Base de dados : MEDLINE
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  1 / 1977 MEDLINE  
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[PMID]:28464919
[Au] Autor:Toth C; Funke S; Nitsche V; Liverts A; Zlachevska V; Gasis M; Wiek C; Hanenberg H; Mahotka C; Schirmacher P; Heikaus S
[Ad] Endereço:Institute of Pathology, Heinrich Heine University Hospital, Medical Faculty, Moorenstrasse 5, 40225, Düsseldorf, Germany. csaba.toth@med.uni-heidelberg.de.
[Ti] Título:The role of apoptosis repressor with a CARD domain (ARC) in the therapeutic resistance of renal cell carcinoma (RCC): the crucial role of ARC in the inhibition of extrinsic and intrinsic apoptotic signalling.
[So] Source:Cell Commun Signal;15(1):16, 2017 May 02.
[Is] ISSN:1478-811X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Renal cell carcinomas (RCCs) display broad resistance against conventional radio- and chemotherapies, which is due at least in part to impairments in both extrinsic and intrinsic apoptotic pathways. One important anti-apoptotic factor that is strongly overexpressed in RCCs and known to inhibit both apoptotic pathways is ARC (apoptosis repressor with a CARD domain). METHODS: Expression and subcellular distribution of ARC in RCC tissue samples and RCC cell lines were determined by immunohistochemistry and fluorescent immunohistochemistry, respectively. Extrinsic and intrinsic apoptosis signalling were induced by TRAIL (TNF-related apoptosis-inducing ligand), ABT-263 or topotecan. ARC knock-down was performed in clearCa-12 cells using lentiviral transduction of pGIPZ. shRNAmir constructs. Extrinsic respectively intrinsic apoptosis were induced by TRAIL (TNF-related apoptosis-inducing ligand), ABT263 or topotecan. Potential synergistic effects were tested by pre-treatment with topotecan and subsequent treatment with ABT263. Activation of different caspases and mitochondrial depolarisation (JC-1 staining) were analysed by flow cytometry. Protein expression of Bcl-2 family members and ARC in RCC cell lines was measured by Western blotting. Statistical analysis was performed by Student's t-test. RESULTS: Regarding the extrinsic pathway, ARC knockdown strongly enhanced TRAIL-induced apoptosis by increasing the activation level of caspase-8. Regarding the intrinsic pathway, ARC, which was only weakly expressed in the nuclei of RCCs in vivo, exerted its anti-apoptotic effect by impairing mitochondrial activation rather than inhibiting p53. Topotecan- and ABT-263-induced apoptosis was strongly enhanced following ARC knockdown in RCC cell lines. In addition, topotecan pre-treatment enhanced ABT-263-induced apoptosis and this effect was amplified in ARC-knockdown cells. CONCLUSION: Taken together, our results are the first to demonstrate the importance of ARC protein in the inhibition of both the extrinsic and intrinsic pathways of apoptosis in RCCs. In this context, ARC cooperates with anti-apoptotic Bcl-2 family members to exert its strong anti-apoptotic effects and is therefore an important factor not only in the therapeutic resistance but also in future therapy strategies (i.e., Bcl-2 inhibitors) in RCC. In sum, targeting of ARC may enhance the therapeutic response in combination therapy protocols.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/metabolismo
Apoptose/efeitos dos fármacos
Carcinoma de Células Renais/patologia
Resistência a Medicamentos Antineoplásicos
Neoplasias Renais/patologia
Proteínas Musculares/metabolismo
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular/efeitos dos fármacos
Compostos de Anilina/farmacologia
Proteínas Reguladoras de Apoptose/deficiência
Proteínas Reguladoras de Apoptose/genética
Linhagem Celular Tumoral
Núcleo Celular/efeitos dos fármacos
Núcleo Celular/metabolismo
Citoplasma/efeitos dos fármacos
Citoplasma/metabolismo
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Seres Humanos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/patologia
Terapia de Alvo Molecular
Proteínas Musculares/deficiência
Proteínas Musculares/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Sulfonamidas/farmacologia
Topotecan/farmacologia
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (Apoptosis Regulatory Proteins); 0 (Muscle Proteins); 0 (NOL3 protein, human); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Sulfonamides); 0 (Tumor Suppressor Protein p53); 7M7YKX2N15 (Topotecan); XKJ5VVK2WD (navitoclax)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12964-017-0170-5


  2 / 1977 MEDLINE  
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[PMID]:29390553
[Au] Autor:Ryu H; Song IC; Choi YS; Yun HJ; Jo DY; Kim JM; Ko YB; Lee HJ
[Ad] Endereço:Department of Internal Medicine.
