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  1 / 1988 MEDLINE  
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[PMID]:29431540
[Au] Autor:Hong JH
[Ad] Endereço:a Department of Urology , Dankook University College of Medicine , Cheonan , Republic of Korea.
[Ti] Título:Pharmacokinetic/pharmacodynamic drug evaluation of enzalutamide for treating prostate cancer.
[So] Source:Expert Opin Drug Metab Toxicol;14(3):361-369, 2018 Mar.
[Is] ISSN:1744-7607
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Enzalutamide is the first approved second-generation androgen receptor (AR) antagonist in the treatment of metastatic castration-resistant prostate cancer (mCRPC) with or without docetaxel-based chemotherapy. Over the past 5 years, a number of attempts were made to determine the efficacy of enzalutamide in the different clinical settings. Areas covered: A literature search was performed at the PubMed, Embase, and Web of Science database to collect the most relevant and impactful studies, including basic science investigations, clinical trials, and reviews. This article focuses on the pharmacology, efficacy, tolerability, and future perspective of enzalutamide. Expert opinion: The treatment paradigm of CRPC has been dramatically challenged of late. Enzalutamide are in wide use because of its favorable efficacy and safety, but primary or acquired resistance to the drug will eventually develop. Further studies are thus necessary to identify appropriate patients who can achieve apparent benefits from enzalutamide alone or in combination with other drugs.
[Mh] Termos MeSH primário: Antagonistas de Receptores de Andrógenos/administração & dosagem
Feniltioidantoína/análogos & derivados
Neoplasias de Próstata Resistentes à Castração/tratamento farmacológico
[Mh] Termos MeSH secundário: Antagonistas de Receptores de Andrógenos/farmacocinética
Antagonistas de Receptores de Andrógenos/farmacologia
Animais
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Protocolos de Quimioterapia Combinada Antineoplásica/farmacocinética
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Resistência a Medicamentos Antineoplásicos
Seres Humanos
Masculino
Metástase Neoplásica
Feniltioidantoína/administração & dosagem
Feniltioidantoína/farmacocinética
Feniltioidantoína/farmacologia
Neoplasias de Próstata Resistentes à Castração/patologia
Taxoides/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Androgen Receptor Antagonists); 0 (MDV 3100); 0 (Taxoids); 15H5577CQD (docetaxel); 2010-15-3 (Phenylthiohydantoin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1440288


  2 / 1988 MEDLINE  
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[PMID]:29206995
[Au] Autor:Wyatt AW; Annala M; Aggarwal R; Beja K; Feng F; Youngren J; Foye A; Lloyd P; Nykter M; Beer TM; Alumkal JJ; Thomas GV; Reiter RE; Rettig MB; Evans CP; Gao AC; Chi KN; Small EJ; Gleave ME
[Ad] Endereço:Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, Canada; Institute of Biosciences and Medical Technology, University of Tampere, Tampere, Finland; Department of Medicine and Department of Radiation Oncology, UCSF Helen Diller Family Comprehensive
[Ti] Título:Concordance of Circulating Tumor DNA and Matched Metastatic Tissue Biopsy in Prostate Cancer.
[So] Source:J Natl Cancer Inst;109(12), 2017 Dec 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Real-time knowledge of the somatic genome can influence management of patients with metastatic castration-resistant prostate cancer (mCRPC). While routine metastatic tissue biopsy is challenging in mCRPC, plasma circulating tumor DNA (ctDNA) has emerged as a minimally invasive tool to sample the tumor genome. However, no systematic comparisons of matched "liquid" and "solid" biopsies have been performed that would enable ctDNA profiling to replace the need for direct tissue sampling. Methods: We performed targeted sequencing across 72 clinically relevant genes in 45 plasma cell-free DNA (cfDNA) samples collected at time of metastatic tissue biopsy. We compared ctDNA alterations with exome sequencing data generated from matched tissue and quantified the concordance of mutations and copy number alterations using the Fisher exact test and Pearson correlations. Results: Seventy-five point six percent of cfDNA samples had a ctDNA proportion greater than 2% of total cfDNA. In these patients, all somatic mutations identified in matched metastatic tissue biopsies were concurrently present in ctDNA. Furthermore, the hierarchy of variant allele fractions for shared mutations was remarkably similar between ctDNA and tissue. Copy number profiles between matched liquid and solid biopsy were highly correlated, and individual copy number calls in clinically actionable genes were 88.9% concordant. Detected alterations included AR amplifications in 22 (64.7%) samples, SPOP mutations in three (8.8%) samples, and inactivating alterations in tumor suppressors TP53 , PTEN , RB1 , APC , CDKN1B , BRCA2 , and PIK3R1 . In several patients, ctDNA sequencing revealed robust changes not present in paired solid biopsy, including clinically relevant alterations in the AR, WNT, and PI3K pathways. Conclusions: Our study shows that, in the majority of patients, a ctDNA assay is sufficient to identify all driver DNA alterations present in matched metastatic tissue and supports development of DNA biomarkers to guide mCRPC patient management based on ctDNA alone.
