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  1 / 180848 MEDLINE  
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[PMID]:29505510
[Au] Autor:Chen XR; Dong JN; Zhang F; Yao TL
[Ad] Endereço:Department of Ultrasound, The Second Affiliated Hospital of Mudanjiang Medical University.
[Ti] Título:Efficacy and safety of image-guidance radiotherapy by helical tomotherapy in patients with lung cancer.
[So] Source:Medicine (Baltimore);97(1):e9243, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aimed to explore the efficacy and toxicity of image-guided stereotactic body radiotherapy (IGSBR) by helical tomotherapy in patients with lung cancer among Chinese Han population.A total of 21 patients with stage I lung cancer were included. They received a total of 60 Gy factions IGSBR. The outcomes included complete response (CR), partial response (PR), stable disease (SD), progress disease (PD), overall response rate (ORR), and overall survival (OS). In addition, toxicities were also recorded in this study.Three-year CR, PR, SD, PD, ORR, and OS were 47.6%, 38.1%, 9.5%, 4.8%, 85.7%, and 48.0 months, respectively. Additionally, mild toxicities were found in this study.This study demonstrated that IGSBR is efficacious for patients with stage I lung cancer with mild toxicities among Chinese Han population.
[Mh] Termos MeSH primário: Carcinoma/radioterapia
Neoplasias Pulmonares/radioterapia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Grupo com Ancestrais do Continente Asiático
Carcinoma Pulmonar de Células não Pequenas/radioterapia
Feminino
Seres Humanos
Masculino
Meia-Idade
Radioterapia Guiada por Imagem
Radioterapia de Intensidade Modulada
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180306
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009243


  2 / 180848 MEDLINE  
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[PMID]:29505507
[Au] Autor:Wang CG; Zeng DX; Huang JA; Jiang JH
[Ad] Endereço:Department of Respiratory and Critical Care, First Affiliated Hospital of Soochow University, Suzhou, P.R. China.
[Ti] Título:Effective assessment of low times MET amplification in pleural effusion after epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) acquired resistance: Cases report.
[So] Source:Medicine (Baltimore);97(1):e9021, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: The mechanism of the first-generation epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) acquired resistance included T790M mutation, cellular-mesenchymal to epithelial transition factor (MET) or EGFR amplification, PIK3CA mutation, and transformation to small cell lung cancer. MET amplification accounted for only about 5% of the resistance cases. PATIENTS CONCERNS: Few report detected MET amplification in pleural effusion. Here, we reported 2 lung adenocarcinoma cases with MET amplification in pleural effusion rapidly responded to crizotinib after EGFR-TKIs acquired resistance. DIAGNOSES: Biopsy via bronchoscopy, next-generation sequencing (NGS) in pleural effusion. INTERVENTIONS: EGFR-TKIs (Icotinib), MET inhibitor crizotinib. OUTCOMES: After a progression-free survival of 9 months and 23months, respectively, both cases progressed accompanying with pleural effusion. Results of NGS in pleural effusion showed MET amplification (2-3 times) in both cases. The 2 patients were treated with a MET inhibitor crizotinib and rapidly responded. CONCLUSION: MET amplification in pleural effusion could predict a perfect response to crizotinib after EGFR-TKIs acquired resistance, even only a low times gene amplification.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Resistência a Medicamentos Antineoplásicos/genética
Neoplasias Pulmonares/genética
Derrame Pleural Maligno/metabolismo
Proteínas Proto-Oncogênicas c-met/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/tratamento farmacológico
Idoso
Feminino
Amplificação de Genes
Seres Humanos
Neoplasias Pulmonares/tratamento farmacológico
Masculino
Meia-Idade
Inibidores de Proteínas Quinases/uso terapêutico
Proteínas Proto-Oncogênicas c-met/metabolismo
Pirazóis/uso terapêutico
Piridinas/uso terapêutico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 0 (Pyrazoles); 0 (Pyridines); 53AH36668S (crizotinib); EC 2.7.10.1 (MET protein, human); EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180306
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009021


  3 / 180848 MEDLINE  
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[PMID]:29421442
[Au] Autor:Wu S; Mao L; Li Y; Yin Y; Yuan W; Chen Y; Ren W; Lu X; Li Y; Chen L; Chen B; Xu W; Tian T; Lu Y; Jiang L; Zhuang X; Chu M; Wu J
[Ad] Endereço:Jiangsu Provincial Key Laboratory of Geriatrics, Department of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
[Ti] Título:RAGE may act as a tumour suppressor to regulate lung cancer development.
