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[PMID]:29332262
[Au] Autor:Karpinsky G; Krawczyk MA; Izycka-Swieszewska E; Fatyga A; Budka A; Balwierz W; Sobol G; Zalewska-Szewczyk B; Rychlowska-Pruszynska M; Klepacka T; Dembowska-Baginska B; Kazanowska B; Gabrych A; Bien E
[Ad] Endereço:Children's Hospital of Michigan, 3901 Beaubien St, Detroit, MI, USA.
[Ti] Título:Tumor expression of survivin, p53, cyclin D1, osteopontin and fibronectin in predicting the response to neo-adjuvant chemotherapy in children with advanced malignant peripheral nerve sheath tumor.
[So] Source:J Cancer Res Clin Oncol;144(3):519-529, 2018 Mar.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Selected cell-cycle regulators and extracellular matrix proteins were found to play roles in malignant peripheral nerve sheath tumor (MPNST) biology. We aimed to analyze whether initial tumor tissue expressions of survivin, p53, cyclin D1, osteopontin (OPN) and fibronectin (FN) correlate with the response to neo-adjuvant CHT (naCHT) in children with advanced inoperable MPNST. METHODS: The study included 26 children with MPNST (M/F 14/12, median age 130 months) treated in Polish centers of pediatric oncology between 1992 and 2013. Tissue expression of markers was studied immunohistochemically in the manually performed tissue microarrays and assessed semi-quantitatively as low and high, based on the rate of positive cells and staining intensity. RESULTS: Good response to naCHT was noted in 47.6%, while poor-in 52.4% of patients. The response to naCHT was influenced negatively by the presence of neurofibromatosis NF1 and high initial tumor tissue expression of OPN, survivin, p53 and cyclin D1. Patients with high tumor expression of either OPN, survivin or p53 and those with simultaneous high expression of ≥ 3 of the markers, responded significantly worse to naCHT, than patients, in whom expression of ≤ 2 markers were detected at diagnosis. Nearly, 85% of patients expressing ≥ 3 markers, responded poor to CHT; while 87.5% of children, expressing ≤ 2 markers, were good responders. CONCLUSION: The initial tumor tissue expression of OPN, survivin, p53 and cyclin D1 may serve as markers to predict response to naCHT in pediatric advanced MPNST. Future studies in more numerous group of patients are needed to confirm these preliminary results.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Biomarcadores Tumorais/metabolismo
Ciclina D1/metabolismo
Citocinas/metabolismo
Proteínas Inibidoras de Apoptose/metabolismo
Neoplasias da Bainha Neural/diagnóstico
Neoplasias da Bainha Neural/tratamento farmacológico
Osteopontina/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Biomarcadores Farmacológicos/metabolismo
Criança
Pré-Escolar
Progressão da Doença
Feminino
Seres Humanos
Lactente
Masculino
Terapia Neoadjuvante
Neoplasias da Bainha Neural/metabolismo
Neoplasias da Bainha Neural/patologia
Neurilemoma/tratamento farmacológico
Neurilemoma/metabolismo
Neurilemoma/patologia
Prognóstico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BIRC5 protein, human); 0 (Biomarkers, Pharmacological); 0 (Biomarkers, Tumor); 0 (CCND1 protein, human); 0 (Cytokines); 0 (Inhibitor of Apoptosis Proteins); 0 (SPP1 protein, human); 0 (migration stimulating factor, human); 106441-73-0 (Osteopontin); 136601-57-5 (Cyclin D1)
[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:180115
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-018-2580-1


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[PMID]:29288364
[Au] Autor:Xu X; Yu S; Sun W; Qin X; Chen Y; Zhou L; Lou R; Dong S; Shen B; Wu J; Zang J; Cao H; Shi M; Zhang Q; Feng J
[Ad] Endereço:Nanjing Medical University Affiliated Cancer Hospital, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Baiziting No.42, Nanjing, 210009, Jiangsu, China.
[Ti] Título:MiRNA signature predicts the response of patients with advanced lung adenocarcinoma to platinum-based treatment.
