Base de dados : MEDLINE
Pesquisa : G05.360.340.024.340.375.500.791.295.300 [Categoria DeCS]
Referências encontradas : 1063 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 107 ir para página                         

  1 / 1063 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29191895
[Au] Autor:Eisenberg R; Varmus H
[Ad] Endereço:University of Michigan Law School, Ann Arbor, MI 48109, USA. rse@umich.edu varmus@med.cornell.edu.
[Ti] Título:Insurance for broad genomic tests in oncology.
[So] Source:Science;358(6367):1133-1134, 2017 12 01.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Análise Mutacional de DNA/economia
Testes Genéticos/economia
Seguro
Neoplasias/genética
[Mh] Termos MeSH secundário: Análise Custo-Benefício
Genes erbB-1
Genômica/economia
Seres Humanos
Oncologia/economia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[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:171202
[St] Status:MEDLINE
[do] DOI:10.1126/science.aao6708


  2 / 1063 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
Texto completo
[PMID]:29336009
[Au] Autor:Sim EH; Yang IA; Wood-Baker R; Bowman RV; Fong KM
[Ad] Endereço:GenesisCare Radiation Oncology, 1 Medical Place, Urraween, Queensland, Australia, 4655.
[Ti] Título:Gefitinib for advanced non-small cell lung cancer.
[So] Source:Cochrane Database Syst Rev;1:CD006847, 2018 01 16.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The role of gefitinib for the treatment of advanced non-small cell lung cancer (NSCLC) is evolving. We undertook a systematic review to evaluate the available evidence from all randomised trials. OBJECTIVES: To determine the effectiveness and safety of gefitinib as first-line, second-line or maintenance treatment for advanced NSCLC. SEARCH METHODS: We performed searches in CENTRAL, MEDLINE and Embase from inception to 17 February 2017. We handsearched relevant conference proceedings, clinical trial registries and references lists of retrieved articles. SELECTION CRITERIA: We included trials assessing gefitinib, alone or in combination with other treatment, compared to placebo or other treatments in the first- or successive-line treatment of patients with NSCLC, excluding compassionate use. DATA COLLECTION AND ANALYSIS: We used the standard Cochrane methodology. Two authors independently assessed the search results to select those with sound methodological quality. We carried out all analyses on an intention-to-treat basis. We recorded the following outcome data: overall survival, progression-free survival, toxicity, tumour response and quality of life. We also collected data for the following subgroups: Asian ethnicity and positive epidermal growth factor receptor (EGFR) mutation. MAIN RESULTS: We included 35 eligible randomised controlled trials (RCTs), which examined 12,089 patients.General populationGefitinib did not statistically improve overall survival when compared with placebo or chemotherapy in either first- or second-line settings. Second-line gefitinib prolonged time to treatment failure (TTF) (hazard ratio (HR) 0.82, 95% confidence interval (CI) 0.75 to 0.90, P < 0.0001) when compared with placebo. Maintenance gefitinib improved progression-free survival (HR 0.70, 95% CI 0.53 to 0.91, P = 0.007) after first-line therapy.Studies in patients of Asian ethnicity or that conducted subgroup analysesSecond-line gefitinib prolonged overall survival over placebo (HR 0.66, 95% CI 0.48 to 0.91, P = 0.01). In the first-line setting, progression-free survival was improved with gefitinib over chemotherapy alone (HR 0.65, 95% CI 0.43 to 0.98, P = 0.04, moderate quality of evidence). Gefitinib given in combination with a chemotherapy regimen improved progression-free survival versus either gefitinib alone or chemotherapy alone (HR 0.69, 95% CI 0.49 to 0.96, P = 0.03; HR 0.69, 95% CI 0.62 to 0.77, P < 0.00001, respectively). In the second-line setting, progression-free survival was superior in patients given gefitinib over placebo or chemotherapy (HR 0.69, 95% CI 0.52 to 0.91, P = 0.009; HR 0.71, 95% CI 0.57 to 0.88, P = 0.002; moderate quality of evidence, respectively). Combining gefitinib with chemotherapy in the second-line