Base de dados : MEDLINE
Pesquisa : D13.444.154.500 [Categoria DeCS]
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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


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[PMID]:28460431
[Au] Autor:Du J; Wu X; Tong X; Wang X; Wei J; Yang Y; Chang Z; Mao Y; Shao YW; Liu B
[Ad] Endereço:The Comprehensive Cancer Centre of Drum Tower Hospital, Medical School of Nanjing University, Clinical Cancer Institute of Nanjing University, Nanjing, Jiangsu, 210008, China.
[Ti] Título:Circulating tumor DNA profiling by next generation sequencing reveals heterogeneity of crizotinib resistance mechanisms in a gastric cancer patient with MET amplification.
[So] Source:Oncotarget;8(16):26281-26287, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Crizotinib has been used to counter MET gene amplification in a number of different human malignancies. Transient response to crizotinib in MET-amplified gastric cancer has been reported, but the mechanisms of resistance are not well studied. Here, we reported a stage IV gastric cancer patient with high levels of MET amplification. The implementation of crizotinib treatment led to significant symptomatic improvement in the first 2 months, but was followed by rapid disease progression. Periodic mutation profiling of patient's circulating tumor DNA (ctDNA) by next generation sequencing (NGS) revealed a number of genetic alterations including re-occurrence of MET amplification, multiple secondary MET mutations, a dramatic increase of FGFR2 gene relative copy number as well as mutations in other downstream and bypassing elements, which may collectively related to the patient's cancer progression. Our results illustrate the complex and heterogeneous molecular mechanisms for crizotinib resistance in this patient, and demonstrate the great potential of ctDNA profiling for treatment decision-making and prognosis in clinical practice.
[Mh] Termos MeSH primário: DNA Tumoral Circulante
Resistência a Medicamentos Antineoplásicos/genética
Amplificação de Genes
Proteínas Proto-Oncogênicas c-met/genética
Pirazóis/farmacologia
Piridinas/farmacologia
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Adulto
Linhagem Celular Tumoral
Feminino
Perfilação da Expressão Gênica
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Modelos Biológicos
Modelos Moleculares
Mutação
Estadiamento de Neoplasias
Tomografia Computadorizada com Tomografia por Emissão de Pósitrons
Conformação Proteica
Inibidores de Proteínas Quinases/farmacologia
Inibidores de Proteínas Quinases/uso terapêutico
Proteínas Proto-Oncogênicas c-met/química
Pirazóis/uso terapêutico
Piridinas/uso terapêutico
Neoplasias Gástricas/diagnóstico
Neoplasias Gástricas/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Circulating Tumor DNA); 0 (Protein Kinase Inhibitors); 0 (Pyrazoles); 0 (Pyridines); 53AH36668S (crizotinib); EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15457


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[PMID]:29243990
[Au] Autor:Agah S; Akbari A; Talebi A; Masoudi M; Sarveazad A; Mirzaei A; Nazmi F
[Ad] Endereço:a Colorectal Research Center , Iran University of Medical Sciences , Tehran , Iran.
[Ti] Título:Quantification of Plasma Cell-Free Circulating DNA at Different Stages of Colorectal Cancer.
[So] Source:Cancer Invest;35(10):625-632, 2017 Nov 26.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cell-free circulating DNAs (cfcDNAs) have been recognized as promising biomarkers for a number of cancers. This study aimed to quantify the cfcDNA in colorectal cancer to assess its potential value as biomarker. Quantification of baseline cfcDNA was determined as the amount of free glyceraldehyde 3-phosphate dehydrogenase (GAPDH) in plasma, using quantitative real-time polymerase chain reaction (PCR). The calculated area under the curve (AUC) of receiver operating characteristic (ROC) for cfcDNA was 0.875 (95% CI, 0.811-0.94), which was indicative of a high discriminatory power (p < 0.001) and significant accuracy in distinguishing cancer patients from healthy individuals. The quantification of cfcDNA could be useful for clinical settings of CRC.
[Mh] Termos MeSH primário: DNA Tumoral Circulante/análise
Neoplasias Colorretais/patologia
Reação em Cadeia da Polimerase em Tempo Real/métodos
[Mh] Termos MeSH secundário: Área Sob a Curva
Biomarcadores Tumorais/análise
Estudos de Casos e Controles
Neoplasias Colorretais/sangue
Neoplasias Colorretais/genética
Feminino
Seres Humanos
Masculino
Estadiamento de Neoplasias
Curva ROC
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Circulating Tumor DNA)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2017.1408814



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