[So] Source:Gene;651:86-93, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Although the correlation of the RAGE rs2070600 polymorphism and cancer risk has been confirmed, detailed studies with functional and experimental evaluations are lacking. In this study, we first aimed to examine whether this polymorphism is associated with cancer risk based on the latest published data, and consistent with previous meta-analyses, a significant association between the rs2070600 polymorphism and cancer risk was observed (A versus G: OR = 1.25; 95% CI = 1.12-1.40). In additional stratified analyses based on cancer type, rs2070600 was significantly associated with an increased risk of lung cancer (A versus G: OR = 1.20; 95% CI = 1.09-1.33). Moreover, TCGA database showed that the expression level of RAGE was significantly lower in lung cancer tumour tissues than in adjacent non-tumour tissues, which was validated in the GEO database. Additionally, eQTL analysis indicated that the rs2070600 polymorphism may modify the expression level of RAGE in lung squamous cell carcinoma tissues (P = 0.09). Finally, we performed functional experiments in lung cancer cells and preliminarily demonstrated that RAGE may act as a tumour suppressor in lung cancer development. These findings provide evidence that the variant A allele of rs2070600 may decrease the expression of the tumour suppressor gene RAGE, thereby increasing lung cancer risk.
[Mh] Termos MeSH primário: Genes Supressores de Tumor
Neoplasias Pulmonares/genética
Polimorfismo de Nucleotídeo Único
Receptor para Produtos Finais de Glicação Avançada/genética
[Mh] Termos MeSH secundário: Linhagem Celular
Linhagem Celular Tumoral
Expressão Gênica
Predisposição Genética para Doença
Seres Humanos
Neoplasias Pulmonares/patologia
Fenótipo
Locos de Características Quantitativas
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Receptor for Advanced Glycation End Products)
[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:180209
[St] Status:MEDLINE


  4 / 180848 MEDLINE  
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[PMID]:29364966
[Au] Autor:Maleki Vareki S; Salim KY; Danter WR; Koropatnick J
[Ad] Endereço:Cancer Research Laboratory Program, Lawson Health Research Institute, London, Ontario, Canada.
[Ti] Título:Novel anti-cancer drug COTI-2 synergizes with therapeutic agents and does not induce resistance or exhibit cross-resistance in human cancer cell lines.
[So] Source:PLoS One;13(1):e0191766, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Emerging drug-resistance and drug-associated toxicities are two major factors limiting successful cancer therapy. Combinations of chemotherapeutic drugs have been used in the clinic to improve patient outcome. However, cancer cells can acquire resistance to drugs, alone or in combination. Resistant tumors can also exhibit cross-resistance to other chemotherapeutic agents, resulting in sub-optimal treatment and/or treatment failure. Therefore, developing novel oncology drugs that induce no or little acquired resistance and with a favorable safety profile is essential. We show here that combining COTI-2, a novel clinical stage agent, with multiple chemotherapeutic and targeted agents enhances the activity of these drugs in vitro and in vivo. Importantly, no overt toxicity was observed in the combination treatment groups in vivo. Furthermore, unlike the tested chemotherapeutic drugs, cancer cells did not develop resistance to COTI-2. Finally, some chemo-resistant tumor cell lines only showed mild cross-resistance to COTI-2 while most remained sensitive to it.
