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[PMID]:29309720
[Au] Autor:Abdel-Rahman O; Elsayed Z; Mohamed H; Eltobgy M
[Ad] Endereço:Clinical Oncology, Faculty of Medicine, Ain Shams University, Lofty Elsayed Street, Cairo, Egypt, 11335.
[Ti] Título:Radical multimodality therapy for malignant pleural mesothelioma.
[So] Source:Cochrane Database Syst Rev;1:CD012605, 2018 Jan 08.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Malignant pleural mesothelioma is an almost always fatal tumour, for which palliative platinum-based chemotherapy is currently the standard treatment. Multimodal therapeutic strategies incorporating surgery, radiation therapy or photodynamic therapy and chemotherapy have been recommended for selected patients but there is no consensus about their effectiveness. OBJECTIVES: To assess the benefits and harms of radical multimodal treatment options (including radical surgery ± radical radiotherapy ± photodynamic therapy ± systemic therapy) compared to each other or to palliative treatments, for people with malignant pleural mesothelioma. SEARCH METHODS: We reviewed data from the Cochrane Lung Cancer group's Specialised Register, Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE and Embase. We also checked reference lists of primary original studies, review articles and relevant conference proceedings manually for further related articles up to 21 March 2017. SELECTION CRITERIA: We included parallel-group randomised controlled trials of multimodal therapy for people with malignant pleural mesothelioma (stages I, II or III) that measured at least one of the following endpoints: overall survival, health-related health-related quality of life, adverse events or progression-free survival. We considered studies regardless of language or publication status. DATA COLLECTION AND ANALYSIS: Two review authors independently extracted relevant information on participant characteristics, interventions, study outcomes, and data on the outcomes for this review, as well as information on the design and methodology of the studies. Two review authors assessed the risk of bias in the included trials using pre-defined 'Risk of bias' domains. We assessed the methodological quality using GRADE. MAIN RESULTS: We conducted this review in accordance with the published Cochrane protocol. Two randomised clinical trials with 104 participants fulfilled our inclusion criteria. Both trials were at high risk of bias (for outcomes other than overall survival), and we rated the evidence as moderate quality for overall survival and low quality for all other outcomes. One trial compared combined extrapleural pneumonectomy (EPP) plus neoadjuvant platinum-based chemotherapy plus postoperative high-dose hemithoracic radiotherapy with combined EPP plus platinum-based chemotherapy. The other trial compared EPP plus postoperative hemithoracic radiotherapy with standard (non-radical) therapy alone following platinum-based chemotherapy (patients in the standard therapy arm received continued oncological management according to local policy, which could include further chemotherapy or palliative radiotherapy).For the first trial, median overall survival calculated from registration was 20.8 months (95% confidence interval (CI) 14.4 to 27.8) in the no-radiotherapy group and 19.3 months (95% CI 11.5 to 21.8) in the radiotherapy group. For the second trial, median overall survival was 14.4 months (95% CI 5.3 to 18.7) for patients allocated to EPP and 19.5 months (95% CI 13.4 to time not yet reached) for patients randomised to standard non-radical therapy. In the second trial, 12 serious adverse events were reported during the study period: ten in the EPP group and two in the non-radical therapy group. Overall health-related quality of life scores were not different between the two arms in either study. We could not perform a meta-analysis of the two included trials due to clinical heterogeneity. We also identified three ongoing trials evaluating the topic of our review. AUTHORS' CONCLUSIONS: The overall strength of the evidence gathered in this review is low and there is a lack of available evidence to support the use of radical multimodality therapy in routine clinical practice (particularly as one trial suggests greater harm). Given the added cost of multimodality treatment and the possible increase in risk of adverse effects, the lack of evidence of their effectiveness probably means that these interventions should currently be limited to clinical trials alone.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Terapia Combinada/métodos
Neoplasias Pulmonares/terapia
Mesotelioma/terapia
Pneumonectomia/métodos
[Mh] Termos MeSH secundário: Seres Humanos
Neoplasias Pulmonares/mortalidade
Mesotelioma/mortalidade
Compostos de Platina/uso terapêutico
Dosagem Radioterapêutica
Ensaios Clínicos Controlados Aleatórios como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Platinum Compounds)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD012605.pub2


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[PMID]:29226731
[Au] Autor:Hamilton G; Rath B
[Ad] Endereço:a Department of Surgery , Medical University of Vienna , Vienna , Austria.
