Supuran CT; Williams KJ; White A
[Ad] Endereço:Division of Diabetes, Endocrinology & Gastroenterology, University of Manchester, Manchester, United Kingdom.
[Ti] Título:Novel carbonic anhydrase IX-targeted therapy enhances the anti-tumour effects of cisplatin in small cell lung cancer.
[So] Source:Int J Cancer;142(1):191-201, 2018 Jan 01.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Small cell lung cancer (SCLC) has an extremely poor prognosis and methods of improving chemotherapeutic intervention are much sought after. A promising approach lies in inhibiting the tumour-associated enzyme, carbonic anhydrase IX (CA IX), which supports tumour cell survival. The aim of this study was to assess the potential of CA IX inhibition using 4-(3'-(3″,5″-dimethylphenyl)ureido)phenyl sulfamate (S4), for the treatment of human SCLC alone and in combination with cisplatin chemotherapy. Treating SCLC cell lines (DMS 79 and COR-L24) with 100 µM S4 reduced viability in vitro and enhanced cell death when combined with 7 µM cisplatin, most prominently under hypoxic conditions (0.1% O ). When either cell line was grown as a xenograft tumour in nude mice, intraperitoneal injection of 50 mg/kg S4 alone and in combination with 3 mg/kg cisplatin led to significantly reduced tumour growth. Combination therapy was superior to single agents and response was greatly accentuated when administering repeated doses of cisplatin in DMS 79 tumours. The mechanism of therapeutic response was investigated in vitro, where S4 treatment increased apoptosis under hypoxic conditions in both DMS 79 and COR-L24 cells. DMS 79 tumours receiving S4 in vivo also displayed increased apoptosis and necrosis. Combining S4 with cisplatin reduced both the area of hypoxia and CA IX-positive cells within tumours and increased necrosis, suggesting hypoxia-specific targeting. This study presents a novel, targeted approach to improving current SCLC therapy via inhibition of CA IX, which enhances apoptosis and significantly inhibits xenograft tumour growth when administered alone and in combination with cisplatin chemotherapy.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Anidrase Carbônica IX/antagonistas & inibidores
Inibidores Enzimáticos/farmacologia
Neoplasias Pulmonares/tratamento farmacológico
Compostos de Fenilureia/farmacologia
Carcinoma de Pequenas Células do Pulmão/tratamento farmacológico
Ácidos Sulfônicos/farmacologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Cisplatino/farmacologia
Sinergismo Farmacológico
Seres Humanos
Camundongos
Camundongos Nus
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-(3'-(3'',5''-dimethylphenyl)ureido)phenyl sulfamate); 0 (Antineoplastic Agents); 0 (Enzyme Inhibitors); 0 (Phenylurea Compounds); 0 (Sulfonic Acids); 9NFU33906Q (sulfamic acid); EC 4.2.1.1 (Carbonic Anhydrase IX); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.31042


  7 / 937 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28965419
[Au] Autor:Ramya PVS; Angapelly S; Angeli A; Digwal CS; Arifuddin M; Babu BN; Supuran CT; Kamal A
[Ad] Endereço:a Department of Medicinal Chemistry , National Institute of Pharmaceutical Education and Research (NIPER) , Hyderabad , India.
[Ti] Título:Discovery of curcumin inspired sulfonamide derivatives as a new class of carbonic anhydrase isoforms I, II, IX, and XII inhibitors.
[So] Source:J Enzyme Inhib Med Chem;32(1):1274-1281, 2017 Dec.