[Ti] Título:ERCC1 expression status predicts the response and survival of patients with metastatic or recurrent cervical cancer treated via platinum-based chemotherapy.
[So] Source:Medicine (Baltimore);96(51):e9402, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The deoxyribonucleic acid (DNA) repair gene encoding the excision-repair cross-complementation group 1 (ERCC1) protein is known to predict the response to platinum-based chemotherapy. Our aim was to explore whether ERCC1 expression predicted tumor response and survival in patients with recurrent or metastatic cervical cancer treated via platinum-based chemotherapy. We analyzed 32 such patients. ERCC1 expression was assessed immunohistochemically in pretreatment biopsy samples. Of the 32 patients, 13 (40.6%) were ERCC1 high. ERCC1-low patients exhibited a significantly higher response rate (73.7%) than did others (15.4%). The median progression-free survival differed significantly by ERCC1 status, being 135 days in ERCC1-high and 242 days in ERCC1-low patients (hazard ratio, 2.428; 95% confidence interval, 1.145-5.148, P = .032). Overall survival was significantly longer in ERCC1-low (617 days) than in ERCC1-high (320 days) patients (hazard ratio, 2.322; 95% confidence interval, 1.051-5.29; P = .037). Thus, pretreatment ERCC1 expression status can be used to predict tumor response and survival of patients with recurrent or metastatic uterine cervical cancer receiving platinum-based chemotherapy.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Biomarcadores Tumorais/metabolismo
Carcinoma/tratamento farmacológico
Proteínas de Ligação a DNA/metabolismo
Endonucleases/metabolismo
Neoplasias do Colo do Útero/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Antineoplásicos/uso terapêutico
Carboplatina/uso terapêutico
Carcinoma/metabolismo
Carcinoma/mortalidade
Carcinoma/secundário
Cisplatino/uso terapêutico
Feminino
Fluoruracila/uso terapêutico
Seguimentos
Seres Humanos
Imuno-Histoquímica
Meia-Idade
Recidiva Local de Neoplasia/tratamento farmacológico
Recidiva Local de Neoplasia/metabolismo
Recidiva Local de Neoplasia/mortalidade
Paclitaxel/uso terapêutico
Neoplasias Pélvicas/patologia
Estudos Retrospectivos
Análise de Sobrevida
Topotecan/uso terapêutico
Resultado do Tratamento
Neoplasias do Colo do Útero/metabolismo
Neoplasias do Colo do Útero/mortalidade
Neoplasias do Colo do Útero/secundário
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biomarkers, Tumor); 0 (DNA-Binding Proteins); 7M7YKX2N15 (Topotecan); BG3F62OND5 (Carboplatin); EC 3.1.- (ERCC1 protein, human); EC 3.1.- (Endonucleases); P88XT4IS4D (Paclitaxel); Q20Q21Q62J (Cisplatin); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009402


  3 / 1977 MEDLINE  
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[PMID]:28448304
[Au] Autor:Rosen VM; Guerra I; McCormack M; Nogueira-Rodrigues A; Sasse A; Munk VC; Shang A
[Ad] Endereço:*Optum, Eden Prairie, MN; †Mapi Group, Uxbridge; and ‡University College London Hospitals, London, UK; §Federal University, Belo Horizonte; and ∥State University of Campinas, Campinas, Brazil; and ¶F. Hoffmann-La Roche Ltd, Basel, Switzerland.
[Ti] Título:Systematic Review and Network Meta-Analysis of Bevacizumab Plus First-Line Topotecan-Paclitaxel or Cisplatin-Paclitaxel Versus Non-Bevacizumab-Containing Therapies in Persistent, Recurrent, or Metastatic Cervical Cancer.
[So] Source:Int J Gynecol Cancer;27(6):1237-1246, 2017 Jul.