[So] Source:J Cancer Res Clin Oncol;144(3):431-438, 2018 Mar.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Accumulating literature proved that miRNAs can regulate the sensitivity of platinum and act as a promising candidate to predict the response of patients with lung adenocarcinoma to chemotherapy. However, most studies on miRNAs were restricted to in vitro experiments. This study aimed to evaluate whether miRNAs alone or in combination (miRNA signature) can act as predictive biomarkers of platinum-based chemotherapy in patients with lung adenocarcinoma. METHODS: Eight miRNAs that most probably predict the efficacy of platinum were screened in 111 tumor tissues of lung adenocarcinoma. Univariate and multivariate Cox analyses, Kaplan-Meier survival curve analysis, Chi-square test, and univariate and multivariate logistic regression analyses were employed to determine whether miRNA expression is associated with the response of patients to platinum-based chemotherapy. The maximum significant odds ratio value was acquired by multiple cycles of multivariate logistic regression analysis. The cut-off points of miRNAs were obtained. A miRNA chemo-sensibility index (CI) formula was established, and its prediction performance was confirmed in another independent set (n = 31). RESULTS: Underexpression of three miRNAs (miRNA-21, miRNA-125b, and miRNA-224) was independently associated with the chemotherapy sensitivity of patients with lung adenocarcinoma. The miRNA CI formula containing these three miRNAs was calculated as (1.364 × miR-21) + (1.323 × miR-125b) + (1.131 × miR-224). A high CI was related to platinum-based chemotherapy resistance, and its prediction performance was confirmed in the testing set. The MAPK, PI3K-Akt, Ras, and cGMP-PKG signaling pathways were considered to be most probably correlated with platinum resistance. CONCLUSION: Our miRNA CI formula can act as an independent predictor to predict the response of patients with lung adenocarcinoma to platinum-based chemotherapy.
[Mh] Termos MeSH primário: Adenocarcinoma
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Biomarcadores Tumorais/genética
Cisplatino/administração & dosagem
Resistência a Medicamentos Antineoplásicos/genética
Neoplasias Pulmonares
MicroRNAs/genética
Transcriptoma
[Mh] Termos MeSH secundário: Adenocarcinoma/diagnóstico
Adenocarcinoma/tratamento farmacológico
Adenocarcinoma/genética
Adulto
Biomarcadores Farmacológicos/metabolismo
Feminino
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Neoplasias Pulmonares/diagnóstico
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/genética
Masculino
Análise de Sequência com Séries de Oligonucleotídeos
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Pharmacological); 0 (Biomarkers, Tumor); 0 (MicroRNAs); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2562-8


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[PMID]:29221581
[Au] Autor:Yancey SW; Keene ON; Albers FC; Ortega H; Bates S; Bleecker ER; Pavord I
[Ad] Endereço:Respiratory Therapeutic Area, GlaxoSmithKline, Research Triangle Park, NC. Electronic address: steve.w.yancey@gsk.com.
[Ti] Título:Biomarkers for severe eosinophilic asthma.
[So] Source:J Allergy Clin Immunol;140(6):1509-1518, 2017 Dec.
[Is] ISSN:1097-6825
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The last decade has seen the approval of several new biologics for the treatment of severe asthma-targeting specific endotypes and phenotypes. This review will examine how evidence generated from the mepolizumab clinical development program showed that blood eosinophil counts, rather than sputum or tissue eosinophil counts, evolved as a pharmacodynamic and predictive biomarker for the efficacy of treatment with mepolizumab in patients with severe eosinophilic asthma. Based on the available evidence and combined with clinical judgement, a baseline blood eosinophil threshold of 150 cells/µL or greater or a historical blood eosinophil threshold of 300 cells/µL or greater will allow selection of patients with severe eosinophilic asthma who are most likely to achieve clinically significant reductions in the rate of exacerbations with mepolizumab treatment.
[Mh] Termos MeSH primário: Asma/diagnóstico
Células Sanguíneas/patologia
Eosinófilos/patologia
Eosinofilia Pulmonar/diagnóstico
Escarro/citologia
[Mh] Termos MeSH secundário: Animais
Antiasmáticos/uso terapêutico
Anticorpos Monoclonais Humanizados/uso terapêutico
Asma/tratamento farmacológico
Biomarcadores Farmacológicos/metabolismo
Progressão da Doença
Seres Humanos
Interleucina-5/imunologia
Contagem de Leucócitos
Valor Preditivo dos Testes
Eosinofilia Pulmonar/tratamento farmacológico
Índice de Gravidade de Doença
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Asthmatic Agents); 0 (Antibodies, Monoclonal, Humanized); 0 (Biomarkers, Pharmacological); 0 (Interleukin-5); 90Z2UF0E52 (mepolizumab)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE


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[PMID]:29036176
[Au] Autor:Chan SL; Chua APG; Aminkeng F; Chee CBE; Jin S; Loh M; Gan SH; Wang YT; Brunham LR
[Ad] Endereço:Translational Laboratory in Genetic Medicine, Agency for Science, Technology and Research, Singapore and the National University of Singapore, Singapore.