[Mh] Termos MeSH primário: DNA Tumoral Circulante/sangue
Neoplasias de Próstata Resistentes à Castração/genética
Neoplasias de Próstata Resistentes à Castração/patologia
[Mh] Termos MeSH secundário: Proteína da Polipose Adenomatosa do Colo/genética
Proteína BRCA2/genética
Biomarcadores Tumorais/sangue
Biomarcadores Tumorais/genética
Inibidor de Quinase Dependente de Ciclina p27/genética
Variações do Número de Cópias de DNA
Seres Humanos
Biópsia Líquida
Masculino
Mutação
Metástase Neoplásica
Proteínas Nucleares/genética
PTEN Fosfo-Hidrolase/genética
Fosfatidilinositol 3-Quinases/genética
Receptores Androgênicos/genética
Proteínas Repressoras/genética
Proteínas de Ligação a Retinoblastoma/genética
Proteína Supressora de Tumor p53/genética
Ubiquitina-Proteína Ligases/genética
Via de Sinalização Wnt/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APC protein, human); 0 (Adenomatous Polyposis Coli Protein); 0 (BRCA2 Protein); 0 (BRCA2 protein, human); 0 (Biomarkers, Tumor); 0 (CDKN1B protein, human); 0 (Circulating Tumor DNA); 0 (Nuclear Proteins); 0 (RB1 protein, human); 0 (Receptors, Androgen); 0 (Repressor Proteins); 0 (Retinoblastoma Binding Proteins); 0 (SPOP protein, human); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.1.- (PIK3R1 protein, human); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx118


  3 / 1988 MEDLINE  
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[PMID]:28453701
[Au] Autor:Sartor O; Coleman RE; Nilsson S; Heinrich D; Helle SI; O'Sullivan JM; Vogelzang NJ; Bruland Ø; Kobina S; Wilhelm S; Xu L; Shan M; Kattan MW; Parker C
[Ad] Endereço:Departments of Medicine and Urology, Tulane Cancer Center, New Orleans, USA.
[Ti] Título:An exploratory analysis of alkaline phosphatase, lactate dehydrogenase, and prostate-specific antigen dynamics in the phase 3 ALSYMPCA trial with radium-223.
[So] Source:Ann Oncol;28(5):1090-1097, 2017 05 01.
[Is] ISSN:1569-8041
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background: Baseline clinical variables are prognostic for overall survival (OS) in patients with castration-resistant prostate cancer (CRPC). Their prognostic and predictive value with agents targeting bone metastases, such as radium-223, is not established. Patients and methods: The radium-223 ALSYMPCA trial enrolled patients with CRPC and symptomatic bone metastases. Prognostic potential of baseline variables was assessed using Cox models. Percentage changes in biomarker levels from baseline were evaluated during the trial period; changes from baseline to week 12 were evaluated for association with OS and surrogacy. Results: Eastern Cooperative Oncology Group performance status, total alkaline phosphatase (tALP), lactate dehydrogenase (LDH), and prostate-specific antigen (PSA) at baseline were associated with OS (P ≤ 0.0003) in the intent-to-treat population (radium-223, N = 614; placebo, N = 307). tALP declined from baseline within 4 weeks after beginning radium-223, by week 12 declining in 87% of radium-223 and 23% of placebo patients (P < 0.001). LDH declined in 51% and 34% (P = 0.003), whereas PSA declined in 27% and 14% (P = 0.160). Mean tALP change from baseline was 32.2% decrease with radium-223 and 37.2% increase with placebo. Radium-223 patients with tALP decline from baseline to week 12 (confirmed ≥3 weeks from week 12) had 55% lower risk of death (hazard ratio = 0.45; 95% CI 0.34-0.61) versus those with no confirmed tALP decline. Proportional treatment effect (PTE) values for tALP, LDH, and PSA changes from baseline at week 12 as OS surrogate markers were 0.34 (95% CI: 0-0.746), 0.07 (95% CI: 0-0.211), and 0 (95% CI: 0-0.082), respectively. Conclusions: Significant tALP declines (versus placebo) occurred as early as 4 weeks after beginning radium-223 therapy. tALP or LDH declines at 12 weeks correlated with longer OS, but did not meet statistical surrogacy requirements. Dynamic changes in tALP and LDH during radium-223 treatments may be useful to monitor, but do not serve as surrogates for survival.