[Mh] Termos MeSH primário: Aminoquinolinas/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Tiossemicarbazonas/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Carcinoma Pulmonar de Células não Pequenas/patologia
Linhagem Celular Tumoral
Cisplatino/administração & dosagem
Desoxicitidina/administração & dosagem
Desoxicitidina/análogos & derivados
Resistência a Medicamentos Antineoplásicos
Neoplasias Pulmonares/patologia
Camundongos
Paclitaxel/administração & dosagem
Vimblastina/administração & dosagem
Vimblastina/análogos & derivados
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aminoquinolines); 0 (COTI-2 compound); 0 (Thiosemicarbazones); 0W860991D6 (Deoxycytidine); 5V9KLZ54CY (Vinblastine); B76N6SBZ8R (gemcitabine); P88XT4IS4D (Paclitaxel); Q20Q21Q62J (Cisplatin); Q6C979R91Y (vinorelbine)
[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:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191766


  5 / 180848 MEDLINE  
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[PMID]:29339155
[Au] Autor:Kuwabara J; Umakoshi A; Abe N; Sumida Y; Ohsumi S; Usa E; Taguchi K; Choudhury ME; Yano H; Matsumoto S; Kunieda T; Takahashi H; Yorozuya T; Watanabe Y; Tanaka J
[Ad] Endereço:Department of Gastrointestinal Surgery and Surgical Oncology, Graduate School of Medicine, Ehime University, Toon, Ehime, Japan.
[Ti] Título:Truncated CD200 stimulates tumor immunity leading to fewer lung metastases in a novel Wistar rat metastasis model.
[So] Source:Biochem Biophys Res Commun;496(2):542-548, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD200 mediates immunosuppression in immune cells that express its receptor, CD200R. There are two CD200 variants; truncated CD200 that lacks the part of N-terminal sequence necessary for CD200R binding (CD200S) and full-length CD200 (CD200L). We established a novel lung metastasis model by subcutaneously transplanting C6 glioma cells into the backs of neonatal Wistar rats. All transplanted rats developed large back tumors, nearly 90% of which bore lung metastases. To compare the effects of CD200S and CD200L on tumor immunity, CD200L (C6-L)- or CD200S (C6-S)-expressing C6 cells were similarly transplanted. The results showed that 100% of rats with C6-L tumors developed lung metastases, while metastases were found in only 44% of rats with C6-S tumors (n = 25). Tumors disappeared in approximately 20% of the C6-S-bearing rats, and these animals evaded death 180 d after transplantation, while all C6-L tumor-bearing rats died after 45 d. Next generation sequencing revealed that C6-S tumors expressed chemokines and granzyme B at much higher levels than C6-L tumors. Flow cytometry revealed that C6-S tumors contained more dead cells and more CD45 cells, including natural killer cells and CD8 lymphocytes. In particular, multiple subsets of dendritic cells expressing CD11c, MHC class II, CD8, and/or CD103 were more abundant in C6-S than in C6-L tumors. These results suggested that CD200S induced the accumulation of multiple dendritic cell subsets that activated cytotoxic T lymphocytes, leading to the elimination of metastasizing tumor cells.
[Mh] Termos MeSH primário: Antígenos CD/imunologia
Glioma/imunologia
Glioma/patologia
Neoplasias Pulmonares/imunologia
Neoplasias Pulmonares/secundário
[Mh] Termos MeSH secundário: Animais
Antígenos CD/genética
Células Dendríticas/imunologia
Células Dendríticas/patologia
Regulação Neoplásica da Expressão Gênica
Glioma/genética
Tolerância Imunológica
Imunidade Celular
Pulmão/imunologia
Pulmão/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Mutação
Ratos Wistar
Linfócitos T Citotóxicos/imunologia
Linfócitos T Citotóxicos/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (antigens, CD200)
[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:180118
[St] Status:MEDLINE


  6 / 180848 MEDLINE  
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[PMID]:29337059
[Au] Autor:Lin L; Li M; Lin L; Xu X; Jiang G; Wu L
[Ad] Endereço:Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China; Tongji University School of Medicine, Shanghai 200092, China.
[Ti] Título:FPPS mediates TGF-ß1-induced non-small cell lung cancer cell invasion and the EMT process via the RhoA/Rock1 pathway.