[Ti] Título:Association and clinical utility of NAT2 in the prediction of isoniazid-induced liver injury in Singaporean patients.
[So] Source:PLoS One;12(10):e0186200, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: Isoniazid (INH) is part of the first-line-therapy for tuberculosis (TB) but can cause drug-induced liver injury (DILI). Several candidate single nucleotide polymorphisms (SNPs) have been previously identified but the clinical utility of these SNPs in the prediction of INH-DILI remains uncertain. The aim of this study was to assess the association between selected candidate SNPs and the risk of INH-DILI and to assess the clinical validity of associated variants in a Singaporean population. METHODS: This was a case-control study where 24 INH-DILI cases and 79 controls were recruited from the TB control unit in a tertiary hospital. Logistic regression was used to test for the association between candidate SNPs and INH-DILI. NAT2 acetylator status was inferred from genotypes and tested for association with INH-DILI. Finally, clinical validity measures were estimated for significant variants. RESULTS: Two SNPs in NAT2 (rs1041983 and rs1495741) and NAT2 slow acetylators (SA) were significantly associated with INH-DILI (OR (95% CI) = 13.86 (4.30-44.70), 0.10 (0.03-0.33) and 9.98 (3.32-33.80), respectively). Based on an INH-DILI prevalence of 10%, the sensitivity, specificity, positive and negative predictive values of NAT2 SA were 75%, 78%, 28% and 97%, respectively. The population attributable fraction (PAF) and number needed to test (NNT) for NAT2 SA were estimated to be 0.67 and 4.08, respectively. A model with clinical and NAT2 acetylator status provided significantly better prediction for INH-DILI than a clinical model alone (area under receiver operating characteristic curve = 0.863 vs. 0.766, respectively, p = 0.027). CONCLUSIONS: We show the association between NAT2 SA and INH-DILI in a Singaporean population and demonstrated its clinical utility in the prediction of INH-DILI.
[Mh] Termos MeSH primário: Antituberculosos/toxicidade
Arilamina N-Acetiltransferase/genética
Doença Hepática Induzida por Substâncias e Drogas/genética
Isoniazida/toxicidade
[Mh] Termos MeSH secundário: Antituberculosos/uso terapêutico
Biomarcadores Farmacológicos
Estudos de Casos e Controles
Feminino
Predisposição Genética para Doença
Seres Humanos
Isoniazida/uso terapêutico
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único
Prognóstico
Singapura
Tuberculose/complicações
Tuberculose/tratamento farmacológico
Tuberculose/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antitubercular Agents); 0 (Biomarkers, Pharmacological); EC 2.3.1.5 (Arylamine N-Acetyltransferase); EC 2.3.1.5 (NAT2 protein, human); V83O1VOZ8L (Isoniazid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171017
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186200


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[PMID]:28792525
[Au] Autor:Covell DG
[Ad] Endereço:Information Technology Branch, Developmental Therapeutics Program, National Cancer Institute, Frederick, MD, United States of America.
[Ti] Título:A data mining approach for identifying pathway-gene biomarkers for predicting clinical outcome: A case study of erlotinib and sorafenib.