[Ti] Título:Pharmacogenetics of platinum-based chemotherapy in non-small cell lung cancer: predictive validity of polymorphisms of ERCC1.
[So] Source:Expert Opin Drug Metab Toxicol;14(1):17-24, 2018 Jan.
[Is] ISSN:1744-7607
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The efficacy of platinum-based chemotherapy for patients with non-small cell lung cancer (NSCLC) is limited by chemoresistance. Platinum drugs damage DNA by introducing intrastrand and interstrand crosslinks which result in cell death. Excision repair cross-complementing 1 (ERCC1) is a member of the nucleotide excision repair (NER) pathway which erases such defects. Single nucleotide polymorphisms (SNPs) in ERCC1 impair this activity and have been suggested to predict the response to chemotherapy. Area covered: Among the polymorphisms of proteins involved in uptake, metabolism, cytotoxicity and efflux of platinum drugs, codon 118 C/T and C8092A in ERCC1 are the best characterized SNPs studied for their predictive power. Here, the divergent results for studies of these markers in NSCLC are summarized and the reasons for this contradictory data discussed. Expert opinion: Cytotoxicity of platinum compounds comprise complex cellular processes for which DNA repair may not constitute the rate limiting step. These drugs are administered as doublets to histologically diverse patients and, furthermore, the NER pathway in ERCC1 wildtype cohorts may be still impaired by the chemotherapeutics applied. At present, assessment of a limited number of polymorphism in DNA repair proteins is not reliably associated with response to treatment in NSCLC patients.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Proteínas de Ligação a DNA/genética
Endonucleases/genética
Neoplasias Pulmonares/tratamento farmacológico
[Mh] Termos MeSH secundário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Dano ao DNA/efeitos dos fármacos
Reparo do DNA/genética
Resistência a Medicamentos Antineoplásicos
Seres Humanos
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Compostos de Platina/administração & dosagem
Polimorfismo de Nucleotídeo Único
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Platinum Compounds); EC 3.1.- (ERCC1 protein, human); EC 3.1.- (Endonucleases)
[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:171212
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1416095


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[PMID]:28453256
[Au] Autor:Cao P; Mooney R; Tirughana R; Abidi W; Aramburo S; Flores L; Gilchrist M; Nwokafor U; Haber T; Tiet P; Annala AJ; Han E; Dellinger T; Aboody KS; Berlin JM
[Ti] Título:Intraperitoneal Administration of Neural Stem Cell-Nanoparticle Conjugates Targets Chemotherapy to Ovarian Tumors.
[So] Source:Bioconjug Chem;28(6):1767-1776, 2017 06 21.
[Is] ISSN:1520-4812
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ovarian cancer is particularly aggressive once it has metastasized to the abdominal cavity (stage III). Intraperitoneal (IP) as compared to intravenous (IV) administration of chemotherapy improves survival for stage III ovarian cancer, demonstrating that concentrating chemotherapy at tumor sites has therapeutic benefit; unfortunately, IP therapy also increases toxic side effects, thus preventing its completion in many patients. The ability to target chemotherapy selectively to ovarian tumors while sparing normal tissue would improve efficacy and decrease toxicities. We have previously shown that tumor-tropic neural stem cells (NSCs) dramatically improve the intratumoral distribution of nanoparticles (NPs) when given intracerebrally near an orthotopic brain tumor or into a flank xenograft tumor. Here, we show that NPs either conjugated to the surface of NSCs or loaded within the cells are selectively delivered to and distributed within ovarian tumors in the abdominal cavity following IP injection, with no evidence of localization to normal tissue. IP administration is significantly more effective than IV administration, and NPs carried by NSCs show substantially deeper penetration into tumors than free NPs. The NSCs and NPs target and localize to ovarian tumors within 1 h of administration. Pt-loaded silica NPs (SiNP[Pt]) were developed that can be transported in NSCs, and it was found that the NSC delivery of SiNP[Pt] (NSC-SiNP[Pt]) results in higher levels of Pt in tumors as compared to free drug or SiNP[Pt]. To the best of our knowledge, this work represents the first demonstration that cells given IP can target the delivery of drug-loaded NPs.