[Mh] Termos MeSH primário: Neoplasias de Próstata Resistentes à Castração/radioterapia
Compostos Radiofarmacêuticos/uso terapêutico
Rádio (Elemento)/uso terapêutico
[Mh] Termos MeSH secundário: Fosfatase Alcalina/metabolismo
Biomarcadores Tumorais/metabolismo
Seres Humanos
Calicreínas/metabolismo
Estimativa de Kaplan-Meier
L-Lactato Desidrogenase/metabolismo
Masculino
Análise Multivariada
Prognóstico
Modelos de Riscos Proporcionais
Antígeno Prostático Específico/metabolismo
Neoplasias de Próstata Resistentes à Castração/enzimologia
Neoplasias de Próstata Resistentes à Castração/mortalidade
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Radiopharmaceuticals); 0 (Radium-223); EC 1.1.1.27 (L-Lactate Dehydrogenase); EC 3.1.3.1 (Alkaline Phosphatase); EC 3.4.21.- (Kallikreins); EC 3.4.21.- (kallikrein-related peptidase 3, human); EC 3.4.21.77 (Prostate-Specific Antigen); W90AYD6R3Q (Radium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/annonc/mdx044


  4 / 1988 MEDLINE  
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[PMID]:29241166
[Au] Autor:De Luca R; Costa RP; Tripoli V; Murabito A; Cicero G
[Ad] Endereço:Department of Surgical, Oncological, and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo, Italy.
[Ti] Título:The Clinical Efficacy of Radium-223 for Bone Metastasis in Patients with Castration-Resistant Prostate Cancer: An Italian Clinical Experience.
[So] Source:Oncology;94(3):161-166, 2018.
[Is] ISSN:1423-0232
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Prostate cancer frequently causes bone metastases and skeletal events that impair quality of life (QoL) and survival. The alpha emitter radium-223 is a new drug that improves treatment in men with castration-resistant prostate cancer (CRPC) and bone metastases. Our aim was to evaluate the effectiveness of radium-223. SUBJECTS AND METHODS: In this retrospective study we enrolled 48 subjects. Pain reduction, alkaline phosphatase (ALP), time to first symptomatic skeletal event, and QoL were the variables we evaluated. RESULTS: Radium-223 was well tolerated, with a manageable toxicity profile and a modest objective response rate. A considerable difference in serum ALP levels before and after treatment was observed, with a significant correlation between pain relief and QoL, which showed a value of R2 to 0.44 with a slope of 1.50 (p = 0.0021). CONCLUSIONS: Radium-223 showed a clinical benefit, with a reduction in pain symptoms in 58% of patients. Radium-223 was shown to be an effective and well-tolerated therapeutic option in patients with metastatic CRPC progressing after docetaxel plus prednisone treatment.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Neoplasias Ósseas/tratamento farmacológico
Neoplasias Ósseas/secundário
Neoplasias de Próstata Resistentes à Castração/patologia
Radioisótopos/uso terapêutico
Rádio (Elemento)/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Seres Humanos
Itália
Masculino
Meia-Idade
Prednisona/uso terapêutico
Neoplasias de Próstata Resistentes à Castração/tratamento farmacológico
Qualidade de Vida
Estudos Retrospectivos
Taxoides/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Radioisotopes); 0 (Radium-223); 0 (Taxoids); 15H5577CQD (docetaxel); VB0R961HZT (Prednisone); W90AYD6R3Q (Radium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1159/000485102


  5 / 1988 MEDLINE  
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[PMID]:29299751
[Au] Autor:Honecker F; Wedding U; Kallischnigg G; Schroeder A; Klier J; Frangenheim T; Weißbach L
[Ad] Endereço:Tumor and Breast Center ZeTuP St Gallen, Rorschacher Str 150, 9006, St Gallen, Switzerland.
[Ti] Título:Risk factors for unplanned discontinuation of scheduled treatment in elderly patients with castration-resistant prostate cancer: results of the IBuTu study.