[So] Source:PLoS One;12(8):e0181991, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A novel data mining procedure is proposed for identifying potential pathway-gene biomarkers from preclinical drug sensitivity data for predicting clinical responses to erlotinib or sorafenib. The analysis applies linear ridge regression modeling to generate a small (N~1000) set of baseline gene expressions that jointly yield quality predictions of preclinical drug sensitivity data and clinical responses. Standard clustering of the pathway-gene combinations from gene set enrichment analysis of this initial gene set, according to their shared appearance in molecular function pathways, yields a reduced (N~300) set of potential pathway-gene biomarkers. A modified method for quantifying pathway fitness is used to determine smaller numbers of over and under expressed genes that correspond with favorable and unfavorable clinical responses. Detailed literature-based evidence is provided in support of the roles of these under and over expressed genes in compound efficacy. RandomForest analysis of potential pathway-gene biomarkers finds average treatment prediction errors of 10% and 22%, respectively, for patients receiving erlotinib or sorafenib that had a favorable clinical response. Higher errors were found for both compounds when predicting an unfavorable clinical response. Collectively these results suggest complementary roles for biomarker genes and biomarker pathways when predicting clinical responses from preclinical data.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Mineração de Dados/métodos
Cloridrato de Erlotinib/uso terapêutico
Neoplasias/genética
Neoplasias/metabolismo
Niacinamida/análogos & derivados
Compostos de Fenilureia/uso terapêutico
[Mh] Termos MeSH secundário: Biomarcadores Farmacológicos/metabolismo
Biomarcadores Tumorais/genética
Biomarcadores Tumorais/metabolismo
Análise por Conglomerados
Bases de Dados Factuais
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Modelos Lineares
Análise em Microsséries
Neoplasias/tratamento farmacológico
Niacinamida/uso terapêutico
Prognóstico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biomarkers, Pharmacological); 0 (Biomarkers, Tumor); 0 (Phenylurea Compounds); 25X51I8RD4 (Niacinamide); 9ZOQ3TZI87 (sorafenib); DA87705X9K (Erlotinib Hydrochloride)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181991


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[PMID]:28737909
[Au] Autor:Anthony NG; Baiget J; Berretta G; Boyd M; Breen D; Edwards J; Gamble C; Gray AI; Harvey AL; Hatziieremia S; Ho KH; Huggan JK; Lang S; Llona-Minguez S; Luo JL; McIntosh K; Paul A; Plevin RJ; Robertson MN; Scott R; Suckling CJ; Sutcliffe OB; Young LC; Mackay SP
[Ad] Endereço:Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde , 161 Cathedral Street, Glasgow G4 0NR, Scotland, United Kingdom.
[Ti] Título:Inhibitory Kappa B Kinase α (IKKα) Inhibitors That Recapitulate Their Selectivity in Cells against Isoform-Related Biomarkers.
[So] Source:J Med Chem;60(16):7043-7066, 2017 Aug 24.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IKKß plays a central role in the canonical NF-kB pathway, which has been extensively characterized. The role of IKKα in the noncanonical NF-kB pathway, and indeed in the canonical pathway as a complex with IKKß, is less well understood. One major reason for this is the absence of chemical tools designed as selective inhibitors for IKKα over IKKß. Herein, we report for the first time a series of novel, potent, and selective inhibitors of IKKα. We demonstrate effective target engagement and selectivity with IKKα in U2OS cells through inhibition of IKKα-driven p100 phosphorylation in the noncanonical NF-kB pathway without affecting IKKß-dependent IKappa-Bα loss in the canonical pathway. These compounds represent the first chemical tools that can be used to further characterize the role of IKKα in cellular signaling, to dissect this from IKKß and to validate it in its own right as a target in inflammatory diseases.
[Mh] Termos MeSH primário: Quinase I-kappa B/antagonistas & inibidores
Inibidores de Proteínas Quinases/farmacologia
Pirimidinas/farmacologia
Pirróis/farmacologia
[Mh] Termos MeSH secundário: Animais
Biomarcadores Farmacológicos/metabolismo
Linhagem Celular Tumoral
Desenho de Drogas
Seres Humanos
Quinase I-kappa B/química
Camundongos
Simulação de Acoplamento Molecular
Simulação de Dinâmica Molecular
Subunidade p52 de NF-kappa B/metabolismo
Isoformas de Proteínas/antagonistas & inibidores
Isoformas de Proteínas/química
Inibidores de Proteínas Quinases/síntese química
Inibidores de Proteínas Quinases/química
Pirimidinas/síntese química
Pirimidinas/química
Pirróis/síntese química
Pirróis/química
Transdução de Sinais/efeitos dos fármacos
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Pharmacological); 0 (NF-kappa B p52 Subunit); 0 (Protein Isoforms); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); 0 (Pyrroles); EC 2.7.11.10 (CHUK protein, human); EC 2.7.11.10 (I-kappa B Kinase); EC 2.7.11.10 (IKBKB protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170725
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.7b00484


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[PMID]:28704552
[Au] Autor:Alonso-Dominguez JM; Casado LF; Anguita E; Gomez-Casares MT; Buño I; Ferrer-Marín F; Arenas A; Del Orbe R; Ayala R; Llamas P; Salgado RN; Osorio S; Sanchez-Godoy P; Burgaleta C; Mahíllo-Fernández I; Garcia-Gutierrez V; Steegmann JL; Martinez-Lopez J
[Ad] Endereço:Hospital Universitario Fundación Jiménez Díaz, Instituto de Investigación Sanitaria Fundación Jiménez Díaz (IIS-FJD), UAM, Madrid, Spain.