[So] Source:Biochem Biophys Res Commun;496(2):536-541, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Farnesyl pyrophosphate synthase (FPPS), a key enzyme in the mevalonate pathway, was recently shown to play a role in cancer progression. However, its role in non-small cell lung cancer (NSCLC) metastasis and the underlying mechanism remain unclear. In this study, FPPS expression was significantly correlated with TNM stage, and metastasis. Inhibition or knockdown of FPPS blocked TGF-ß1-induced cell invasion and epithelial-to-mesenchymal transition (EMT) process. FPPS expression of FPPS was induced by TGF-ß1 and FPPS promoted cell invasion and EMT via the RhoA/Rock1 pathway. In conclusion, FPPS mediates TGF-ß1-induced lung cancer cell invasion and EMT via the RhoA/Rock1 pathway. These findings suggest new treatment strategies to reduce mortality associated with metastasis in patients with NSCLC.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/metabolismo
Transição Epitelial-Mesenquimal
Geraniltranstransferase/metabolismo
Neoplasias Pulmonares/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
Quinases Associadas a rho/metabolismo
Proteína rhoA de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Idoso
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Linhagem Celular Tumoral
Feminino
Regulação Neoplásica da Expressão Gênica
Geraniltranstransferase/análise
Geraniltranstransferase/genética
Seres Humanos
Pulmão/metabolismo
Pulmão/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Masculino
Meia-Idade
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Transforming Growth Factor beta1); EC 2.5.1.10 (Geranyltranstransferase); EC 2.7.11.1 (ROCK1 protein, human); EC 2.7.11.1 (rho-Associated Kinases); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[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:180117
[St] Status:MEDLINE


  7 / 180848 MEDLINE  
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[PMID]:28749044
[Au] Autor:Li X; Fu Y; Miao J; Li H; Hu B
[Ad] Endereço:Department of Thoracic Surgery, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
[Ti] Título:Video-assisted thoracoscopic lobectomy after percutaneous coronary intervention in lung cancer patients with concomitant coronary heart disease.
[So] Source:Thorac Cancer;8(5):477-481, 2017 Sep.
[Is] ISSN:1759-7714
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In recent years, based on clinical observations, the number of lung cancer patients with concomitant coronary heart disease (CHD) has gradually increased. However, because of the requirement of long-term anticoagulant therapy after percutaneous coronary intervention (PCI), some of these patients lose the opportunity for surgical treatment, resulting in tumor progression. The objective of this study was to determine the appropriate timing of video-assisted thoracic surgery (VATS) lobectomy after PCI without increasing perioperative cardiovascular risk. METHODS: This study retrospectively analyzed clinical data of patients with a combination of NSCLC and CHD who underwent selective pulmonary lobectomy by VATS in the early postoperative PCI period between 2010 and 2015 at Beijing Chaoyang Hospital, China. RESULTS: Fourteen patients received VATS lobectomy after PCI. The disease had progressed to T stage in two patients after PCI. No perioperative death occurred. Two patients suffered postoperative atrial fibrillation: one had a pulmonary infection, and the other had acute coronary syndrome. All patients recovered and were discharged. CONCLUSION: For NSCLC patients with severe CHD, the use of VATS lobectomy in the early postoperative PCI period could not only advance the timing of surgery, but may also control perioperative hemorrhage and CHD event risks within acceptable ranges, which could provide more patients with an opportunity to undergo surgical treatment.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/cirurgia
Doença das Coronárias/cirurgia
Neoplasias Pulmonares/cirurgia
[Mh] Termos MeSH secundário: Idoso
Comorbidade
Feminino
Seres Humanos
Masculino
Meia-Idade
Intervenção Coronária Percutânea
Pneumonectomia/métodos
Estudos Retrospectivos
Cirurgia Torácica Vídeoassistida/métodos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[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:170728
[St] Status:MEDLINE
[do] DOI:10.1111/1759-7714.12471


  8 / 180848 MEDLINE  
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[PMID]:28745824
[Au] Autor:Ma D; Wang J; Hao X; Wang Y; Hu X; Xing P; Li J
[Ad] Endereço:Department of Medical Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
[Ti] Título:Gemcitabine combined with cisplatin as adjuvant chemotherapy for non-small cell lung cancer: A retrospective analysis.
[So] Source:Thorac Cancer;8(5):482-488, 2017 Sep.