[Is] ISSN:1525-1438
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Despite advances in cervical cancer prevention and diagnosis, outcomes for patients given a diagnosis of advanced and recurrent disease are poor. In the GOG240 trial, the addition of bevacizumab to paclitaxel-topotecan or paclitaxel-cisplatin has been shown to prolong survival compared with paclitaxel-topotecan or paclitaxel-cisplatin in patients with persistent, recurrent, or metastatic disease. However, standards of care vary between regions and countries. The purpose of this systematic review and network meta-analysis was to enable a comparison between bevacizumab + chemotherapy with multiple monotherapy or combination chemotherapy regimens in the treatment for women with advanced, recurrent, or persistent cervical cancer. METHODS/MATERIALS: A systematic literature review was conducted to identify randomized or nonrandomized controlled trials of patients with recurrent, persistent, or metastatic cervical cancer published in English from 1999 to 2015. A feasibility study was performed to assess the heterogeneity of the trials, and a network meta-analysis was conducted. Fixed- and random-effects models were fitted to calculate the hazard ratio for overall survival (OS) for all pairwise comparisons and ranking of all interventions. RESULTS: Twenty-three studies (19 trials) met inclusion criteria and were included in the review. Sample sizes ranged from 69 to 452, and median patient age ranged from 45 to 53 years. There was a trend toward prolonged OS with cisplatin-paclitaxel-bevacizumab and topotecan-paclitaxel-bevacizumab compared with all non-bevacizumab-containing therapies. Cisplatin-paclitaxel-bevacizumab had the highest probability of being the most efficacious compared with all regimens (68.1%), and cisplatin monotherapy had the lowest (0%). CONCLUSIONS: The results of this network meta-analysis show that bevacizumab in combination with paclitaxel-topotecan or paclitaxel-cisplatin is likely to prolong OS over other non-bevacizumab-containing chemotherapies (eg, paclitaxel-carboplatin), which were not included in the GOG240 trial. In patients with advanced, persistent, and recurrent cervical cancer, cisplatin-paclitaxel-bevacizumab and topotecan-paclitaxel-bevacizumab showed the highest efficacy in all regimens investigated in this analysis.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Recidiva Local de Neoplasia/tratamento farmacológico
Neoplasias do Colo do Útero/tratamento farmacológico
[Mh] Termos MeSH secundário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Bevacizumab/administração & dosagem
Cisplatino/administração & dosagem
Feminino
Seres Humanos
Metástase Neoplásica
Recidiva Local de Neoplasia/patologia
Paclitaxel/administração & dosagem
Topotecan/administração & dosagem
Neoplasias do Colo do Útero/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
2S9ZZM9Q9V (Bevacizumab); 7M7YKX2N15 (Topotecan); P88XT4IS4D (Paclitaxel); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1097/IGC.0000000000001000


  4 / 1977 MEDLINE  
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[PMID]:28927790
[Au] Autor:Yang CJ; Song ZL; Goto M; Hsu PL; Zhang XS; Yang QR; Liu YQ; Wang MJ; Morris-Natschke SL; Shang XF; Lee KH
[Ad] Endereço:School of Pharmacy, Lanzhou University, Lanzhou 730000, PR China.
[Ti] Título:Design, semisynthesis and potent cytotoxic activity of novel 10-fluorocamptothecin derivatives.
[So] Source:Bioorg Med Chem Lett;27(20):4694-4697, 2017 10 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fluorination is a well-known strategy for improving the bioavailability of bioactive molecules in the lead optimization phase of drug discovery projects. In an attempt to improve the antitumor activity of camptothecins (CPTs), novel 10-fluoro-CPT derivatives were designed, synthesized and evaluated for cytotoxicity against five human cancer cell lines (A-549, MDA-MB-231, KB, KB-VIN and MCF-7). All of the derivatives showed more potent in vitro cytotoxic activity than the clinical CPT-derived drug irinotecan against the tumor cell lines tested, and most of them showed comparable or superior potency to topotecan. Remarkably, compounds 16b (IC , 67.0nM) and 19b (IC , 99.2nM) displayed the highest cytotoxicity against the multidrug-resistant (MDR) KB-VIN cell line and merit further development as preclinical drug candidates for treating cancer, including MDR phenotype. Our study suggested that incorporation of a fluorine atom into position 10 of CPT is an effective method for discovering new potent CPT derivatives.