[So] Source:J Cancer Res Clin Oncol;144(3):571-577, 2018 Mar.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To gain knowledge about the factors associated with discontinuation of scheduled treatment in elderly men with castration-resistant prostate cancer (CRPC). METHODS: Patients ≥ 70 years with CRPC starting a new line of treatment were included in a prospective cohort study. A geriatric assessment (CGA) was performed at baseline, including comorbidity, mobility, functional/mental/nutritional status, as well as depression. Furthermore, pain intensity, quality of life, ECOG-performance status, and physicians' and patients' perception of health were documented. Reasons for and factors associated with discontinuation of scheduled treatment were analysed by univariate and multivariate analysis. RESULTS: After inclusion of 177 of 300 planned patients, the study was closed due to slow recruitment. 160 patients were eligible for final analysis. Median age was 77.5 years. 46% received chemotherapy, and 54% hormonal treatment. Discontinuation of scheduled treatment occurred in 91 patients (57.6%). The main reasons were progressive disease/death in 63%, adverse events/toxicity in 22%, and withdrawal of consent in 8%. In bivariate analyses, factors associated with discontinuation of treatment were age ≥ 80 years, ECOG PS ≥ 2, compromised/poor health status (physicians'/patients' assessment), and compromised functional or nutritional status. In multivariate analysis, the only remaining factor independently associated with discontinuation of scheduled treatment was impairment of activities of daily living (ADL < 100 points) (OR = 4.2 for discontinuation; p < 0.05). CONCLUSION: Despite limitations due to early termination of the study, our results demonstrate that discontinuation of scheduled treatment was common, and that compromised ADL seems to be a significant risk factor for treatment failure in elderly patients with CRPC.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Neoplasias de Próstata Resistentes à Castração/tratamento farmacológico
Neoplasias de Próstata Resistentes à Castração/epidemiologia
Suspensão de Tratamento
[Mh] Termos MeSH secundário: Atividades Cotidianas
Fatores Etários
Idoso
Idoso de 80 Anos ou mais
Estudos de Coortes
Comorbidade
Esquema de Medicação
Avaliação Geriátrica
Nível de Saúde
Seres Humanos
Masculino
Qualidade de Vida
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[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:180105
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2577-1


  6 / 1988 MEDLINE  
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[PMID]:29374713
[Au] Autor:Cheng WL; Huang CY; Tai CJ; Chang YJ; Hung CS
[Ad] Endereço:Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan, R.O.C.
[Ti] Título:Maspin Enhances the Anticancer Activity of Curcumin in Hormone-refractory Prostate Cancer Cells.
[So] Source:Anticancer Res;38(2):863-870, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Androgen deprivation therapy remains the principal treatment for patients with advanced prostate cancer, though, most patients will eventually develop hormone-refractory prostate cancer (HRPC). Androgen ablation mediated maspin-induction has been identified in cancer patients. However, the role of maspin on the anticancer activity of curcumin derived from turmeric (Curcuma longa) in HRPC cells has not been elucidated. MATERIALS AND METHODS: The anticancer action of curcumin in hormone-independent prostate cancer cells (DU145, and PC-3) was determined by measures of cell survival rate. The cause of maspin silencing on the anti-tumor abilities of curcumin in PC-3 cells was evaluated by measures of cell survival rate, cell-cycle distribution, and apoptosis signaling analysis. RESULTS: Our present study showed that PC-3 cells (with higher maspin expression) were more sensitive than DU145 cells to curcumin treatment (with lower maspin expression). RNA interference-mediated maspin silencing reduced curcumin sensitivity of PC-3 cells, as evidenced by reduced apoptotic cell death. After exposure to curcumin, maspin-knockdown cells showed lower expression levels of pro-apoptotic proteins, Bad and Bax, as compared with control cells. CONCLUSION: Maspin can enhance the sensitivity of HRPC cells to curcumin treatment.
[Mh] Termos MeSH primário: Curcumina/farmacologia
Neoplasias de Próstata Resistentes à Castração/terapia
Serpinas/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Apoptose/genética
Linhagem Celular Tumoral
Regulação para Baixo
Técnicas de Silenciamento de Genes
Seres Humanos
Masculino
Neoplasias de Próstata Resistentes à Castração/tratamento farmacológico
Neoplasias de Próstata Resistentes à Castração/genética
Neoplasias de Próstata Resistentes à Castração/metabolismo
Serpinas/biossíntese
Serpinas/deficiência
Serpinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (SERPIN-B5); 0 (Serpins); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE


  7 / 1988 MEDLINE  
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[PMID]:27776343
[Au] Autor:Fradet A; Bouchet M; Delliaux C; Gervais M; Kan C; Benetollo C; Pantano F; Vargas G; Bouazza L; Croset M; Bala Y; Leroy X; Rosol TJ; Rieusset J; Bellahcène A; Castronovo V; Aubin JE; Clézardin P; Duterque-Coquillaud M; Bonnelye E
[Ad] Endereço:InsermUMR1033, F-69372 Lyon, France.