[Ti] Título:PTCH1 is a reliable marker for predicting imatinib response in chronic myeloid leukemia patients in chronic phase.
[So] Source:PLoS One;12(7):e0181366, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Patched homolog 1 gene (PTCH1) expression and the ratio of PTCH1 to Smoothened (SMO) expression have been proposed as prognostic markers of the response of chronic myeloid leukemia (CML) patients to imatinib. We compared these measurements in a realistic cohort of 101 patients with CML in chronic phase (CP) using a simplified qPCR method, and confirmed the prognostic power of each in a competing risk analysis. Gene expression levels were measured in peripheral blood samples at diagnosis. The PTCH1/SMO ratio did not improve PTCH1 prognostic power (area under the receiver operating characteristic curve 0.71 vs. 0.72). In order to reduce the number of genes to be analyzed, PTCH1 was the selected measurement. High and low PTCH1 expression groups had significantly different cumulative incidences of imatinib failure (IF), which was defined as discontinuation of imatinib due to lack of efficacy (5% vs. 25% at 4 years, P = 0.013), probabilities of achieving a major molecular response (81% vs. 53% at first year, P = 0.02), and proportions of early molecular failure (14% vs. 43%, P = 0.015). Every progression to an advanced phase (n = 3) and CML-related death (n = 2) occurred in the low PTCH1 group (P<0.001 for both comparisons). PTCH1 was an independent prognostic factor for the prediction of IF. We also validated previously published thresholds for PTCH1 expression. Therefore, we confirmed that PTCH1 expression can predict the imatinib response in CML patients in CP by applying a more rigorous statistical analysis. Thus, PTCH1 expression is a promising molecular marker for predicting the imatinib response in CML patients in CP.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Biomarcadores Tumorais/fisiologia
Mesilato de Imatinib/uso terapêutico
Leucemia Mieloide de Fase Crônica/tratamento farmacológico
Receptor Patched-1/fisiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Farmacológicos
Feminino
Regulação Leucêmica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Leucemia Mieloide de Fase Crônica/diagnóstico
Leucemia Mieloide de Fase Crônica/genética
Masculino
Meia-Idade
Prognóstico
Estudos Retrospectivos
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biomarkers, Pharmacological); 0 (Biomarkers, Tumor); 0 (PTCH protein, human); 0 (Patched-1 Receptor); 8A1O1M485B (Imatinib Mesylate)
[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:170714
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181366


  8 / 1361 MEDLINE  
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[PMID]:28700478
[Au] Autor:Xing Y; Liu X; Yan M; Chen T; Lu F; Xu B; Gong Y; Chu F; Lei H
[Ad] Endereço:aSchool of Chinese Pharmacy, Beijing University of Chinese Medicine bNational Anti-Doping Laboratory, China Anti-Doping Agency cCollege of Applied Statistics, Beijing University of Technology, Beijing, China.
[Ti] Título:Impact of nonsteroidal aromatase inhibitors on steroid profile in a Chinese population.