[Mh] Termos MeSH primário: Antineoplásicos/síntese química
Antineoplásicos/farmacologia
Camptotecina/análogos & derivados
Camptotecina/farmacologia
Desenho de Drogas
[Mh] Termos MeSH secundário: Antineoplásicos/química
Camptotecina/síntese química
Linhagem Celular Tumoral
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Ensaios de Seleção de Medicamentos Antitumorais
Flúor/química
Seres Humanos
Relação Estrutura-Atividade
Topotecan/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 284SYP0193 (Fluorine); 7M7YKX2N15 (Topotecan); XT3Z54Z28A (Camptothecin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE


  5 / 1977 MEDLINE  
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[PMID]:28825853
[Au] Autor:Pignata S; Scambia G; Bologna A; Signoriello S; Vergote IB; Wagner U; Lorusso D; Murgia V; Sorio R; Ferrandina G; Sacco C; Cormio G; Breda E; Cinieri S; Natale D; Mangili G; Pisano C; Cecere SC; Di Napoli M; Salutari V; Raspagliesi F; Arenare L; Bergamini A; Bryce J; Daniele G; Piccirillo MC; Gallo C; Perrone F
[Ad] Endereço:Sandro Pignata, Carmela Pisano, Sabrina Chiara Cecere, Marilena Di Napoli, Laura Arenare, Alice Bergamini, Jane Bryce, Gennaro Daniele, Maria Carmela Piccirillo, and Francesco Perrone, Istituto Nazionale per lo Studio e la Cura dei Tumori-Fondazione G. Pascale, IRCCS; Simona Signoriello and Ciro Gal
[Ti] Título:Randomized Controlled Trial Testing the Efficacy of Platinum-Free Interval Prolongation in Advanced Ovarian Cancer: The MITO-8, MaNGO, BGOG-Ov1, AGO-Ovar2.16, ENGOT-Ov1, GCIG Study.
[So] Source:J Clin Oncol;35(29):3347-3353, 2017 Oct 10.
[Is] ISSN:1527-7755
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose Platinum-based chemotherapy (PBC) for patients with progressing ovarian cancer (OC) is more effective with a longer time interval from previous platinum treatment (platinum-free interval [PFI]). In 1999, it was hypothesized that prolonging PFI with single-agent non-PBC (NPBC) may offer a strategy to improve overall outcome. MITO-8 aimed to verify this hypothesis commonly used in clinical practice although it has not been prospectively tested. Methods MITO-8 is an open-label, prospective, randomized, superiority trial. Patients with OC who experienced disease progression 6 to 12 months after their last platinum treatment were randomly assigned 1:1 to the experimental sequence of NPBC followed by PBC at subsequent relapse or the standard reverse treatment sequence. Overall survival (OS) was the primary end point. Results Two hundred fifteen patients were enrolled (standard arm [n = 108]; experimental arm [n = 107]). The trial ended before planned because of slow enrollment. PFI was prolonged in the experimental arm (median, 7.8 v 0.01 months). There was no OS benefit in the experimental arm (median, 21.8 v 24.5 months; hazard ratio, 1.38; 95% CI, 0.99 to 1.94; P = .06). Progression-free survival after the sequence was significantly shorter in the experimental arm (median, 12.8 v 16.4 months; hazard ratio, 1.41; 95% CI, 1.04 to 1.92; P = .025). Global quality-of-life change after three cycles was worse in the experimental arm. Slight differences were observed in the incidence of adverse effects. Conclusion MITO-8 supports the recommendation that PBC not be delayed in favor of an NPBC in patients with partially platinum-sensitive OC. PBC should be used as a control arm in future trials of new drugs in this setting.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Neoplasias Ovarianas/tratamento farmacológico
[Mh] Termos MeSH secundário: Idoso
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Carboplatina/administração & dosagem
Desoxicitidina/administração & dosagem
Desoxicitidina/análogos & derivados
Dioxóis/administração & dosagem
Progressão da Doença
Intervalo Livre de Doença
Doxorrubicina/administração & dosagem
Doxorrubicina/análogos & derivados
Esquema de Medicação
Término Precoce de Ensaios Clínicos
Europa (Continente)
Feminino
Seres Humanos
Estimativa de Kaplan-Meier
Meia-Idade
Recidiva Local de Neoplasia
Neoplasias Ovarianas/mortalidade
Neoplasias Ovarianas/patologia
Paclitaxel/administração & dosagem
Polietilenoglicóis/administração & dosagem
Estudos Prospectivos