[Is] ISSN:1759-7714
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: This study was conducted to evaluate the value of gemcitabine combined with cisplatin as adjuvant chemotherapy for radical resection of non-small cell lung cancer. METHODS: Data of 100 patients who had undergone radical resection of non-small cell lung cancer and were treated with cisplatin/gemcitabine as adjuvant chemotherapy between June 2007 and December 2010 at the Chinese Academy of Medical Sciences were reviewed. RESULTS: The median age was 59 years (range 36-73); 82% of the patients were male. Forty-two percent had adenocarcinoma and 55% had squamous cell carcinoma. Most patients had pathologic IIB (29%) and IIIA (44%) stage disease. Eighty-five percent of patients completed four cycles of chemotherapy, with 76% completing the planned full dose. The main reason for a reduced gemcitabine dose in 13 patients was grade 3/4 neutropenia or thrombocytopenia. The median dose and dose intensity were 8377.1 mg/m and 708 mg/(m /week) for gemcitabine and 293.38 mg/m and 25.24 mg/(m /week) for cisplatin, respectively. During follow-up the median disease-free survival was 33.8 months (95% confidence interval [CI] 15.938-51.676). Patients with squamous cell carcinoma (hazard ratio [HR] 0.404, 95% CI 0.241-0.676; P = 0.001) and pathologic stage I (HR 4.379, 95% CI 1.721-11.142; P = 0.002) achieved better disease-free survival. The survival rates at one, two, and five years were 94%, 77%, and 55%, while the survival rates without recurrence were 64%, 53%, and 39%, respectively. CONCLUSION: As an adjuvant chemotherapy regimen, gemcitabine with cisplatin is well tolerated. Patients with squamous cell carcinomas or pathologic stage I achieve better results.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Cisplatino/administração & dosagem
Desoxicitidina/análogos & derivados
Neoplasias Pulmonares/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Carcinoma Pulmonar de Células não Pequenas/patologia
Carcinoma Pulmonar de Células não Pequenas/cirurgia
Quimioterapia Adjuvante
Cisplatino/uso terapêutico
Desoxicitidina/administração & dosagem
Desoxicitidina/uso terapêutico
Feminino
Seres Humanos
Neoplasias Pulmonares/patologia
Neoplasias Pulmonares/cirurgia
Masculino
Meia-Idade
Estadiamento de Neoplasias
Estudos Retrospectivos
Análise de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0W860991D6 (Deoxycytidine); B76N6SBZ8R (gemcitabine); Q20Q21Q62J (Cisplatin)
[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:170727
[St] Status:MEDLINE
[do] DOI:10.1111/1759-7714.12472


  9 / 180848 MEDLINE  
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[PMID]:28742247
[Au] Autor:Zhiwei W; Yuan J; Yihui Y; Xin H; Jingtao C; Lei S; Yongjian D
[Ti] Título:Ventana immunohistochemistry assay for anaplastic lymphoma kinase gene rearrangement detection in patients with non-small cell lung cancer: A meta-analysis.
[So] Source:Thorac Cancer;8(5):471-476, 2017 Sep.