setting was superior to gefitinib alone (HR 0.65, 95% CI 0.43 to 0.97, P = 0.04). As maintenance therapy, gefitinib improved progression-free survival when compared with placebo (HR 0.42, 95% CI 0.33 to 0.54, P < 0.00001).Patients with EGFR mutation-positive tumoursStudies in patients with EGFR mutation-positive tumours showed an improvement in progression-free survival in favour of gefitinib over first-line and second-line chemotherapy (HR 0.47, 95% CI 0.36 to 0.61, P < 0.00001; HR 0.24, 95% CI 0.12 to 0.47, P < 0.0001, respectively). Gefitinib as maintenance therapy following chemotherapy improved overall and progression-free survival (HR 0.39, 95% CI 0.15 to 0.98, P = 0.05; HR 0.17, 95% CI 0.07 to 0.41, P < 0.0001, respectively) in one phase III study when compared to placebo.Toxicities from gefitinib included skin rash, diarrhoea and liver transaminase derangements. Toxicities from chemotherapy included anaemia, neutropenia and neurotoxicity.In terms of quality of life, gefitinib improved Functional Assessment of Cancer Therapy-Lung (FACT-L) (standardised mean difference (SMD) 10.50, 95% CI 9.55 to 11.45, P < 0.000001), lung cancer subscale (SMD 3.63, 95% CI 3.08 to 4.19, P < 0.00001) and Trial Outcome Index (SMD 9.87, 95% CI 1.26 to 18.48, P < 0.00001) scores when compared with chemotherapy. AUTHORS' CONCLUSIONS: This systematic review shows that gefitinib, when compared with standard first- or second-line chemotherapy or maintenance therapy, probably has a beneficial effect on progression-free survival and quality of life in selected patient populations, particularly those with tumours bearing sensitising EGFR mutations.Patients with EGFR mutations lived longer when given maintenance gefitinib than those given placebo.One study conducted subgroup analysis and showed that gefitinib improved overall survival over placebo in the second-line setting in patients of Asian ethnicity. All other studies did not detect any benefit on overall survival. The data analysed in this review were very heterogenous. We were limited in the amount of data that could be pooled, largely due to variations in study design. The risk of bias in most studies was moderate, with some studies not adequately addressing potential selection, attrition and reporting bias. This heterogeneity may have an impact on the applicability of the resultsCombining gefitinib with chemotherapy appears to be superior in improving progression-free survival to either gefitinib or chemotherapy alone, however further data and phase III studies in these settings are required.Gefitinib has a favourable toxicity profile when compared with current chemotherapy regimens. Although there is no improvement in overall survival, gefitinib compares favourably with cytotoxic chemotherapy in patients with EGFR mutations with a prolongation of progression-free survival and a lesser side effect profile.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Neoplasias Pulmonares/tratamento farmacológico
Quinazolinas/uso terapêutico
[Mh] Termos MeSH secundário: Antineoplásicos/efeitos adversos
Carcinoma Pulmonar de Células não Pequenas/etnologia
Carcinoma Pulmonar de Células não Pequenas/genética
Intervalo Livre de Doença
Genes erbB-1
Seres Humanos
Neoplasias Pulmonares/etnologia
Neoplasias Pulmonares/genética
Mutação
Qualidade de Vida
Quinazolinas/efeitos adversos
Ensaios Clínicos Controlados Aleatórios como Assunto
Falha de Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Quinazolines); S65743JHBS (gefitinib)
[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:180117
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD006847.pub2


  3 / 1063 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29352306
[Au] Autor:Peraldo-Neia C; Cavalloni G; Fenocchio E; Cagnazzo C; Gammaitoni L; Cereda S; Nasti G; Satolli MA; Aprile G; Reni M; Avallone A; Spadi R; Venesio T; Martin V; Doglioni C; Frattini M; Aglietta M; Leone F
[Ad] Endereço:Medical Oncology, Fondazione del Piemonte per l'Oncologia (FPO), IRCCS-Institute of Candiolo, Candiolo, Italy.
[Ti] Título:Prognostic and predictive role of EGFR pathway alterations in biliary cancer patients treated with chemotherapy and anti-EGFR.