Tetra-Hidroisoquinolinas/administração & dosagem
Fatores de Tempo
Topotecan/administração & dosagem
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Dioxoles); 0 (Tetrahydroisoquinolines); 0 (liposomal doxorubicin); 0W860991D6 (Deoxycytidine); 30IQX730WE (Polyethylene Glycols); 7M7YKX2N15 (Topotecan); 80168379AG (Doxorubicin); B76N6SBZ8R (gemcitabine); BG3F62OND5 (Carboplatin); ID0YZQ2TCP (trabectedin); P88XT4IS4D (Paclitaxel)
[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:170822
[St] Status:MEDLINE
[do] DOI:10.1200/JCO.2017.73.4293


  6 / 1977 MEDLINE  
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[PMID]:28797568
[Au] Autor:Koosha F; Neshasteh-Riz A; Takavar A; Eyvazzadeh N; Mazaheri Z; Eynali S; Mousavi M
[Ad] Endereço:Department of Medical Physics and Biomedical Engineering, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Radiation Biology Research Center, Iran University of Medical Sciences, Tehran, Iran.
[Ti] Título:The combination of A-966492 and Topotecan for effective radiosensitization on glioblastoma spheroids.
[So] Source:Biochem Biophys Res Commun;491(4):1092-1097, 2017 Sep 30.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Radiotherapy is one of the modalities in the treatment of glioblastoma patients, but glioma tumors are resistant to radiation and also chemotherapy drugs. Thus, researchers are investigating drugs which have radiosensitization capabilities in order to improve radiotherapy. PARP enzymes and topoisomerase I enzymes have a critical role in repairing DNA damage in tumor cells. Thus, inhibiting activity of these enzymes helps stop DNA damage repair and increase DSB lethal damages. In the current study, we investigated the combination of TPT as a topoisomerase I inhibitor, and A-966492 as a novel PARP inhibitor for further radiosensitization. U87MG cells (a human glioblastoma cell line) were cultured in Poly-Hema coated flasks to reach 300 µm-diameter spheroids. Treatments were accomplished by using non-toxic concentrations of A-966492 and Topotecan. The surviving fraction of treated cells was determined by clonogenic assay after treatment with drugs and 6 MV X-ray. The γ-H2AX expression was measured by an immunofluorescence staining method to examine the influence of A-966492, TPT and radiation on the induction of double stranded DNA breaks. Treatments using the A-966492 drug were conducted in concentration of 1 µM. Combining A-966492 and TPT with radiation yielded enhanced cell killing, as demonstrated by a sensitizer enhancement ratio at 50% survival (SER ) 1.39 and 1.16 respectively. Radio- and chemo-sensitization was further enhanced when A-966492 was combined with both X-ray and TPT, with SER of 1.53. Also γ-H2AX expression was higher in the group treated with a combination of drugs and radiation. A-966492 is an effective PARP inhibitor and has significant radio-sensitivity on U87MG spheroids. By accumulating cells in the S phase and by inhibiting the DNA damage repair, TPT enhanced radio-sensitivity. A-966492 combined with TPT as a topoisomerase I inhibitor had additive radio-sensitizing effects. As a result, applying PARP and topoisomerase I inhibitors can be a suitable strategy for improving radiotherapy in clinics.
[Mh] Termos MeSH primário: Benzimidazóis/farmacologia
Glioblastoma/tratamento farmacológico
Esferoides Celulares/efeitos dos fármacos
Inibidores da Topoisomerase I/farmacologia
Topotecan/farmacologia
[Mh] Termos MeSH secundário: Benzimidazóis/administração & dosagem
Linhagem Celular Tumoral
DNA Topoisomerases Tipo I/metabolismo
Seres Humanos
Tolerância a Radiação/efeitos dos fármacos
Relação Estrutura-Atividade
Inibidores da Topoisomerase I/administração & dosagem
Topotecan/administração & dosagem
Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(2-fluoro-4-(pyrrolidin-2-yl)phenyl)-1H-benzimidazole-4-carboxamide); 0 (Benzimidazoles); 0 (Topoisomerase I Inhibitors); 7M7YKX2N15 (Topotecan); EC 5.99.1.2 (DNA Topoisomerases, Type I)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE


  7 / 1977 MEDLINE  
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[PMID]:28643177
[Au] Autor:Murai J
[Ad] Endereço:Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA. junko.murai@nih.gov.