[Is] ISSN:1475-6374
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A series of curcumin inspired sulfonamide derivatives was prepared from various chalcones and 4-sulfamoyl benzaldehyde via Claisen-Schmidt condensation. All new compounds were assayed as inhibitors of four human isoforms of the metalloenzyme carbonic anhydrase (hCA, EC 4.2.1.1) isoforms hCA I, II, IX and XII. Interesting inhibitory activities were observed against all these isoforms. hCA I, an isoform involved in several eye diseases was inhibited moderately with K s in the range of 191.8-904.2 nM, hCA II, an antiglaucoma drug target was highly inhibited by the new sulfonamides, with K s in the range of 0.75-8.8 nM. hCA IX, a tumor-associated isoform involved in cancer progression and metastatic spread was potently inhibited by the new sulfonamides, with K s in the range of 2.3-87.3 nM, whereas hCA XII, and antiglaucoma and anticancer drug target, was inhibited with K s in the range of 6.1-71.8 nM. It is noteworthy that one of the new compounds, 5d, was found to be almost 9 times more selective against hCA II (K = 0.89 nM) over hCA IX and hCA XII, whereas 5e was 3 and 70 times more selective against hCA II (K = 0.75 nM) over hCA IX and hCA XII, respectively.
[Mh] Termos MeSH primário: Inibidores da Anidrase Carbônica/farmacologia
Curcumina/farmacologia
Descoberta de Drogas
Sulfonamidas/farmacologia
[Mh] Termos MeSH secundário: Antígenos de Neoplasias/metabolismo
Anidrase Carbônica I/antagonistas & inibidores
Anidrase Carbônica I/metabolismo
Anidrase Carbônica II/antagonistas & inibidores
Anidrase Carbônica II/metabolismo
Anidrase Carbônica IX/antagonistas & inibidores
Anidrase Carbônica IX/metabolismo
Inibidores da Anidrase Carbônica/síntese química
Inibidores da Anidrase Carbônica/química
Anidrases Carbônicas/metabolismo
Curcumina/síntese química
Curcumina/química
Relação Dose-Resposta a Droga
Seres Humanos
Estrutura Molecular
Relação Estrutura-Atividade
Sulfonamidas/síntese química
Sulfonamidas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Carbonic Anhydrase Inhibitors); 0 (Sulfonamides); EC 4.2.1.- (Carbonic Anhydrase I); EC 4.2.1.- (Carbonic Anhydrase II); EC 4.2.1.1 (CA9 protein, human); EC 4.2.1.1 (Carbonic Anhydrase IX); EC 4.2.1.1 (Carbonic Anhydrases); EC 4.2.1.1 (carbonic anhydrase XII); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171003
[St] Status:MEDLINE
[do] DOI:10.1080/14756366.2017.1380638


  8 / 937 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28962657
[Au] Autor:Zhu L; Guo Y; Wang L; Fan X; Xiong X; Fang K; Xu D
[Ad] Endereço:Department of Ultrasound, Southwest Hospital, Third Military Medical University, 30 Gaotanyan Street, Shapingba District, Chongqing, 400038, China.
[Ti] Título:Construction of ultrasonic nanobubbles carrying CAIX polypeptides to target carcinoma cells derived from various organs.
[So] Source:J Nanobiotechnology;15(1):63, 2017 Sep 29.
[Is] ISSN:1477-3155
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ultrasound molecular imaging is a novel diagnostic approach for tumors, whose key link is the construction of targeted ultrasound contrast agents. However, available targeted ultrasound contrast agents for molecular imaging of tumors are only achieving imaging in blood pool or one type tumor. No targeted ultrasound contrast agents have realized targeted ultrasound molecular imaging of tumor parenchymal cells in a variety of solid tumors so far. Carbonic anhydrase IX (CAIX) is highly expressed on cell membranes of various malignant solid tumors, so it's a good target for ultrasound molecular imaging. Here, targeted nanobubbles carrying CAIX polypeptides for targeted binding to a variety of malignant tumors were constructed, and targeted binding ability and ultrasound imaging effect in different types of tumors were evaluated. RESULTS: The mean diameter of lipid targeted nanobubbles was (503.7 ± 78.47) nm, and the polypeptides evenly distributed on the surfaces of targeted nanobubbles, which possessed the advantages of homogenous particle size, high stability, and good safety. Targeted nanobubbles could gather around CAIX-positive cells (786-O and Hela cells), while they cannot gather around CAIX-negative cells (BxPC-3 cells) in vitro, and the affinity of targeted nanobubbles to CAIX-positive cells were significantly higher than that to CAIX-negative cells (P < 0.05). Peak intensity and duration time of targeted nanobubbles and blank nanobubbles were different in CAIX-positive transplanted tumor tissues in vivo (P < 0.05). Moreover, targeted nanobubbles in CAIX-positive transplanted tumor tissues produced higher peak intensity and longer duration time than those in CAIX-negative transplanted tumor tissues (P < 0.05). Finally, immunofluorescence not only confirmed targeted nanobubbles could pass through blood vessels to enter in tumor tissue spaces, but also clarified imaging differences of targeted nanobubbles in different types of transplanted tumor tissues. CONCLUSIONS: Targeted nanobubbles carrying CAIX polypeptides can specifically enhance ultrasound imaging in CAIX-positive transplanted tumor tissues and could potentially be used in early diagnosis of a variety of solid tumors derived from various organs.