[Mh] Termos MeSH primário: Sistemas de Liberação de Medicamentos/métodos
Nanopartículas/química
Células-Tronco Neurais/transplante
Neoplasias Ovarianas/tratamento farmacológico
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Injeções Intraperitoneais
Nanopartículas/administração & dosagem
Células-Tronco Neurais/química
Compostos de Platina/administração & dosagem
Compostos de Platina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Platinum Compounds)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1021/acs.bioconjchem.7b00237


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[PMID]:27770282
[Au] Autor:Petrelli F; Barni S; Bregni G; de Braud F; Di Cosimo S
[Ad] Endereço:Medical Oncology Unit, ASST Bergamo Ovest, Piazzale Ospedale 1, 24047, Treviglio, BG, Italy. faupe@libero.it.
[Ti] Título:Platinum salts in advanced breast cancer: a systematic review and meta-analysis of randomized clinical trials.
[So] Source:Breast Cancer Res Treat;160(3):425-437, 2016 12.
[Is] ISSN:1573-7217
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The interest in platinum salts in breast cancer (BC) therapy has been recently renewed as inhibition of DNA damage response may enhance the effects of DNA-damaging agents in BC tumors with high genomic instability. The present systematic review and meta-analysis of randomized trials were performed to assess the efficacy and safety of therapy with platinum salts in patients with locally advanced or metastatic (hereinafter advanced) BC. METHODS: We searched PubMed, EMBASE, SCOPUS, Web of Science, the Cochrane Library, and CINAHL for phase II/III clinical trials that assessed efficacy of platinum-based therapy in patients with advanced BC. Pooled estimates of overall response rate (RR), median progression-free survival (PFS) and overall survival (OS) were computed using random or fixed effects models. RESULTS: Data on 4625 patients from 23 phase II and III trials (11 with cisplatin, 11 with carboplatin, and 1 with either agents respectively) were analyzed. Estimates for RR, PFS, and OS were obtained from 23, 13, and 15 studies, respectively. Although at the cost of significantly increased fatigue, hematological and gastrointestinal toxicity, compared with non-platinum schemas, cisplatin, and carboplatin prolonged OS (HR 0.91; 95 % CI 0.83-1.00, p = 0.04), PFS (HR 0.84; 95 % CI 0.73-0.97, p = 0.01), and RR (HR 1.27; 95 % CI 1.03-1.57, p = 0.03). CONCLUSIONS: Despite some limitations of the studies examined, including partial information on hormonal receptor and HER2 status, the use of platinum salts significantly prolonged OS, and PFS of patients with advanced BC with no unexpected toxicity.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Neoplasias da Mama/tratamento farmacológico
Neoplasias da Mama/patologia
Compostos de Platina/uso terapêutico
[Mh] Termos MeSH secundário: Antineoplásicos/administração & dosagem
Antineoplásicos/efeitos adversos
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Neoplasias da Mama/mortalidade
Ensaios Clínicos Fase II como Assunto
Ensaios Clínicos Fase III como Assunto
Feminino
Seres Humanos
Estadiamento de Neoplasias
Compostos de Platina/administração & dosagem
Compostos de Platina/efeitos adversos
Modelos de Riscos Proporcionais
Viés de Publicação
Ensaios Clínicos Controlados Aleatórios como Assunto
Análise de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Platinum Compounds)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171209
[Lr] Data última revisão:
171209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161103
[St] Status:MEDLINE
[do] DOI:10.1007/s10549-016-4025-3


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[PMID]:28945187
[Au] Autor:Raudenska M; Krejcova L; Richtera L; Heger Z; Hrabeta J; Eckschlager T; Stiborova M; Adam V; Kratochvilova M; Masarik M; Gumulec J
[Ad] Endereço:1 Department of Physiology, Faculty of Medicine, Masaryk University, Brno, Czech Republic.