[So] Source:PLoS One;13(1):e0191593, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The association of anti-EGFR to gemcitabine and oxaliplatin (GEMOX) chemotherapy did not improve survival in biliary tract carcinoma (BTC) patients. Multiple mechanisms might be involved in the resistance to anti-EGFR. Here, we explored the mutation profile of EGFR extracellular domain (ECD), of tyrosine kinase domain (TKD), and its amplification status. EGFR mutational status of exons 12, 18-21 was analyzed in 57 tumors by Sanger sequencing. EGFR amplification was evaluated in 37 tumors by Fluorescent In Situ Hybridization (FISH). Kaplan-Meier curves were calculated using the log-rank test. Six patients had mutations in exon 12 of EGFR ECD and 7 in EGFR TKD. Neither EGFR ECD nor TKD mutations affected progression free survival (PFS) or overall survival (OS) in the entire population. In the panitumumab plus GEMOX (P-GEMOX) arm, ECD mutated patients had a worse OS, while EGFR TKD mutated patients had a trend towards shorter PFS and OS. Overall, the presence of mutations in EGFR or in its transducers did not affect PFS or OS, while the extrahepatic cholangiocarcinoma (ECC) mutated patients had a worse prognosis compared to WT. Nineteen out of 37 tumors were EGFR amplified, but the amplification did not correlate with survival. ECC EGFR amplified patients had improved OS, whereas the amplification significantly correlated with poor PFS (p = 0.03) in gallbladder carcinoma patients. The high molecular heterogeneity is a predominant feature of BTC: the alterations found in this work seem to have a prognostic impact rather than a predictive role towards anti-EGFR therapy.
[Mh] Termos MeSH primário: Neoplasias do Sistema Biliar/tratamento farmacológico
Neoplasias do Sistema Biliar/genética
Genes erbB-1
Mutação
Receptor do Fator de Crescimento Epidérmico/genética
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/administração & dosagem
Anticorpos Monoclonais/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Neoplasias dos Ductos Biliares/tratamento farmacológico
Neoplasias dos Ductos Biliares/genética
Neoplasias dos Ductos Biliares/metabolismo
Neoplasias do Sistema Biliar/metabolismo
Colangiocarcinoma/tratamento farmacológico
Colangiocarcinoma/genética
Colangiocarcinoma/metabolismo
Análise Mutacional de DNA
Desoxicitidina/administração & dosagem
Desoxicitidina/análogos & derivados
Desoxicitidina/uso terapêutico
Neoplasias da Vesícula Biliar/tratamento farmacológico
Neoplasias da Vesícula Biliar/genética
Neoplasias da Vesícula Biliar/metabolismo
Amplificação de Genes
Seres Humanos
Hibridização in Situ Fluorescente
Estimativa de Kaplan-Meier
Compostos Organoplatínicos/administração & dosagem
Compostos Organoplatínicos/uso terapêutico
Prognóstico
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
Receptor do Fator de Crescimento Epidérmico/metabolismo
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Organoplatinum Compounds); 04ZR38536J (oxaliplatin); 0W860991D6 (Deoxycytidine); 6A901E312A (panitumumab); B76N6SBZ8R (gemcitabine); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[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:180121
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191593


  4 / 1063 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29365415
[Au] Autor:Du J; Wang Z; Yang L; Di J; Zhang JG; Wang TY; Liu DG
[Ad] Endereço:Department of Pathology, Beijing Hospital, National Center of Gerontology, Beijing 100730, China.
[Ti] Título:[Evaluation of Consistency in detection of epidermal growth factor receptor gene T790M mutation in plasma and tumor specimens of patients with lung adenocarcinoma].
[So] Source:Zhonghua Zhong Liu Za Zhi;40(1):35-39, 2018 Jan 23.