[Mh] Termos MeSH primário: Anidrase Carbônica IX/análise
Carcinoma/diagnóstico por imagem
Imagem Molecular/métodos
Nanocápsulas/química
Peptídeos/química
Ultrassonografia/métodos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Células HeLa
Seres Humanos
Camundongos Endogâmicos BALB C
Tamanho da Partícula
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nanocapsules); 0 (Peptides); EC 4.2.1.1 (Carbonic Anhydrase IX)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171001
[St] Status:MEDLINE
[do] DOI:10.1186/s12951-017-0307-0


  9 / 937 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28940980
[Au] Autor:Angapelly S; Sri Ramya PV; Angeli A; Supuran CT; Arifuddin M
[Ad] Endereço:Department of Medicinal Chemistry, National Institute of Pharmaceutical Education & Research (NIPER), Hyderabad, 500037, India.
[Ti] Título:Sulfocoumarin-, Coumarin-, 4-Sulfamoylphenyl-Bearing Indazole-3-carboxamide Hybrids: Synthesis and Selective Inhibition of Tumor-Associated Carbonic Anhydrase Isozymes IX and XII.
[So] Source:ChemMedChem;12(19):1578-1584, 2017 Oct 09.
[Is] ISSN:1860-7187
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:A series of sulfocoumarin-, coumarin-, and 4-sulfamoylphenyl-bearing indazole-3-carboxamide hybrids were synthesized and investigated as inhibitors of the human carbonic anhydrase (hCA, EC 4.2.1.1) isoforms I and II (cytosolic isozymes), as well as hCA IX and XII (transmembrane, tumor-associated enzymes). Compounds 6 a-g (amide derivatives) and 7 a-h (triazoles) act as "prodrugs", and their hydrolysis products are the de facto CA inhibitors. These compounds displayed sub-micromolar to high-nanomolar inhibitory activity against hCA isoforms IX and XII, which were recently validated as antitumor drug targets. Moreover, no inhibition of the off-target hCA I and II isoforms was observed. Compounds 8 a-f (another set of triazoles) exhibited nanomolar inhibition against hCA isoforms I, II, IX and XII, among which compounds 8 c, 8 d, and 8 f were found to inhibit the tumor-associated hypoxia-induced hCA isoform IX with K values of 1.8, 2.3, and 2.0 nm respectively. Further exploration of these compounds could be useful for the development of novel antitumor agents with selective mechanisms of CA inhibitory action.