[Ti] Título:VPA does not enhance platinum binding to DNA in cisplatin-resistant neuroblastoma cancer cells.
[So] Source:Tumour Biol;39(9):1010428317711656, 2017 Sep.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuroblastoma represents a malignancy of the sympathetic nervous system characteristic by biological heterogeneity. Thus, chemotherapy exhibits only low effectivity in curing high-risk forms. Previous studies revealed the cytotoxic potential of valproate on neuroblastoma cells. Nevertheless, these studies omitted effects of hypoxia, despite its undeniable tumorigenic role. In this study, we addressed the question whether valproate promotes binding of platinum-based anti-cancer drugs (cisplatin, carboplatin and oxaliplatin) to DNA and role of hypoxia, cellular antioxidant capacity and cisplatin resistance in this process. Following parameters differed significantly when cells were exposed to treatment with platinum-based drugs: elevation of platinum content bound to DNA, elevation of total thiol content, GSH/GSSG ratio, glutathione reductase and peroxidase, superoxide dismutase and elevation of antioxidant capacity. Hypoxia caused a decrease in cytosine/adenine peak, and no changes in platinum-DNA binding properties were observed. After valproate co-treatment, oxidative stress-related parameters and cytosine/adenine peak were only elevated. The amount of platinum bound to DNA was not changed significantly. Valproate is not able to enhance platinum binding to DNA in neuroblastoma cells, neither in case of intrinsic resistance (UKF-NB-4) nor in case of acquired resistance (UKF-NB-4 ). Therefore, another mechanism different from increase in platinum binding to DNA should be considered as a synergistic effect of valproate by cisplatin treatment.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Neuroblastoma/patologia
Compostos de Platina/farmacologia
Ácido Valproico/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
DNA/efeitos dos fármacos
Sinergismo Farmacológico
Seres Humanos
Estresse Oxidativo/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Platinum Compounds); 614OI1Z5WI (Valproic Acid); 9007-49-2 (DNA)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317711656


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[PMID]:28916659
[Au] Autor:Chen F; Xu G; Qin X; Jin X; Gou S
[Ad] Endereço:Jiangsu Province Hi-Tech Key Laboratory for Biomedical Research, Pharmaceutical Research Center and School of Chemistry and Chemical Engineering, Southeast University, Nanjing, China.
[Ti] Título:Hybrid of DNA-targeting Chlorambucil with Pt(IV) Species to Reverse Drug Resistance.
[So] Source:J Pharmacol Exp Ther;363(2):221-239, 2017 Nov.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Two hybrids of Pt(IV) species were designed and prepared by addition of a chlorambucil unit to the axial positions of the Pt(IV) complexes derived from DN603 and DN604. In vitro studies of two hybrids against two pairs of cisplatin sensitive and resistant cancer cell lines indicated that compound had superior antitumor activity to cisplatin and chlorambucil via suppressing DNA damage repair to reverse drug resistance. Mechanistic investigation suggested that the potent antitumor activity of compound arose from its major suppression of CK2-mediated MRE11-RAD50-NBS1(MRN) complex promotion of DNA double-strand break (DSB) repair. In nude mice with A549/CDDP xenografts, compound exhibited higher anticancer efficacy than cisplatin and chlorambucil by reversing drug resistance, displayed improved effectiveness, and had no toxicity effects. Overall, compound is a promising drug candidate, which could promote the anticancer activity and reverse drug resistance by attenuating CK2-induced MRN-dependent DSB repair.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Antineoplásicos/farmacologia
Clorambucila/farmacologia
DNA de Neoplasias/efeitos dos fármacos
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Compostos de Platina/farmacologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacocinética
Antineoplásicos Alquilantes/farmacocinética
Cálcio/metabolismo
Caseína Quinase II/antagonistas & inibidores
Linhagem Celular Tumoral
Clorambucila/farmacocinética
Cisplatino/farmacologia
Reparo do DNA/efeitos dos fármacos
Desenho de Drogas
Feminino
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Platina/metabolismo
Compostos de Platina/farmacocinética
Ratos Sprague-Dawley
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Antineoplastic Agents, Alkylating); 0 (DNA, Neoplasm); 0 (Platinum Compounds); 18D0SL7309 (Chlorambucil); 49DFR088MY (Platinum); EC 2.7.11.1 (Casein Kinase II); Q20Q21Q62J (Cisplatin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170917
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.117.243451


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[PMID]:28816138
[Au] Autor:Davuluri R; Jiang W; Fang P; Xu C; Komaki R; Gomez DR; Welsh J; Cox JD; Crane CH; Hsu CC; Lin SH
[Ad] Endereço:Department of Radiation Oncology, The University of Arizona, Tucson, Arizona.