[So] Source:Medicine (Baltimore);96(28):e7411, 2017 Jul.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Steroid profiling was introduced to determine the endogenous steroid misuse in sports. Thus, screening for the exogenous use of these prohibited substances can be established by monitoring a range of endogenous steroids, which constitute the steroid profile and evaluate their concentrations and ratios against reference values. The steroid profiling is currently based on population statistics. As large interindividual variations exist, athlete biological passport (ABP) analysis is ongoing. This study aimed to identify new biomarker(s) for aromatase inhibitor detection in sports using statistical analysis and adapt the model into ABP analysis.Forty-one Chinese nonathlete volunteers (21 males and 20 females) were administered 3 nonsteroidal aromatase inhibitors (aminoglutethimide, letrozole, and anastrozole) independently. Statistical analysis was performed on 16 steroid profile parameters.After administration, the concentrations of endogenous androgen biomarkers including testosterone (T), epitestosterone, androsterone (AN), etiocholanolone (ETIO), 5α-diol, 5ß-diol, and dehydroepiandrosterone were increased, while the level of estrogen was decreased. These biomarkers returned to the baselines levels within 1 month. In females, the concentrations of endogenous biomarkers were affected by nonsteroidal aromatase inhibitors, without a common trend. Three new endogenous biomarkers (AN/estrone, ETIO/estrone, and T/estrone) elevated significantly after treatment. The 3 new models were more sensitive than the World Anti-Doping Agency ratio biomarkers. They were also effective in exponentially weighted moving average chart analysis.Verification experiment demonstrated that the biomarker T/estrone was valid in judging the steroidal aromatase inhibitor abuse. The screening of these new endogenous biomarkers can provide additional parameters to support ABP monitoring and specific information regarding the administered steroids.
[Mh] Termos MeSH primário: Aminoglutetimida/farmacologia
Inibidores da Aromatase/farmacologia
Hormônios/sangue
Nitrilos/farmacologia
Esteroides/sangue
Triazóis/farmacologia
[Mh] Termos MeSH secundário: Biomarcadores Farmacológicos/sangue
Doping nos Esportes
Feminino
Seres Humanos
Masculino
Modelos Biológicos
Método Simples-Cego
Transtornos Relacionados ao Uso de Substâncias/sangue
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Aromatase Inhibitors); 0 (Biomarkers, Pharmacological); 0 (Hormones); 0 (Nitriles); 0 (Steroids); 0 (Triazoles); 0O54ZQ14I9 (Aminoglutethimide); 2Z07MYW1AZ (anastrozole); 7LKK855W8I (letrozole)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170730
[Lr] Data última revisão:
170730
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007411


  9 / 1361 MEDLINE  
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[PMID]:28673254
[Au] Autor:Ongubo DM; Lim R; Tweya H; Stanley CC; Tembo P; Broadhurst R; Gugsa S; Ngongondo M; Speight C; Heller T; Phiri S; Hosseinipour MC
[Ad] Endereço:Tulane University School of Public Health and Tropical Medicine, New Orleans, USA.
[Ti] Título:A cross-sectional study to evaluate second line virological failure and elevated bilirubin as a surrogate for adherence to atazanavir/ritonavir in two urban HIV clinics in Lilongwe, Malawi.
[So] Source:BMC Infect Dis;17(1):461, 2017 Jul 03.
[Is] ISSN:1471-2334
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Malawi's national antiretroviral therapy program provides atazanavir/ritonavir-based second line regimens which cause concentration-dependent rise in indirect bilirubin. We sought to determine if elevated bilirubin, as a surrogate of atazanavir/ritonavir adherence, can aid in the evaluation of second line virological failure in Malawi. METHODS: We conducted a cross-sectional study of HIV-infected patients ≥15 years who were on boosted protease inhibitor-based second line antiretroviral therapy for at least 6 months in two urban HIV clinics in Lilongwe, Malawi. Antiretroviral therapy history and adherence data were extracted from the electronic medical records and blood was drawn for viral load, complete blood count, total bilirubin, and CD4 cell count at a clinic visit. Factors associated with virological failure were assessed using multivariate logistic regression model. RESULTS: Out of 376 patients on second line antiretroviral therapy evaluated, 372 (98.9%) were on atazanavir/ritonavir-based therapy and 142 (37.8%) were male. Mean age was 40.9 years (SD ± 10.1), mean duration on second line antiretroviral therapy was 41.9 months (SD ± 27.6) and 256 patients (68.1%) had elevated bilirubin >1.3 mg/dL. Overall, 35 (9.3%) patients had viral load >1000 copies/ml (virological failure). Among the virologically failing vs. non-failing patients, bilirubin was elevated in 34.3% vs. 72.0% respectively (p < 0.001), although adherence by pill count was similar (62.9% vs. 60.7%, p = 0.804). The odds of virological failure were higher for adults aged 25-40 years (adjusted odds ratio (aOR) 2.5, p = 0.048), those with CD4 cell count <100 (aOR 17.5, p < 0.001), and those with normal bilirubin levels (aOR 5.4, p < 0.001); but were lower for the overweight/obese patients (aOR 0.3, p = 0.026). Poor pill count adherence (aOR 0.7, p = 0.4) and male gender (aOR 1.2, p = 0.698) were not associated with second line virological failure. CONCLUSIONS: Among patients receiving atazanavir/ritonavir-based second line antiretroviral therapy, bilirubin levels better predicted virological failure than pill count adherence. Therefore, strategic use of bilirubin and viral load testing to target adherence counseling and support may be cost-effective in monitoring second line antiretroviral therapy adherence and virological failure. Drug resistance testing targeted for patients with virological failure despite elevated bilirubin levels would facilitate timely switch to third line antiretroviral regimens whenever available.