[Is] ISSN:0253-3766
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To evaluate the consistency in detection of T790M mutation of epidermal growth factor receptor gene (EGFR) in plasma and tumor samples of patients with lung adenocarcinoma. The tumor tissues or cytological specimens of 12 patients with operable lung adenocarcinoma(stage â… -â…¢A) and 100 patients with advanced stage â…¢B-â…£ lung adenocarcinoma were collected, among which 11 patients showed acquired resistance for gefitinib (11/100). In the same period, peripheral blood samples were collected from all patients and 50 healthy volunteers. Amplification refractory mutation system (ARMS) was used to detect EGFR mutations in tumor specimens. Next Generation Sequencing(NGS) based circulating single-molecule amplification and resequencing technology (cSMART)was performed to quantitatively detect the EGFR mutations in circulating tumor DNA (ctDNA) from plasma specimens. The sensitivity, specificity and concordance rate of EGFR T790M mutation between plasma and tissue specimens from 100 advanced stage patients were 50.0%, 72.9% and 72.0%, respectively. For L858R mutation and exon 19 deletion mutations, the above mentioned sensitivity, specificity and concordance rate were 91.7%, 100.0%, and 98.0%, as well as 79.2%, 100.0% and 95.0%, respectively. The L858R mutation and exon 19 deletion mutations were not detected in plasma of 50 healthy volunteers, whereasT790M mutation(1.0±0.0 copies) was found in 7 individuals(7/50, 14.0%). Similarly, in 12 resectable patients, 4 (4/12, 33.3%) T790M mutations were found in plasma (1.2±0.2 copies), but no L858R mutation and 19 exon deletion mutations. In comparison, 28.0% of patients with advanced lung adenocarcinoma (28/100)had detectable T790M mutation in plasma with copy numbers (34.0±22.7 copies). Furthermore, the copy numbers of T790M were 268.2±119.9 in plasma of 5 cases with acquired gefitinib-resistance. In patients with advanced stages of lung adenocarcinoma, the detection of T790M mutation in plasma and tumor specimens is low. The T790M mutation also exists in the plasma of some healthy controls, suggesting that T790M mutation participates in EGFR signaling pathway and it might function in healthy population.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Genes erbB-1
Neoplasias Pulmonares/genética
Mutação
[Mh] Termos MeSH secundário: Adenocarcinoma/tratamento farmacológico
Antineoplásicos/uso terapêutico
Éxons
Voluntários Saudáveis
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Neoplasias Pulmonares/tratamento farmacológico
Quinazolinas/uso terapêutico
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Quinazolines); S65743JHBS (gefitinib)
[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:180125
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0253-3766.2018.01.006


  5 / 1063 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29245278
[Au] Autor:Wu Y; Zhu Z; Chen Y; Chai Y
[Ad] Endereço:Department of Thoracic Surgery, the Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
[Ti] Título:Tonsillar metastasis of nonsmall cell lung cancer with G719S mutation in exon 18: A case report.
[So] Source:Medicine (Baltimore);96(49):e9003, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Lung cancer has the highest mortality of all malignant tumors and is becoming the leading cause of death in China. Surgical resection is the best treatment for early non-small-cell lung carcinoma. But postoperative tumor recurrence is very common. Brain, bone and liver are the most common metastatic sites of lung cancer. PATIENT CONCERNS: A 59-year-old woman was admitted to our hospital finding a lung nodule in physical examination. No other obvious symptoms were obsessed in this patient. No remarkable abnormality was detected in preoperative laboratory tests and physical examination. DIAGNOSES: A ground-glass nodule was detected on the left inferior lobe in the imaging examination. No metastases were detected before the surgery and early-stage lung cancer was supposed. INTERVENTION: This patient underwent a radical resection of lung cancer successfully and enjoyed a peaceful postoperative rehabilitation. OUTCOMES: Although pathological diagnosed confirmed early stage lung adenocarcinoma (T1N0M0). The patient had tumor recurrence 7 months after operation. Gene sequencing confirmed the G719S mutation in exon 18 of the EGFR gene and target therapy, chemotherapy and radiotherapy were all given to this patient successively, but they were all unresponsive. The patient died 26 months after surgery. LESSONS: We herein first report G719S mutation in lung adenocarcinoma with tonsillar metastasis. Generally, the tumor responded poorly to treatment and progressed quickly, which didn't achieve the desired effect. G719S mutant is supposed to be the cause of poor responsive to treatment.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/patologia
Genes erbB-1/genética
Neoplasias Pulmonares/patologia
Neoplasias Tonsilares/secundário
[Mh] Termos MeSH secundário: Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/terapia
China
Feminino
Seres Humanos
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/terapia
Meia-Idade
Neoplasias Tonsilares/genética
Neoplasias Tonsilares/terapia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009003


  6 / 1063 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28936923
[Au] Autor:Alvarez K; Orellana P; Villarroel C; Contreras L; Kawachi H; Kobayashi M; Wielandt AM; De la Fuente M; Triviño JC; Kronberg U; Carvallo P; López-Köstner F
[Ad] Endereço:1 Laboratorio de Oncología y Genética Molecular, Unidad de Coloproctología, Clínica Las Condes, Santiago, Chile.