[Ti] Título:Lymphocyte Nadir and Esophageal Cancer Survival Outcomes After Chemoradiation Therapy.
[So] Source:Int J Radiat Oncol Biol Phys;99(1):128-135, 2017 Sep 01.
[Is] ISSN:1879-355X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Host immunity may affect the outcome in patients with esophageal cancer. We sought to identify factors that influenced absolute lymphocyte count (ALC) nadir during chemoradiation therapy (CRT) for esophageal cancer (EC) and looked for clinically relevant associations with survival. METHODS AND MATERIALS: 504 patients with stage I-III EC (2007-2013) treated with neoadjuvant or definitive CRT with weekly ALC determinations made during treatment were analyzed. Grade of lymphopenia from ALC nadir during CRT was based on Common Terminology Criteria for Adverse Events version 4.0. Associations of ALC nadir with survival were examined using multivariate Cox proportional hazards analysis (MVA) and competing risks regression analysis. RESULTS: The median follow-up time was 36 months. The incidences of grade 1, 2, 3, and 4 ALC nadir during CRT were 2%, 12%, 59%, and 27%, respectively. The impact was lymphocyte-specific because this was not seen for monocyte or neutrophil count. On MVA, grade 4 ALC nadir (G4 nadir) was significantly associated with worse overall and disease-specific survival outcomes. Predictors of G4 nadir included distal tumor location, definitive CRT, taxane/5-fluorouracil chemotherapy, and photon-based radiation type (vs proton-based). Radiation type strongly influenced the mean body dose exposure, which was a strong predictor for G4 nadir (odds ratio 1.22 per Gray, P<.001). CONCLUSIONS: G4 nadir during CRT for EC was associated with poor outcomes, suggesting a role of host immunity in disease control. This observation provides a rationale to prospectively test chemotherapeutic and radiation treatment strategies that may have a lower impact on host immunity.
[Mh] Termos MeSH primário: Adenocarcinoma/mortalidade
Adenocarcinoma/terapia
Carcinoma de Células Escamosas/mortalidade
Carcinoma de Células Escamosas/terapia
Quimiorradioterapia/efeitos adversos
Neoplasias Esofágicas/mortalidade
Neoplasias Esofágicas/terapia
Linfopenia/mortalidade
[Mh] Termos MeSH secundário: Adenocarcinoma/imunologia
Adenocarcinoma/patologia
Carcinoma de Células Escamosas/imunologia
Carcinoma de Células Escamosas/patologia
Quimiorradioterapia/métodos
Neoplasias Esofágicas/imunologia
Neoplasias Esofágicas/patologia
Fluoruracila/uso terapêutico
Seres Humanos
Incidência
Estimativa de Kaplan-Meier
Contagem de Linfócitos
Linfopenia/epidemiologia
Linfopenia/etiologia
Meia-Idade
Monócitos/efeitos dos fármacos
Monócitos/efeitos da radiação
Neutrófilos/efeitos dos fármacos
Neutrófilos/efeitos da radiação
Razão de Chances
Compostos de Platina/uso terapêutico
Modelos de Riscos Proporcionais
Terapia com Prótons
Dosagem Radioterapêutica
Análise de Regressão
Estudos Retrospectivos
Linfócitos T/efeitos dos fármacos
Linfócitos T/efeitos da radiação
Taxoides/uso terapêutico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Platinum Compounds); 0 (Taxoids); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE


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[PMID]:28772281
[Au] Autor:Ciuleanu TE; Ahmed S; Kim JH; Mezger J; Park K; Thomas M; Chen J; Poondru S; VanTornout JM; Whitcomb D; Blackhall F
[Ad] Endereço:Oncological Institute I Chiricuta and UMF Iuliu Hatieganu, Cluj-Napoca, Romania.