[Ti] Título:Estrogen related receptor alpha in castration-resistant prostate cancer cells promotes tumor progression in bone.
[So] Source:Oncotarget;7(47):77071-77086, 2016 11 22.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone metastases are one of the main complications of prostate cancer and they are incurable. We investigated whether and how estrogen receptor-related receptor alpha (ERRα) is involved in bone tumor progression associated with advanced prostate cancer. By meta-analysis, we first found that ERRα expression is correlated with castration-resistant prostate cancer (CRPC), the hallmark of progressive disease. We then analyzed tumor cell progression and the associated signaling pathways in gain-of-function/loss-of-function CRPC models in vivo and in vitro. Increased levels of ERRα in tumor cells led to rapid tumor progression, with both bone destruction and formation, and direct impacts on osteoclasts and osteoblasts. VEGF-A, WNT5A and TGFß1 were upregulated by ERRα in tumor cells and all of these factors also significantly and positively correlated withERRα expression in CRPC patient specimens. Finally, high levels of ERRα in tumor cells stimulated the pro-metastatic factor periostin expression in the stroma, suggesting that ERRα regulates the tumor stromal cell microenvironment to enhance tumor progression. Taken together, our data demonstrate that ERRα is a regulator of CRPC cell progression in bone. Therefore, inhibiting ERRα may constitute a new therapeutic strategy for prostate cancer skeletal-related events.
[Mh] Termos MeSH primário: Neoplasias Ósseas/metabolismo
Neoplasias Ósseas/secundário
Neoplasias de Próstata Resistentes à Castração/metabolismo
Receptores Estrogênicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Neoplasias Ósseas/genética
Moléculas de Adesão Celular/metabolismo
Linhagem Celular Tumoral
Progressão da Doença
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Camundongos
Transplante de Neoplasias
Neoplasias de Próstata Resistentes à Castração/genética
Receptores Estrogênicos/genética
Transdução de Sinais
Fator de Crescimento Transformador beta1/metabolismo
Microambiente Tumoral
Fator A de Crescimento do Endotélio Vascular/metabolismo
Proteína Wnt-5a/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (ERRalpha estrogen-related receptor); 0 (POSTN protein, human); 0 (Receptors, Estrogen); 0 (TGFB1 protein, human); 0 (Transforming Growth Factor beta1); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 0 (WNT5A protein, human); 0 (Wnt-5a Protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.12787


  8 / 1988 MEDLINE  
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[PMID]:29241901
[Au] Autor:Degeling K; Schivo S; Mehra N; Koffijberg H; Langerak R; de Bono JS; IJzerman MJ
[Ad] Endereço:Health Technology and Services Research Department, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Enschede, The Netherlands. Electronic address: k.degeling@utwente.nl.
[Ti] Título:Comparison of Timed Automata with Discrete Event Simulation for Modeling of Biomarker-Based Treatment Decisions: An Illustration for Metastatic Castration-Resistant Prostate Cancer.
[So] Source:Value Health;20(10):1411-1419, 2017 12.
[Is] ISSN:1524-4733
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: With the advent of personalized medicine, the field of health economic modeling is being challenged and the use of patient-level dynamic modeling techniques might be required. OBJECTIVES: To illustrate the usability of two such techniques, timed automata (TA) and discrete event simulation (DES), for modeling personalized treatment decisions. METHODS: An early health technology assessment on the use of circulating tumor cells, compared with prostate-specific antigen and bone scintigraphy, to inform treatment decisions in metastatic castration-resistant prostate cancer was performed. Both modeling techniques were assessed quantitatively, in terms of intermediate outcomes (e.g., overtreatment) and health economic outcomes (e.g., net monetary benefit). Qualitatively, among others, model structure, agent interactions, data management (i.e., importing and exporting data), and model transparency were assessed. RESULTS: Both models yielded realistic and similar intermediate and health economic outcomes. Overtreatment was reduced by 6.99 and 7.02 weeks by applying circulating tumor cell as a response marker at a net monetary benefit of -€1033 and -€1104 for the TA model and the DES model, respectively. Software-specific differences were observed regarding data management features and the support for statistical distributions, which were considered better for the DES software. Regarding method-specific differences, interactions were modeled more straightforward using TA, benefiting from its compositional model structure. CONCLUSIONS: Both techniques prove suitable for modeling personalized treatment decisions, although DES would be preferred given the current software-specific limitations of TA. When these limitations are resolved, TA would be an interesting modeling alternative if interactions are key or its compositional structure is useful to manage multi-agent complex problems.