[Mh] Termos MeSH primário: Fármacos Anti-HIV/uso terapêutico
Bilirrubina/análise
Biomarcadores Farmacológicos/análise
Infecções por HIV/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Sulfato de Atazanavir/uso terapêutico
Contagem de Linfócito CD4
Estudos Transversais
Feminino
Seres Humanos
Malaui
Masculino
Adesão à Medicação
Meia-Idade
Ritonavir/uso terapêutico
Falha de Tratamento
Saúde da População Urbana
Carga Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-HIV Agents); 0 (Biomarkers, Pharmacological); 4MT4VIE29P (Atazanavir Sulfate); O3J8G9O825 (Ritonavir); RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE
[do] DOI:10.1186/s12879-017-2528-0


  10 / 1361 MEDLINE  
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[PMID]:28618958
[Au] Autor:Loosen SH; Neumann UP; Trautwein C; Roderburg C; Luedde T
[Ad] Endereço:1 Department of Gastroenterology, Digestive Diseases and Intensive Care Medicine (Department of Medicine III), Division of GI Oncology, University Hospital RWTH Aachen, Aachen, Germany.
[Ti] Título:Current and future biomarkers for pancreatic adenocarcinoma.
[So] Source:Tumour Biol;39(6):1010428317692231, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although pancreatic cancer is only the twelfth most common type of cancer in the world, it features a very unfavorable prognosis. The mortality rate almost equals the incidence rate, corroborating the very poor prognosis of pancreatic cancer. The 5-year survival rate for all stages of pancreatic ductal adenocarcinoma is only 7%. Surgical resection represents the only potentially curative treatment option for pancreatic ductal adenocarcinoma patients but is often not feasible due to the advanced stage of the disease upon diagnosis. For advanced disease, palliative chemotherapy is the treatment of choice although the regimens available to date are untargeted and have extensive side-effect profiles, making them unsuitable for patients with a low performance status. For this reason, early detection of pancreatic cancer is essential in order to provide patients with an optimal therapeutic approach. Up to the present day, carbohydrate antigen 19-9 is the only diagnostic marker approved by the U.S. Food and Drug Administration but its diagnostic potential is limited due to its restricted sensitivity and specificity, supporting the urgent need for novel biomarkers. In addition, prognostic and treatment-predictive biomarkers might provide essential information regarding personalized treatment decisions for individual patients. In this article, we aim to review current and future diagnostic, prognostic, and treatment-predictive biomarkers for pancreatic cancer.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Biomarcadores Tumorais/genética
Antígeno CA-19-9/genética
Neoplasias Pancreáticas/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/diagnóstico
Adenocarcinoma/tratamento farmacológico
Adenocarcinoma/patologia
Antígenos de Neoplasias/genética
Biomarcadores Farmacológicos
Transportador Equilibrativo 1 de Nucleosídeo/genética
Fator 15 de Diferenciação de Crescimento/genética
Seres Humanos
Neoplasias Pancreáticas/diagnóstico
Neoplasias Pancreáticas/tratamento farmacológico
Neoplasias Pancreáticas/patologia
Prognóstico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Biomarkers, Pharmacological); 0 (Biomarkers, Tumor); 0 (CA-19-9 Antigen); 0 (Equilibrative Nucleoside Transporter 1); 0 (Growth Differentiation Factor 15); 0 (PAM4 protein, human); 0 (SLC29A1 protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170705
[Lr] Data última revisão:
170705
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317692231



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