[Ti] Título:Targeting DNA repair and replication stress in the treatment of ovarian cancer.
[So] Source:Int J Clin Oncol;22(4):619-628, 2017 Aug.
[Is] ISSN:1437-7772
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Approximately half of high-grade serous epithelial ovarian cancers incur alterations in genes of homologous recombination (BRCA1, BRCA2, RAD51C, Fanconi anemia genes), and the rest incur alterations in other DNA repair pathways at high frequencies. Such cancer-specific gene alterations can confer selective sensitivity to DNA damaging agents such as cisplatin and carboplatin, topotecan, etoposide, doxorubicin, and gemcitabine. Originally presumed to inhibit DNA repair, PARP inhibitors that have recently been approved by the FDA for the treatment of advanced ovarian cancer also act as DNA damaging agents by inducing PARP-DNA complexes. These DNA damaging agents induce different types of DNA lesions that require various DNA repair genes for the repair, but commonly induce replication fork slowing or stalling, also referred to as replication stress. Replication stress activates DNA repair checkpoint proteins (ATR, CHK1), which prevent further DNA damage. Hence, targeting DNA repair genes or DNA repair checkpoint genes augments the anti-tumor activity of DNA damaging agents. This review describes the rational basis for using DNA repair and DNA repair checkpoint inhibitors as single agents. The review also presents the strategies combining these inhibitors with DNA damaging agents for ovarian cancer therapy based on specific gene alterations.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Reparo do DNA/efeitos dos fármacos
Neoplasias Ovarianas/tratamento farmacológico
Neoplasias Ovarianas/genética
Inibidores de Poli(ADP-Ribose) Polimerases/farmacologia
[Mh] Termos MeSH secundário: Antineoplásicos/uso terapêutico
Proteína BRCA1/genética
Proteína BRCA2/genética
Ciclo Celular/efeitos dos fármacos
Ciclo Celular/genética
Cisplatino/uso terapêutico
Dano ao DNA/efeitos dos fármacos
Replicação do DNA/efeitos dos fármacos
Proteínas de Ligação a DNA/genética
Feminino
Seres Humanos
Terapia de Alvo Molecular/métodos
Neoplasias Epiteliais e Glandulares/tratamento farmacológico
Neoplasias Epiteliais e Glandulares/genética
Neoplasias Epiteliais e Glandulares/patologia
Neoplasias Ovarianas/patologia
Inibidores de Poli(ADP-Ribose) Polimerases/uso terapêutico
Topotecan/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (BRCA1 Protein); 0 (BRCA1 protein, human); 0 (BRCA2 Protein); 0 (BRCA2 protein, human); 0 (DNA-Binding Proteins); 0 (Poly(ADP-ribose) Polymerase Inhibitors); 0 (RAD51C protein, human); 7M7YKX2N15 (Topotecan); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170624
[St] Status:MEDLINE
[do] DOI:10.1007/s10147-017-1145-7


  8 / 1977 MEDLINE  
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[PMID]:28625313
[Au] Autor:Pautier P; Kalbacher E; de la Motte Rouge T; Bonnetain F; Lesoin A
[Ad] Endereço:Département de médecine oncologique, Gustave-Roussy, Villejuif, France; Service d'oncologie médicale, CHRU de Besançon, France. Electronic address: Patricia.PAUTIER@gustaveroussy.fr.
[Ti] Título:Cancer de l'ovaire : la rechute précoce..
[So] Source:Bull Cancer;104 Suppl 1:S32-S38, 2017 May.
[Is] ISSN:1769-6917
[Cp] País de publicação:France
[La] Idioma:fre
[Ab] Resumo:OVARIAN CANCER: EARLY RELAPSE: Early relapse (primary or secondary) is defined by relapse of disease less than 6 months before the last infusion of chemotherapy (with a platinum compound). There is no carcinological surgical indication. Disease should be treated with a non-platinum single agent (pegylated liposomal doxorubicin, weekly paclitaxel, gemcitabine or topotecan). Bevacizumab can be added if patients have not already received it (level of proof 1, grade A).