[Mh] Termos MeSH primário: Simulação por Computador
Técnicas de Apoio para a Decisão
Modelos Econômicos
Neoplasias de Próstata Resistentes à Castração/terapia
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/metabolismo
Tomada de Decisão Clínica
Seres Humanos
Masculino
Medicina de Precisão/métodos
Antígeno Prostático Específico/metabolismo
Neoplasias de Próstata Resistentes à Castração/patologia
Cintilografia/métodos
Avaliação da Tecnologia Biomédica/métodos
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor); EC 3.4.21.77 (Prostate-Specific Antigen)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE


  9 / 1988 MEDLINE  
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[PMID]:28459972
[Au] Autor:van Soest RJ
[Ad] Endereço:Department of Urology, Erasmus University Medical Center, Erasmus MC Cancer Institute, Rotterdam, The Netherlands.
[Ti] Título:Liquid biopsies and plasma DNA: paving the way for personalized medicine in metastatic castration-resistant prostate cancer.
[So] Source:Ann Oncol;28(7):1408-1409, 2017 07 01.
[Is] ISSN:1569-8041
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Medicina de Precisão
Neoplasias de Próstata Resistentes à Castração
[Mh] Termos MeSH secundário: Androstenos
DNA
Seres Humanos
Biópsia Líquida
Masculino
[Pt] Tipo de publicação:EDITORIAL; COMMENT
[Nm] Nome de substância:
0 (Androstenes); 9007-49-2 (DNA)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1093/annonc/mdx208


  10 / 1988 MEDLINE  
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[PMID]:28457729
[Au] Autor:Seipel AH; Whitington T; Delahunt B; Samaratunga H; Mayrhofer M; Wiklund P; Grönberg H; Lindberg J; Egevad L
[Ad] Endereço:Department of Oncology-Pathology, Karolinska Institutet, 171 76 Stockholm, Sweden.
[Ti] Título:Genetic profile of ductal adenocarcinoma of the prostate.
[So] Source:Hum Pathol;69:1-7, 2017 11.
[Is] ISSN:1532-8392
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Despite being discovered almost 50 years ago, little is known regarding the genetic profile of ductal adenocarcinoma of the prostate (DAC). In recent years, progress has been made in the understanding of the genetics of acinar adenocarcinomas, and at least 7 genetically different subtypes have been identified. DAC is known to present at an advanced stage with a high rate of extraprostatic extension and seminal vesicle invasion, and a decreased interval to biochemical recurrence and the development of metastatic disease when compared with acinar adenocarcinoma. Our aim was to investigate the genetic profile of DAC to determine whether there is a genomic rationale for the aggressive behavior associated with this tumor type. Frozen tissue from 11 cases of DAC with paired benign tissue was analyzed. After DNA extraction, copy-number alteration analysis was performed, as well as identification of mutations and indels. We compared the fraction of the DAC genome with copy-number alteration to previous results from 74 primary acinar adenocarcinomas of the prostate. The alteration rate in DAC was comparable to that of acinar adenocarcinoma of high Gleason score. DAC harbored somatic changes seen in advanced and/or metastatic castration-resistant acinar adenocarcinoma, which likely accounts for its aggressive biological behavior.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Carcinoma Ductal/genética
Perfilação da Expressão Gênica/métodos
Neoplasias de Próstata Resistentes à Castração/genética
Neoplasias da Próstata/genética
Transcriptoma
[Mh] Termos MeSH secundário: Idoso
Carcinoma Ductal/secundário
Variações do Número de Cópias de DNA
Análise Mutacional de DNA
Dosagem de Genes
Predisposição Genética para Doença
Seres Humanos
Mutação INDEL
Masculino
Meia-Idade
Gradação de Tumores
Invasividade Neoplásica
Estadiamento de Neoplasias
Fenótipo
Neoplasias da Próstata/patologia
Neoplasias de Próstata Resistentes à Castração/patologia
Carga Tumoral
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180117
[Lr] Data última revisão:
180117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE



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