[Mh] Termos MeSH primário: Amidas/química
Anidrase Carbônica IX/metabolismo
Inibidores da Anidrase Carbônica/síntese química
Anidrases Carbônicas/metabolismo
Cumarínicos/química
[Mh] Termos MeSH secundário: Amidas/síntese química
Amidas/metabolismo
Sítios de Ligação
Anidrase Carbônica I/antagonistas & inibidores
Anidrase Carbônica I/metabolismo
Anidrase Carbônica II/antagonistas & inibidores
Anidrase Carbônica II/metabolismo
Anidrase Carbônica IX/antagonistas & inibidores
Inibidores da Anidrase Carbônica/química
Inibidores da Anidrase Carbônica/metabolismo
Anidrases Carbônicas/química
Domínio Catalítico
Cumarínicos/síntese química
Cumarínicos/metabolismo
Seres Humanos
Indazóis/química
Concentração Inibidora 50
Isoenzimas/antagonistas & inibidores
Isoenzimas/metabolismo
Simulação de Dinâmica Molecular
Neoplasias/enzimologia
Neoplasias/patologia
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amides); 0 (Carbonic Anhydrase Inhibitors); 0 (Coumarins); 0 (Indazoles); 0 (Isoenzymes); EC 4.2.1.- (Carbonic Anhydrase I); EC 4.2.1.- (Carbonic Anhydrase II); EC 4.2.1.1 (Carbonic Anhydrase IX); EC 4.2.1.1 (Carbonic Anhydrases); EC 4.2.1.1 (carbonic anhydrase XII)
[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:170924
[St] Status:MEDLINE
[do] DOI:10.1002/cmdc.201700446


  10 / 937 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28891338
[Au] Autor:Kumar R; Sharma V; Bua S; Supuran CT; Sharma PK
[Ad] Endereço:a Department of Chemistry , Kurukshetra University , Kurukshetra , India.
[Ti] Título:Synthesis and biological evaluation of benzenesulphonamide-bearing 1,4,5-trisubstituted-1,2,3-triazoles possessing human carbonic anhydrase I, II, IV, and IX inhibitory activity.
[So] Source:J Enzyme Inhib Med Chem;32(1):1187-1194, 2017 Dec.
[Is] ISSN:1475-6374
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A library of benzenesulphonamides incorporating 1,2,3-triazole rings functionalised with ester, carboxylic acid, carboxamide, carboxyhydrazide, and hydroxymethyl moieties were synthesised. The carbonic anhydrase (CAs, EC 4.2.1.1) inhibitory activity of the new compounds was assessed against four human (h) isoforms, hCA I, hCA II, hCA IV, and hCA IX. Among them, hCA II and IV are anti-glaucoma drug targets, being involved in aqueous humour secretion within the eye. hCA I was inhibited with Ki's ranging between 8.3 nM and 0.8737 µM. hCA II, the physiologically dominant cytosolic isoform, was excellently inhibited by these compounds, with Ki's in the range of 1.6-9.4 nM, whereas hCA IV was effectively inhibited by most of them, with Ki's in the range of 1.4-55.3 nM. Thirteen of the twenty sulphonamides were found to be excellent inhibitors of tumour associated hCA IX with Ki's ≤ 9.5 nM. Many of the new compounds reported here showed low nM inhibitory action against hCA II, IV, and IX, isoforms involved in glaucoma and some tumours, making them interesting candidates for further medicinal chemistry/pharmacologic studies.
[Mh] Termos MeSH primário: Inibidores da Anidrase Carbônica/farmacologia
Sulfonamidas/farmacologia
Triazóis/farmacologia
[Mh] Termos MeSH secundário: Anidrase Carbônica I/antagonistas & inibidores
Anidrase Carbônica I/metabolismo
Anidrase Carbônica II/antagonistas & inibidores
Anidrase Carbônica II/metabolismo
Anidrase Carbônica IV/antagonistas & inibidores
Anidrase Carbônica IV/metabolismo
Anidrase Carbônica IX/antagonistas & inibidores
Anidrase Carbônica IX/metabolismo
Inibidores da Anidrase Carbônica/síntese química
Inibidores da Anidrase Carbônica/química
Relação Dose-Resposta a Droga
Seres Humanos
Estrutura Molecular
Relação Estrutura-Atividade
Sulfonamidas/síntese química
Sulfonamidas/química
Triazóis/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carbonic Anhydrase Inhibitors); 0 (Sulfonamides); 0 (Triazoles); 98-10-2 (benzenesulfonamide); EC 4.2.1.- (Carbonic Anhydrase I); EC 4.2.1.- (Carbonic Anhydrase II); EC 4.2.1.- (Carbonic Anhydrase IV); EC 4.2.1.1 (Carbonic Anhydrase IX)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170912
[St] Status:MEDLINE
[do] DOI:10.1080/14756366.2017.1367775



página 1 de 94 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