[Ti] Título:Randomised Phase 2 study of maintenance linsitinib (OSI-906) in combination with erlotinib compared with placebo plus erlotinib after platinum-based chemotherapy in patients with advanced non-small cell lung cancer.
[So] Source:Br J Cancer;117(6):757-766, 2017 Sep 05.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Maintenance therapy is important in advanced/metastatic non-small cell lung cancer (NSCLC). Erlotinib as switch maintenance following platinum-based chemotherapy increases survival. Cross-talk between the epidermal growth factor receptor and insulin-like growth factor receptor (IGFR) pathways mediate resistance to individual receptor blockade. This study compared maintenance linsitinib plus erlotinib vs erlotinib plus placebo in patients with NSCLC. METHODS: In this Phase II randomised trial, patients without progression following four cycles of first-line platinum-based chemotherapy (N=205) received continuous schedule maintenance oral linsitinib 150 mg or placebo BID combined with erlotinib 150 mg QD for 21-day cycles. The primary endpoint was progression-free survival (PFS). RESULTS: The study was unblinded early due to linsitinib non-superiority. No difference was found between the two treatment groups in median PFS of 125 days linsitinib vs 129 days placebo (P=0.601); no difference in overall survival (OS) was observed. Tolerability was similar, although in the linsitinib group, treatment-related adverse events and discontinuations were more frequent. No drug-drug interaction was implicated. CONCLUSIONS: Linsitinib maintenance therapy added to erlotinib did not improve PFS or OS in non-progressing NSCLC patients. This highlights the need for robust biomarkers of response for combinations that incorporate IGFR-targeted therapies in maintenance or other therapeutic settings.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Cloridrato de Erlotinib/uso terapêutico
Imidazóis/uso terapêutico
Neoplasias Pulmonares/tratamento farmacológico
Quimioterapia de Manutenção
Pirazinas/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Carcinoma Pulmonar de Células não Pequenas/patologia
Cloridrato de Erlotinib/efeitos adversos
Feminino
Seres Humanos
Imidazóis/efeitos adversos
Estimativa de Kaplan-Meier
Neoplasias Pulmonares/patologia
Masculino
Meia-Idade
Placebos/uso terapêutico
Compostos de Platina/uso terapêutico
Pirazinas/efeitos adversos
Receptores de Somatomedina/antagonistas & inibidores
Receptores de Somatomedina/genética
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (3-(8-amino-1-(2-phenylquinolin-7-yl)imidazo(1,5-a)pyrazin-3-yl)-1-methylcyclobutanol); 0 (Imidazoles); 0 (Placebos); 0 (Platinum Compounds); 0 (Pyrazines); 0 (Receptors, Somatomedin); DA87705X9K (Erlotinib Hydrochloride)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2017.226


  9 / 1640 MEDLINE  
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[PMID]:28761342
[Au] Autor:Zhu H; Zhou B; Chan L; Du Y; Chen T
[Ad] Endereço:Department of Internal Medicine and Orthopedics, Guangdong Provincial Hospital of Traditional Chinese Medicine.
[Ti] Título:Transferrin-functionalized nanographene oxide for delivery of platinum complexes to enhance cancer-cell selectivity and apoptosis-inducing efficacy.