[Ti] Título:EGFR pathway subgroups in Chilean colorectal cancer patients, detected by mutational and expression profiles, associated to different clinicopathological features.
[So] Source:Tumour Biol;39(9):1010428317724517, 2017 Sep.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Colorectal cancer is a multistep process affecting several signaling pathways including EGFR (epidermal growth factor receptor), a therapeutic target for metastatic disease. Our aim was to characterize the mutational and expression profiles of the EGFR pathway in colorectal tumors and to integrate these results according to five previously defined groups. We screened seven genes for mutations ( KRAS-BRAF-PIK3CA-PIK3R1-AKT1-MAP2K1-PTEN) and six proteins (EGFR-p110α-p85α-PTEN-phosphoAKT-phosphoMEK1) by immunohistochemistry, PTEN deletion, and MSI. At least one mutated gene was observed in 68% of tumors ( KRAS 45%, PIK3CA 21%, BRAF 14%, and PTEN 7%). PTEN deletion was observed in 10.7% of tumors and 19.6% were MSI-High. In all, 54% of tumors showed a high EGFR expression, 48% p110α, 4.4% phosphoAKT, and 22% phosphoMEK1; and 43% showed low PTEN expression and 22% p85α. In total, five groups of tumors were defined based on MSI, BRAF, and KRAS mutations. Three groups gather mainly early-stage tumors, whereas a fourth group is mostly conformed by advanced tumors. We described here that 71.4% of tumors from one group have a mutated PI3K/PTEN pathway, in comparison to other groups having 32%, 27%, and 25%. In addition, the five groups are differentiated by molecular features such as EGFR, p85α, p110α, and PTEN, showing variable expression among tumor groups. In conclusion, alterations on the EGFR pathway were found in a high percentage of colorectal cancer patients. Using the integration of diverse molecular markers, we ratified previous classification in an ethnic group having relevant genetic differences and living in a different environmental background, adding complementary molecular targets related to therapy.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Neoplasias Colorretais/patologia
Receptor do Fator de Crescimento Epidérmico/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Chile
Análise Mutacional de DNA
Feminino
Genes erbB-1
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Imuno-Histoquímica
Masculino
Meia-Idade
Reação em Cadeia da Polimerase
Transdução de Sinais/genética
Análise Serial de Tecidos
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[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:170923
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317724517


  7 / 1063 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28854088
[Au] Autor:Reck M; Rabe KF
[Ad] Endereço:From LungenClinic Grosshansdorf and Airway Research Center North, Grosshansdorf (M.R., K.F.R.), the German Center for Lung Research, Giessen (M.R., K.F.R.), University of Lübeck, Lübeck (M.R.), and Christian Albrechts University Kiel, Kiel (K.F.R.) - all in Germany.
[Ti] Título:Precision Diagnosis and Treatment for Advanced Non-Small-Cell Lung Cancer.
[So] Source:N Engl J Med;377(9):849-861, 2017 Aug 31.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Carcinoma Pulmonar de Células não Pequenas/diagnóstico
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Imunoterapia
Neoplasias Pulmonares/diagnóstico
Neoplasias Pulmonares/tratamento farmacológico
[Mh] Termos MeSH secundário: Algoritmos
Broncoscopia/métodos
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Genes erbB-1
Seres Humanos
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Mutação
Estadiamento de Neoplasias
Ultrassonografia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170831
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMra1703413


  8 / 1063 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28768863
[Au] Autor:Pecenka V; Pajer P; Karafiat V; Kasparova P; Dudlova J; Dvorak M
[Ad] Endereço:Institute of Molecular Genetics, Academy of Sciences CR, Prague, Czech Republic pecenkav@img.cas.cz.