[Is] ISSN:1759-7714
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The aim of this study was to evaluate the diagnostic value of Ventana immunohistochemistry (IHC) assay for anaplastic lymphoma kinase (ALK) gene rearrangement screening in patients with non-small cell lung cancer (NSCLC). METHODS: Open published studies that reported the diagnostic performance of Ventana IHC assay for ALK gene rearrangement detection in NSCLC patients were extracted from PubMed, Embase, Google scholar, Wanfang, and China National Knowledge Infrastructure. The general information and number of true positive (tp), false positive (fp), false negative (fn), and true negative (tn) cases identified by Ventana IHC assay were extracted. The diagnostic sensitivity, specificity, positive likelihood ratio (+lr), negative likelihood ratio (-lr), diagnostic odds ratio (dor) and the summary receiver operating characteristic (ROC) curve were calculated using Stata 11.0 software. RESULTS: Ten studies, including 240 ALK positive and 1973 ALK negative NSCLC patients were included in this meta-analysis. The pooled diagnostic sensitivity, specificity, +lr, -lr, and dor were 0.94 (95% confidence interval [CI] 0.85-0.98), 1.00 (95% CI 0.99-1.00), 859.61 (95% CI 60.81-1200.00), 0.06 (95% CI 0.03-0.16), and 1400.00 (95% CI 813.29-23 000.00), respectively. The area under the ROC curve was 0.996 for Ventana IHC assay in detecting ALK gene rearrangement in NSCLC patients. CONCLUSION: The sensitivity and specificity of Ventana IHC assay for the detection of ALK gene rearrangement were high, thus Ventana IHC could substitute fluorescence in situ hybridization for the screening of ALK+ NSCLC patients.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/metabolismo
Rearranjo Gênico
Neoplasias Pulmonares/metabolismo
Receptores Proteína Tirosina Quinases/metabolismo
[Mh] Termos MeSH secundário: Carcinoma Pulmonar de Células não Pequenas/genética
Seres Humanos
Imuno-Histoquímica/métodos
Neoplasias Pulmonares/genética
Proteínas de Fusão Oncogênicas/metabolismo
Curva ROC
Receptores Proteína Tirosina Quinases/genética
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Oncogene Proteins, Fusion); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (anaplastic lymphoma kinase)
[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:170726
[St] Status:MEDLINE
[do] DOI:10.1111/1759-7714.12468


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[PMID]:29191878
[Au] Autor:Klaeger S; Heinzlmeir S; Wilhelm M; Polzer H; Vick B; Koenig PA; Reinecke M; Ruprecht B; Petzoldt S; Meng C; Zecha J; Reiter K; Qiao H; Helm D; Koch H; Schoof M; Canevari G; Casale E; Depaolini SR; Feuchtinger A; Wu Z; Schmidt T; Rueckert L; Becker W; Huenges J; Garz AK; Gohlke BO; Zolg DP; Kayser G; Vooder T; Preissner R; Hahne H; Tõnisson N; Kramer K; Götze K; Bassermann F; Schlegl J; Ehrlich HC; Aiche S; Walch A; Greif PA; Schneider S; Felder ER; Ruland J; Médard G; Jeremias I; Spiekermann K; Kuster B
[Ad] Endereço:Chair of Proteomics and Bioanalytics, Technical University of Munich (TUM), Freising, Germany.
[Ti] Título:The target landscape of clinical kinase drugs.
[So] Source:Science;358(6367), 2017 12 01.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kinase inhibitors are important cancer therapeutics. Polypharmacology is commonly observed, requiring thorough target deconvolution to understand drug mechanism of action. Using chemical proteomics, we analyzed the target spectrum of 243 clinically evaluated kinase drugs. The data revealed previously unknown targets for established drugs, offered a perspective on the "druggable" kinome, highlighted (non)kinase off-targets, and suggested potential therapeutic applications. Integration of phosphoproteomic data refined drug-affected pathways, identified response markers, and strengthened rationale for combination treatments. We exemplify translational value by discovering SIK2 (salt-inducible kinase 2) inhibitors that modulate cytokine production in primary cells, by identifying drugs against the lung cancer survival marker MELK (maternal embryonic leucine zipper kinase), and by repurposing cabozantinib to treat FLT3-ITD-positive acute myeloid leukemia. This resource, available via the ProteomicsDB database, should facilitate basic, clinical, and drug discovery research and aid clinical decision-making.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Descoberta de Drogas/métodos
Terapia de Alvo Molecular
Inibidores de Proteínas Quinases/farmacologia
Proteômica/métodos
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Linhagem Celular Tumoral
Citocinas/metabolismo
Seres Humanos
Leucemia Mieloide Aguda/tratamento farmacológico
Leucemia Mieloide Aguda/enzimologia
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/enzimologia
Camundongos
Inibidores de Proteínas Quinases/química
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Ensaios Antitumorais Modelo de Xenoenxerto
Tirosina Quinase 3 Semelhante a fms/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cytokines); 0 (Protein Kinase Inhibitors); EC 2.7.1.- (MELK protein, human); EC 2.7.1.- (salt-inducible kinase-2, human); EC 2.7.10.1 (FLT3 protein, human); EC 2.7.10.1 (fms-Like Tyrosine Kinase 3); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[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



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