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Recidiva Local de Neoplasia/tratamento farmacológico
Neoplasias Ovarianas/tratamento farmacológico
[Mh] Termos MeSH secundário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Bevacizumab/uso terapêutico
Desoxicitidina/análogos & derivados
Desoxicitidina/uso terapêutico
Doxorrubicina/uso terapêutico
Feminino
Seres Humanos
Paclitaxel/uso terapêutico
Topotecan/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0W860991D6 (Deoxycytidine); 2S9ZZM9Q9V (Bevacizumab); 7M7YKX2N15 (Topotecan); 80168379AG (Doxorubicin); B76N6SBZ8R (gemcitabine); P88XT4IS4D (Paclitaxel)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE


  9 / 1977 MEDLINE  
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[PMID]:28545735
[Au] Autor:Francis JH; Iyer S; Gobin YP; Brodie SE; Abramson DH
[Ad] Endereço:Ophthalmic Oncology Service, Memorial Sloan Kettering Cancer Center, New York, New York; Department of Ophthalmology, Weill-Cornell Medical Center, New York, New York. Electronic address: francij1@mskcc.org.
[Ti] Título:Retinoblastoma Vitreous Seed Clouds (Class 3): A Comparison of Treatment with Ophthalmic Artery Chemosurgery with or without Intravitreous and Periocular Chemotherapy.
[So] Source:Ophthalmology;124(10):1548-1555, 2017 Oct.
[Is] ISSN:1549-4713
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To compare the efficacy and toxicity of treating class 3 retinoblastoma vitreous seeds with ophthalmic artery chemosurgery (OAC) alone versus OAC with intravitreous chemotherapy. DESIGN: Retrospective cohort study. PARTICIPANTS: Forty eyes containing clouds (class 3 vitreous seeds) of 40 retinoblastoma patients (19 treated with OAC alone and 21 treated with OAC plus intravitreous and periocular chemotherapy). METHODS: Ocular survival, disease-free survival and time to regression of seeds were estimated with Kaplan-Meier estimates. Ocular toxicity was evaluated by clinical findings and electroretinography: 30-Hz flicker responses were compared at baseline and last follow-up visit. Continuous variables were compared with Student t test, and categorical variables were compared with the Fisher exact test. MAIN OUTCOME MEASURES: Ocular survival, disease-free survival, and time to regression of seeds. RESULTS: There were no disease- or treatment-related deaths and no patient demonstrated externalization of tumor or metastatic disease. There was no significant difference in the age, laterality, disease, or disease status (treatment naïve vs. previously treated) between the 2 groups. The time to regression of seeds was significantly shorter for eyes treated with OAC plus intravitreous chemotherapy (5.7 months) compared with eyes treated with OAC alone (14.6 months; P < 0.001). The 18-month Kaplan-Meier estimates of disease-free survival were significantly worse for the OAC alone group: 67.1% (95% confidence interval, 40.9%-83.6%) versus 94.1% (95% confidence interval, 65%-99.1%) for the OAC plus intravitreous chemotherapy group (P = 0.05). The 36-month Kaplan-Meier estimates of ocular survival were 83.3% (95% confidence interval, 56.7%-94.3%) for the OAC alone group and 100% for the OAC plus intravitreous chemotherapy group (P = 0.16). The mean change in electroretinography responses was not significantly different between groups, decreasing by 11 µV for the OAC alone group and 22 µV for the OAC plus intravitreous chemotherapy group (P = 0.4). CONCLUSIONS: Treating vitreous seed clouds with OAC and intravitreous and periocular chemotherapy, compared with OAC alone, resulted in a shorter time to regression and was associated with fewer recurrences requiring additional treatment and fewer enucleations. The toxicity to the retina does not seem to be significantly worse in the OAC plus intravitreous chemotherapy group.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Inoculação de Neoplasia
Artéria Oftálmica/efeitos dos fármacos
Neoplasias da Retina/tratamento farmacológico
Retinoblastoma/tratamento farmacológico
Corpo Vítreo/patologia
[Mh] Termos MeSH secundário: Carboplatina/administração & dosagem
Pré-Escolar
Estudos de Coortes
Intervalo Livre de Doença
Eletrorretinografia
Feminino
Seres Humanos
Infusões Intra-Arteriais
Injeções Intravítreas
Estimativa de Kaplan-Meier
Masculino
Melfalan/administração & dosagem
Retina/efeitos dos fármacos
Retina/fisiologia
Neoplasias da Retina/patologia
Retinoblastoma/patologia
Estudos Retrospectivos
Topotecan/administração & dosagem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
7M7YKX2N15 (Topotecan); BG3F62OND5 (Carboplatin); Q41OR9510P (Melphalan)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE


  10 / 1977 MEDLINE  
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[PMID]:28513496
[Au] Autor:Rishi P; Sharma T; Sharma M; Maitray A; Dhami A; Aggarwal V; Munusamy S; Ravikumar R; Ramamurthy S
[Ad] Endereço:Shri Bhagwan Mahavir Vitreoretinal Services, Sankara Nethralya, Chennai, Tamil Nadu, India.