[Ti] Título:, , , and Genes Are Recurrently Activated by Provirus Insertion in Liver Tumors Induced by the Retrovirus Myeloblastosis-Associated Virus 2.
[So] Source:J Virol;91(20), 2017 Oct 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Myeloblastosis-associated virus 2 (MAV-2) is a highly tumorigenic simple avian retrovirus. Chickens infected with MAV-2 develop tumors in the kidneys, lungs, and liver with a short latency, less than 8 weeks. Here we report the results of molecular analyses of MAV-2-induced liver tumors that fall into three classes: hepatic hemangiosarcomas (HHSs), intrahepatic cholangiocarcinomas (ICCs), and hepatocellular carcinomas (HCCs). Comprehensive inverse PCR-based screening of 92 chicken liver tumors revealed that in ca. 86% of these tumors, MAV-2 provirus had integrated into one of four gene loci: , , , and Insertionally mutated genes correlated with tumor type: was hit in HHSs, in ICCs, mostly in ICCs, and mostly in HCCs. The provirus insertions led to the overexpression of the affected genes and, in the case of and , also to the truncation of exons encoding the extracellular ligand-binding domains of these transmembrane receptors. The structures of truncated and closely mimic the structures of oncogenic variants of these genes frequently found in human tumors ( and ). These data describe the mechanisms of oncogenesis induced in chickens by the MAV-2 retrovirus. They also show that molecular processes converting cellular regulatory genes to cancer genes may be remarkably similar in chickens and humans. We suggest that the MAV-2 retrovirus-based model can complement experiments performed using mouse models and provide data that could translate to human medicine.
[Mh] Termos MeSH primário: Vírus da Mieloblastose Aviária/fisiologia
Carcinogênese
Genes erbB-1
Neoplasias Hepáticas/virologia
Mutagênese Insercional
Proteínas Proto-Oncogênicas c-met/genética
Receptores Proteína Tirosina Quinases/genética
[Mh] Termos MeSH secundário: Animais
Vírus da Mieloblastose Aviária/genética
Proteínas Aviárias/genética
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/virologia
Galinhas/genética
Colangiocarcinoma/genética
Colangiocarcinoma/virologia
Hemangiossarcoma/genética
Hemangiossarcoma/virologia
Seres Humanos
Neoplasias Hepáticas/genética
Oncogenes
Provírus/genética
Provírus/fisiologia
Integração Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Avian Proteins); EC 2.7.10.1 (Proto-Oncogene Proteins c-met); EC 2.7.10.1 (RON protein); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE


  9 / 1063 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28720682
[Au] Autor:Do H; Molania R; Mitchell PL; Vaiskunaite R; Murdoch JD; Dobrovic A
[Ad] Endereço:Translational Genomics and Epigenomics Laboratory, Olivia Newton-John Cancer Research Institute, Melbourne, Australia; Hongdo.Do@onjcri.org.au Alex.Dobrovic@onjcri.org.au.
[Ti] Título:Reducing Artifactual T790M Mutations in DNA from Formalin-Fixed Paraffin-Embedded Tissue by Use of Thymine-DNA Glycosylase.
[So] Source:Clin Chem;63(9):1506-1514, 2017 Sep.
[Is] ISSN:1530-8561
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: False-positive T790M mutations have been reported in formalin-fixed lung tumors, but the cause of the false positives has not been identified. The T790M mutation results from a C>T change at the cytosine of a CpG dinucleotide. The presence or absence of methylation at this cytosine has different consequences following deamination, resulting in a thymine or uracil, respectively, both of which however result in an artifactual change. Uracil-DNA glycosylase (UDG) can be used to eliminate DNA templates with uracil residues but is not active against artifactual thymines. We therefore investigated the use of thymine-DNA glycosylase (TDG) to reduce artifactual T790M mutations. METHODS: Formalin-fixed normal lung tissues and lung squamous cell carcinomas were tested to measure the frequency of false-positive mutations by use of droplet digital PCR before and after treatment with either UDG or TDG. Methylation at the cytosine at T790 was assessed by pyrosequencing and by analysis of public databases. RESULTS: Artifactual T790M mutations were detected in all of the archival formalin-fixed normal lung and lung squamous cell carcinomas at mutant allele frequencies of 1% or lower. The cytosine at T790 showed high levels of methylation in all lung cancer samples and normal tissues. Pretreatment of the formalin-fixed DNA with either UDG or TDG reduced the false T790M mutations, but a greater reduction was seen with the TDG treatment. CONCLUSIONS: Both U:G and T:G lesions in formalin-fixed tissue are sources of false-positive T790M mutations. This is the first report of the use of TDG to reduce sequence artifacts in formalin-fixed DNA and is applicable to the accurate detection of mutations arising at methylated cytosines.