[So] Source:Int J Nanomedicine;12:5023-5038, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Rational design and construction of delivery nanosystems for anticancer metal complexes is a crucial strategy to improve solubility under physiological conditions and permeability and retention behavior in tumor cells. Therefore, in this study, we designed and synthesize a transferrin (Tf)-conjugated nanographene oxide (NGO) nanosystem as a cancer-targeted nanocarrier of Pt complexes (Tf-NGO@Pt). This nanodelivery system exhibited good solubility under physiological conditions. Moreover, Tf-NGO@Pt showed higher anticancer efficacy against MCF human breast cancer cells than the free Pt complex, and effectively inhibited cancer-cell migration and invasion, with involvement of reactive oxygen species overproduction. In addition, nanolization also enhanced the penetration ability and inhibitory effect of the Pt complex toward MCF7 breast cancer-cell tumor spheroids. The enhancement of anticancer efficacy was positively correlated with increased cellular uptake and cellular drug retention. This study provides a new strategy to facilitate the future application of metal complexes in cancer therapy.
[Mh] Termos MeSH primário: Antineoplásicos/administração & dosagem
Apoptose/efeitos dos fármacos
Sistemas de Liberação de Medicamentos/métodos
Compostos de Platina/administração & dosagem
Transferrina/química
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Neoplasias da Mama/tratamento farmacológico
Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Feminino
Grafite/química
Seres Humanos
Células MCF-7
Nanoestruturas/administração & dosagem
Nanoestruturas/química
Óxidos/farmacologia
Platina/administração & dosagem
Platina/química
Platina/farmacologia
Compostos de Platina/farmacologia
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Oxides); 0 (Platinum Compounds); 0 (Reactive Oxygen Species); 0 (Transferrin); 49DFR088MY (Platinum); 7782-42-5 (Graphite)
[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:170802
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S139207


  10 / 1640 MEDLINE  
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[PMID]:28753429
[Au] Autor:Yu T; Guo F; Yu Y; Sun T; Ma D; Han J; Qian Y; Kryczek I; Sun D; Nagarsheth N; Chen Y; Chen H; Hong J; Zou W; Fang JY
[Ad] Endereço:State Key Laboratory for Oncogenes and Related Genes, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Division of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Cancer Institute,Shanghai Institute of Digestive Disea
[Ti] Título:Fusobacterium nucleatum Promotes Chemoresistance to Colorectal Cancer by Modulating Autophagy.
[So] Source:Cell;170(3):548-563.e16, 2017 Jul 27.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gut microbiota are linked to chronic inflammation and carcinogenesis. Chemotherapy failure is the major cause of recurrence and poor prognosis in colorectal cancer patients. Here, we investigated the contribution of gut microbiota to chemoresistance in patients with colorectal cancer. We found that Fusobacterium (F.) nucleatum was abundant in colorectal cancer tissues in patients with recurrence post chemotherapy, and was associated with patient clinicopathological characterisitcs. Furthermore, our bioinformatic and functional studies demonstrated that F. nucleatum promoted colorectal cancer resistance to chemotherapy. Mechanistically, F. nucleatum targeted TLR4 and MYD88 innate immune signaling and specific microRNAs to activate the autophagy pathway and alter colorectal cancer chemotherapeutic response. Thus, F. nucleatum orchestrates a molecular network of the Toll-like receptor, microRNAs, and autophagy to clinically, biologically, and mechanistically control colorectal cancer chemoresistance. Measuring and targeting F. nucleatum and its associated pathway will yield valuable insight into clinical management and may ameliorate colorectal cancer patient outcomes.
[Mh] Termos MeSH primário: Autofagia
Neoplasias Colorretais/tratamento farmacológico
Neoplasias Colorretais/patologia
Fusobacterium nucleatum/fisiologia
Microbioma Gastrointestinal
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/uso terapêutico
Capecitabina/uso terapêutico
Neoplasias Colorretais/metabolismo
Resistência a Medicamentos Antineoplásicos
Xenoenxertos
Camundongos
MicroRNAs/metabolismo
Transplante de Neoplasias
Compostos de Platina/uso terapêutico
Recidiva
Receptores Toll-Like/metabolismo
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (MIRN18A microRNA, human); 0 (MIRN4802 microRNA, human); 0 (MicroRNAs); 0 (Platinum Compounds); 0 (Toll-Like Receptors); 6804DJ8Z9U (Capecitabine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE



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