[Ti] Título:Intra-arterial chemotherapy for retinoblastoma: Two-year results from tertiary eye-care center in India.
[So] Source:Indian J Ophthalmol;65(4):311-315, 2017 Apr.
[Is] ISSN:1998-3689
[Cp] País de publicação:India
[La] Idioma:eng
[Ab] Resumo:AIM: The aim of this study is to describe treatment outcomes and complications of selective intra-arterial chemotherapy (IAC) for intraocular retinoblastoma (RB). MATERIALS AND METHODS: A retrospective, interventional series of 10 eyes with RB which underwent IAC using melphalan (5 mg/7.5 mg) and topotecan (1 mg), or melphalan (5 mg/7.5 mg) alone. Treatment outcomes were evaluated in terms of tumor control, vitreous seeds (VS) and subretinal seeds (SRS) control, and globe salvage rates. RESULTS: Ten eyes of 10 patients underwent 38 IAC sessions (mean = 3.8; median = 4; range = 3-5 sessions). Following IAC, complete regression of main tumor was seen in 9 eyes (90%) and partial regression in 1 (10%). All four eyes with SRS showed complete regression (100%). Of 5 eyes with VS, 3 eyes (60%) showed complete regression, 1 eye (20%) showed relapse, while 1 eye (20%) showed no response. Globe salvage was achieved in 8 of 10 eyes (80%). Complications included transient ophthalmic artery narrowing (n = 2), branched retinal vein occlusion (n = 1), forehead skin pigmentation (n = 1), and vitreous hemorrhage (n = 2). There was no case of stroke, hemiplegia, metastasis, or death. Transient hematological changes included relative pancytopenia (n = 4), relative leukopenia (n = 5), and relative thrombocytopenia (n = 4). Mean follow-up was 26 months (median = 28, range = 13-36) from the initiation of first IAC. CONCLUSIONS: IAC is an effective therapy for globe preservation in eyes with intraocular RB, in the setting of a developing country like India. Larger studies with longer follow-up are required to validate these results.
[Mh] Termos MeSH primário: Melfalan/administração & dosagem
Neoplasias da Retina/tratamento farmacológico
Retinoblastoma/tratamento farmacológico
Topotecan/administração & dosagem
[Mh] Termos MeSH secundário: Antineoplásicos Alquilantes/administração & dosagem
Pré-Escolar
Relação Dose-Resposta a Droga
Feminino
Seguimentos
Seres Humanos
Incidência
Índia/epidemiologia
Lactente
Injeções Intra-Arteriais
Masculino
Neoplasias da Retina/diagnóstico
Neoplasias da Retina/epidemiologia
Retinoblastoma/diagnóstico
Retinoblastoma/epidemiologia
Estudos Retrospectivos
Fatores de Tempo
Inibidores da Topoisomerase I/administração & dosagem
Resultado do Tratamento
Ultrassonografia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (Topoisomerase I Inhibitors); 7M7YKX2N15 (Topotecan); Q41OR9510P (Melphalan)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170518
[St] Status:MEDLINE
[do] DOI:10.4103/ijo.IJO_843_16



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