[Mh] Termos MeSH primário: DNA Glicosilases/metabolismo
Erros de Diagnóstico/prevenção & controle
Genes erbB-1/genética
Técnicas de Diagnóstico Molecular/métodos
Mutação/genética
Inclusão em Parafina
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Reações Falso-Positivas
Seres Humanos
Técnicas de Diagnóstico Molecular/normas
Neoplasias/diagnóstico
Neoplasias/genética
Timina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.2.2.- (DNA Glycosylases); QR26YLT7LT (Thymine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170720
[St] Status:MEDLINE
[do] DOI:10.1373/clinchem.2017.271932


  10 / 1063 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28635230
[Au] Autor:Yin H; Liao CG; Wang YQ; Li Z; Fan LL; Qian ML; Lu N
[Ad] Endereço:Medical College of Shihezi University, Shihezi 832000, China.
[Ti] Título:[The expression of programmed death receptor 1 in non-small cell lung cancer and its clinicopathological features and prognosis showed a connection with epidermal growth factor receptor gene mutations].
[So] Source:Zhonghua Zhong Liu Za Zhi;39(6):419-423, 2017 Jun 23.
[Is] ISSN:0253-3766
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the relationships between the expression of programmed death 1 (PD-1) and the epidermal growth factor receptor (EGFR) gene mutations in non-small cell lung cancer (NSCLC). The study also attempted to investigate the clinicopathological features and prognosis in NSCLC patients. The expression of PD-1 protein in 88 cases of NSCLC tumor tissues and adjacent tissues was detected by immunohistochemistry. The mutations of EGFR in NSCLC were detected by Polymerase Chain Reaction-Amplification Refractory Mutation System(PCR-ARMS) method. The expression of PD-1 and patients' clinical characteristics and prognosis were analyzed. PD-1 was positive in 63.6%(56/88) NSCLC tumor tissues, which was significantly higher than that in adjacent normal tissues (21.6%, 19/88) ( <0.05). EGFR gene mutations were found in 43 cases (48.9%), in which 30 cases (69.8%)were PD-1 positive expression. 45 cases had the wild types of EGFR gene, in which 26 cases (57.8%) were PD-1 positive. There were 24 cases of 19Del EGFR mutations, including 20 cases (83.3%) of PD-1 positive expression. 19 patients had 21L858 EGFR mutations, including 10 cases (52.6%) of PD-1 positive expression. The expression of PD-1 in NSCLC was related to patients' smoking status, lymph node metastasis and EGFR gene mutations ( <0.05). The median progression-free survival time of patients with PD-1 positive and negative expression was 7.03 and 18.66 months, respectively ( =0.007). In patients with wild-type EGFR gene, the median progression-free survival time of PD-1 positive and negative expression was 25.21 and 38.24 months, respectively. The difference was statistically significant ( =0.024). The median progression-free survival time in 43 cases of EGFR mutant patients with PD-1 positive and negative expression was 21.23 and 31.44 months. The difference was not statistically significant ( =0.128). PD-1 expresses in both EGFR mutant and wild-type NSCLC, and its expression levelis different with various EGFR mutations. The expression of PD-1 in NSCLC is related to the prognosis of patients, and the prognosis of patients with positive PD-1 expression was poor.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/metabolismo
Genes erbB-1/genética
Neoplasias Pulmonares/metabolismo
Mutação
Receptor de Morte Celular Programada 1/metabolismo
[Mh] Termos MeSH secundário: Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/mortalidade
Intervalo Livre de Doença
Feminino
Seres Humanos
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/mortalidade
Metástase Linfática
Masculino
Reação em Cadeia da Polimerase
Prognóstico
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0253-3766.2017.06.004



página 1 de 107 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde