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[PMID]:29211701
[Au] Autor:Zhong J; Deng Y; Zhang P; Li S; Huang H; Wang B; Zhang H; Peng L; Yang R; Xu J; Yuan J
[Ad] Endereço:State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, China.
[Ti] Título:New Grading System for Limbal Dermoid: A Retrospective Analysis of 261 Cases Over a 10-Year Period.
[So] Source:Cornea;37(1):66-71, 2018 Jan.
[Is] ISSN:1536-4798
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To establish a new scoring system for limbal dermoid, in order to unify the diagnostic criteria and assess the prognosis. METHODS: A retrospective study was conducted on 261 patients with limbal dermoid. The basic information, clinical features, and pathology of dermoids were recorded, and the prognosis at 1 year after keratoplasty was assessed at follow-up. A new visual scoring system was created for the area of corneal involvement, the area of conjunctival involvement, and the surface shape. RESULTS: There were 154 females and 107 males with mean age of 4 ± 3 years at surgery. After scoring, 59% (136) of patients were classified as grade I, 26% (60) as grade II, and 14% (33) as grade III. The pathological results were 124 dermoid cases, 76 lipodermoid, 5 complex choristoma, and 10 epibulbar osseous choristoma. Moreover, patients with lower clinical scores presented a better prognosis; the mean logarithm of the minimum angle of resolution (logMAR) best-corrected visual acuity in grade I patients was 0.38 ± 0.05, which was better than the grade II value of 0.61 ± 0.09 (P < 0.05) and the grade III value of 0.94 ± 0.11 (P < 0.001). CONCLUSIONS: New grading systems for limbal dermoid were useful for clinical diagnosis and may have prognostic value in predicting visual acuity. A lower-grade dermoid exhibited better vision postoperatively.
[Mh] Termos MeSH primário: Doenças da Córnea/diagnóstico
Cisto Dermoide/diagnóstico
Neoplasias Oculares/diagnóstico
Limbo da Córnea/patologia
[Mh] Termos MeSH secundário: Pré-Escolar
Doenças da Córnea/cirurgia
Cisto Dermoide/cirurgia
Neoplasias Oculares/cirurgia
Feminino
Seres Humanos
Lactente
Limbo da Córnea/cirurgia
Masculino
Gradação de Tumores
Procedimentos Cirúrgicos Oftalmológicos
Prognóstico
Estudos Retrospectivos
Acuidade Visual/fisiologia
[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:171207
[St] Status:MEDLINE
[do] DOI:10.1097/ICO.0000000000001429


  2 / 14096 MEDLINE  
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[PMID]:29267504
[Au] Autor:Mendes GA; Haag T; Trott G; Rech CGSL; Ferreira NP; Oliveira MC; Kohek MB; Pereira-Lima JFS
[Ad] Endereço:Programa de Pós-Graduação em Patologia, Universidade Federal de Ciências da Saúde de Porto Alegre, Porto Alegre, RS, Brasil.
[Ti] Título:Expression of E-cadherin, Slug and NCAM and its relationship to tumor invasiveness in patients with acromegaly.
[So] Source:Braz J Med Biol Res;51(2):e6808, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Pituitary adenomas account for 10-15% of primary intracranial tumors. Growth hormone (GH)-secreting adenomas account for 13% of all pituitary adenomas and cause acromegaly. These tumors can be aggressive, invade surrounding structures and are highly recurrent. The objective of this study was to evaluate E-cadherin, Slug and neural cell adhesion molecule (NCAM) expression in GH-secreting pituitary adenomas and its relationship to tumor invasiveness. A cross-sectional study of patients who underwent hypophysectomy due to GH-secreting pituitary adenoma from April 2007 to December 2014 was carried out. The medical records were reviewed to collect clinical data. Immediately after surgery, tumor samples were frozen in liquid nitrogen and stored in a biofreezer at -80°C for assessment of E-cadherin 1 (CDH1), SLUG (SNAI2), and NCAM (NCAM1) by real-time PCR. The samples were fixed in formalin and embedded in paraffin for immunohistochemical analysis of E-cadherin and NCAM. Thirty-five patients with acromegaly were included in the study. Of these, 65.7% had invasive tumors. Immunohistochemically, E-cadherin was expressed in 96.7% of patients, and NCAM in 80% of patients. There was no statistically significant relationship between tumor grade or invasiveness and immunohistochemical expression of these markers. Regarding gene expression, 50% of cases expressed CDH1, none expressed SNAI2, and 53.3% expressed NCAM1. There was no statistically significant relationship between tumor grade or invasiveness and gene expression of CDH1, SNAI2, and NCAM1. The absence of Slug overexpression and of E-cadherin and NCAM suppression suggests that expression of these markers is not associated with tumor invasiveness in GH-secreting pituitary adenomas.
[Mh] Termos MeSH primário: Acromegalia/patologia
Adenoma/patologia
Caderinas/análise
Moléculas de Adesão de Célula Nervosa/análise
Neoplasias Hipofisárias/patologia
Fatores de Transcrição da Família Snail/análise
[Mh] Termos MeSH secundário: Acromegalia/genética
Acromegalia/metabolismo
Adenoma/química
Adenoma/genética
Adolescente
Adulto
Idoso
Biomarcadores Tumorais/análise
Antígeno CD56/análise
Estudos Transversais
Feminino
Expressão Gênica
Seres Humanos
Imuno-Histoquímica
Masculino
Meia-Idade
Gradação de Tumores
Invasividade Neoplásica
Neoplasias Hipofisárias/química
Neoplasias Hipofisárias/genética
Reação em Cadeia da Polimerase em Tempo Real
Estatísticas não Paramétricas
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CD56 Antigen); 0 (Cadherins); 0 (NCAM1 protein, human); 0 (Neural Cell Adhesion Molecules); 0 (SNAI1 protein, human); 0 (Snail Family Transcription Factors)
[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:171222
[St] Status:MEDLINE


  3 / 14096 MEDLINE  
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[PMID]:29206996
[Au] Autor:Fokas E; Ströbel P; Fietkau R; Ghadimi M; Liersch T; Grabenbauer GG; Hartmann A; Kaufmann M; Sauer R; Graeven U; Hoffmanns H; Raab HR; Hothorn T; Wittekind C; Rödel C; German Rectal Cancer Study Group
[Ad] Endereço:Department of Radiotherapy and Oncology, University of Frankfurt, Frankfurt, Germany.
[Ti] Título:Tumor Regression Grading After Preoperative Chemoradiotherapy as a Prognostic Factor and Individual-Level Surrogate for Disease-Free Survival in Rectal 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: We investigated tumor regression grading (TRG) as a prognostic marker and individual-level surrogate for disease-free survival (DFS) in patients with rectal carcinoma treated within the Chirurgische Arbeitsgemeinschaft fur Onkologie/Arbeitsgemeinschaft Radiologische Onkologie/Arbeitsgemeinschaft Internistische Onkologie (CAO/ARO/AIO)-04 randomized trial. Methods: TRG was recorded prospectively using the Dworak classification in 1179 patients after preoperative fluorouracil-based chemoradiotherapy (CRT) with or without oxaliplatin. Multivariable analysis was performed using Cox regression models adjusted for treatment arm, resection status, and pathologic stage. Individual-level surrogacy of TRG for DFS was examined using the four Prentice criteria (PC1-4). All statistical tests were two-sided. Results: With a median follow-up of 50 months, the addition of oxaliplatin to fluorouracil-based CRT led to statistically significantly improved three-year DFS (75.9%, 95% CI = 72.3 to 79.5, vs 71.3%, 95% CI = 67.6 to 74.9, P = .04, PC 1) and a shift toward more advanced TRG groups ( P < .001, PC 2) compared with CRT with fluorouracil alone. The three-year DFS was 64.6% (95% CI = 57.3 to 71.9), 77.6% (95% CI = 74.5 to 80.7), and 92.3% (95% CI = 88.4 to 96.2) for TRG 0 + 1 (poor regression), TRG 2 + 3 (intermediate regression), and TRG 4 (complete regression), respectively ( P < .001, PC 3). TRG constituted an independent prognostic factor for DFS (TRG 2 + 3 vs TRG 0 + 1, HR = 0.68, 95% CI = 0.51 to 0.90, P = .007). Due to multicollinearity, TRG 4 and pathologic stage could not be tested within the same model. The treatment effect on DFS was captured by TRG, satisfying individual-level PC4. Conclusions: Higher TRG after preoperative CRT predicted a favorable long-term outcome. At the individual patient level, TRG was a surrogate marker for DFS. Further phase III trials are needed to validate TRG as a surrogate at trial level.
[Mh] Termos MeSH primário: Carcinoma/secundário
Carcinoma/terapia
Recidiva Local de Neoplasia
Neoplasias Retais/patologia
Neoplasias Retais/terapia
[Mh] Termos MeSH secundário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Quimiorradioterapia Adjuvante
Intervalo Livre de Doença
Feminino
Fluoruracila/administração & dosagem
Seguimentos
Seres Humanos
Masculino
Margens de Excisão
Gradação de Tumores
Recidiva Local de Neoplasia/patologia
Neoplasia Residual
Compostos Organoplatínicos/administração & dosagem
Período Pré-Operatório
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Organoplatinum Compounds); 04ZR38536J (oxaliplatin); U3P01618RT (Fluorouracil)
[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/djx095


  4 / 14096 MEDLINE  
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[PMID]:28464446
[Au] Autor:Zumsteg ZS; Zelefsky MJ; Woo KM; Spratt DE; Kollmeier MA; McBride S; Pei X; Sandler HM; Zhang Z
[Ad] Endereço:Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
[Ti] Título:Unification of favourable intermediate-, unfavourable intermediate-, and very high-risk stratification criteria for prostate cancer.
[So] Source:BJU Int;120(5B):E87-E95, 2017 11.
[Is] ISSN:1464-410X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To improve on the existing risk-stratification systems for prostate cancer. PATIENTS AND METHODS: This was a retrospective investigation including 2 248 patients undergoing dose-escalated external beam radiotherapy (EBRT) at a single institution. We separated National Comprehensive Cancer Network (NCCN) intermediate-risk prostate cancer into 'favourable' and 'unfavourable' groups based on primary Gleason pattern, percentage of positive biopsy cores (PPBC), and number of NCCN intermediate-risk factors. Similarly, NCCN high-risk prostate cancer was stratified into 'standard' and 'very high-risk' groups based on primary Gleason pattern, PPBC, number of NCCN high-risk factors, and stage T3b-T4 disease. Patients with unfavourable-intermediate-risk (UIR) prostate cancer had significantly inferior prostate-specific antigen relapse-free survival (PSA-RFS, P < 0.001), distant metastasis-free survival (DMFS, P < 0.001), prostate cancer-specific mortality (PCSM, P < 0.001), and overall survival (OS, P < 0.001) compared with patients with favourable-intermediate-risk (FIR) prostate cancer. Similarly, patients with very high-risk (VHR) prostate cancer had significantly worse PSA-RFS (P < 0.001), DMFS (P < 0.001), and PCSM (P = 0.001) compared with patients with standard high-risk (SHR) prostate cancer. Moreover, patients with FIR and low-risk prostate cancer had similar outcomes, as did patients with UIR and SHR prostate cancer. RESULTS: Consequently, we propose the following risk-stratification system: Group 1, low risk and FIR; Group 2, UIR and SHR; and Group 3, VHR. These groups have markedly different outcomes, with 8-year distant metastasis rates of 3%, 9%, and 29% (P < 0.001) for Groups 1, 2, and 3, respectively, and 8-year PCSM of 1%, 4%, and 13% (P < 0.001) after EBRT. This modified stratification system was significantly more accurate than the three-tiered NCCN system currently in clinical use for all outcomes. CONCLUSION: Modifying the NCCN risk-stratification system to group FIR with low-risk patients and UIR with SHR patients, results in modestly improved prediction of outcomes, potentially allowing better personalisation of therapeutic recommendations.
[Mh] Termos MeSH primário: Gradação de Tumores
Neoplasias da Próstata/patologia
[Mh] Termos MeSH secundário: Idoso
Seres Humanos
Masculino
Meia-Idade
Recidiva Local de Neoplasia/mortalidade
Recidiva Local de Neoplasia/patologia
Estadiamento de Neoplasias
Guias de Prática Clínica como Assunto
Prognóstico
Próstata/patologia
Antígeno Prostático Específico/sangue
Prostatectomia
Neoplasias da Próstata/sangue
Neoplasias da Próstata/mortalidade
Estudos Retrospectivos
Medição de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.21.77 (Prostate-Specific Antigen)
[Em] Mês de entrada:1802
[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:10.1111/bju.13903


  5 / 14096 MEDLINE  
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[PMID]:28460481
[Au] Autor:Kang HJ; Chung DH; Sung CO; Yoo SH; Yu E; Kim N; Lee SH; Song JY; Kim CJ; Choi J
[Ad] Endereço:Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
[Ti] Título:SHP2 is induced by the HBx-NF-κB pathway and contributes to fibrosis during human early hepatocellular carcinoma development.
[So] Source:Oncotarget;8(16):27263-27276, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The non-receptor tyrosine phosphatase SHP2 has scaffolding functions in signal transduction cascades downstream of growth receptors. A recent study suggested that SHP2 acts as a tumor suppressor during hepatocellular carcinoma (HCC) development. Herein we examined whether SHP2 links the HBx-NF-κB pathway to EGFR signaling during HCC development. The overexpression of HBx or NF-κB led to increased SHP2 expression via NF-κB binding to the Shp2 promoter. EGF treatment induced ERK activation as well as the rapid assembly of SHP2, EGFR, and Gab1. Upon LPS stimulation, NF-κB-SHP2-ERK activation and phosphorylated STAT3 levels exhibited a negative correlation in vitro. By contrast, in patients with HBV-associated HCC, NF-κB-SHP2-ERK and IL-6-JAK-STAT3 pathway activity levels were concomitantly higher in adjacent non-neoplastic tissues than in HCC tissues. The immunohistochemical analysis of 162 tissues of patients with HCC revealed that SHP2 levels were significantly higher in non-neoplastic background tissues than in corresponding HCC tissues and considerably increased in background liver tissues with advanced fibrosis (P < 0.001). SHP2 expression increased gradually from normal liver to chronic hepatitis, cirrhosis, and background liver with a dysplastic nodule, but was decreased or lost in dysplastic nodules and HCC. This is the first report to describe the existence of the HBx-NF-κB-SHP2 pathway, linking HBV infection to the EGFR-RAS-RAF-MAPK pathway in the liver. SHP2 depletion from the negative crosstalk between NF-κB and STAT3 accelerates HCC development.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/etiologia
Carcinoma Hepatocelular/metabolismo
Neoplasias Hepáticas/etiologia
Neoplasias Hepáticas/metabolismo
NF-kappa B/metabolismo
Proteína Tirosina Fosfatase não Receptora Tipo 11/genética
Transativadores/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Carcinoma Hepatocelular/patologia
Carcinoma Hepatocelular/cirurgia
Linhagem Celular Tumoral
Feminino
Fibrose
Regulação Neoplásica da Expressão Gênica
Vírus da Hepatite B/fisiologia
Seres Humanos
Cirrose Hepática/etiologia
Cirrose Hepática/metabolismo
Cirrose Hepática/patologia
Neoplasias Hepáticas/patologia
Neoplasias Hepáticas/cirurgia
Masculino
Meia-Idade
Modelos Biológicos
Gradação de Tumores
Estadiamento de Neoplasias
Regiões Promotoras Genéticas
Ligação Proteica
Proteína Tirosina Fosfatase não Receptora Tipo 11/metabolismo
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Proteínas ras/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (STAT3 Transcription Factor); 0 (Trans-Activators); 0 (hepatitis B virus X protein); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11); EC 3.6.5.2 (ras Proteins)
[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.15930


  6 / 14096 MEDLINE  
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[PMID]:28460468
[Au] Autor:Jiang L; Su X; Zhang T; Yin X; Zhang M; Fu H; Han H; Sun Y; Dong L; Qian J; Xu Y; Fu X; Gavine PR; Zhou Y; Tian K; Huang J; Shen D; Jiang H; Yao Y; Han B; Gu Y
[Ad] Endereço:Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
[Ti] Título:PD-L1 expression and its relationship with oncogenic drivers in non-small cell lung cancer (NSCLC).
[So] Source:Oncotarget;8(16):26845-26857, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In order to explore the potential patient population who could benefit from anti PD-1/PD-L1 mono or combination therapies, this study aimed to profile a panel of immunotherapy related biomarkers (PD-1, PD-L1, CTLA-4 and CD8) and targeted therapy biomarkers (EGFR, KRAS, ALK, ROS1 and MET) in NSCLC.Tumor samples from 297 NSCLC patients, including 156 adenocarcinomas (AD) and 129 squamous cell carcinomas (SCC), were analyzed using immunohistochemistry, immunofluorescence, sequencing and fluorescence in situ hybridization.43.1% of NSCLC patients had PD-L1 positive staining on ≥ 5% tumor cells (TC). Furthermore, dual color immunofluorescence revealed that the majority of PD-L1/CD8 dual positive tumor infiltrating lymphocytes (TIL) had infiltrated into the tumor core. Finally, combined analysis of all eight biomarkers showed that tumor PD-L1 positivity overlapped with known alterations in NSCLC oncogenic tumor drivers in 26% of SCC and 76% of AD samples.Our illustration of the eight biomarkers' overlap provides an intuitive overview of NSCLC for personalized therapeutic strategies using anti-PD-1/PD-L1 immune therapies, either as single agents, or in combination with targeted therapies. For the first time, we also report that PD-L1 and CD8 dual positive TILs are predominantly located within the tumor core.
[Mh] Termos MeSH primário: Antígeno B7-H1/genética
Biomarcadores Tumorais
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Expressão Gênica
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Antígeno B7-H1/metabolismo
Antígeno CTLA-4/genética
Antígeno CTLA-4/metabolismo
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Carcinoma Pulmonar de Células não Pequenas/cirurgia
Transformação Celular Neoplásica/genética
Feminino
Amplificação de Genes
Seres Humanos
Imuno-Histoquímica
Hibridização in Situ Fluorescente
Neoplasias Pulmonares/metabolismo
Neoplasias Pulmonares/cirurgia
Linfócitos do Interstício Tumoral/imunologia
Linfócitos do Interstício Tumoral/metabolismo
Masculino
Meia-Idade
Mutação
Gradação de Tumores
Estadiamento de Neoplasias
Receptor de Morte Celular Programada 1/genética
Receptor de Morte Celular Programada 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-H1 Antigen); 0 (Biomarkers, Tumor); 0 (CD274 protein, human); 0 (CTLA-4 Antigen); 0 (Programmed Cell Death 1 Receptor)
[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.15839


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[PMID]:28460465
[Au] Autor:McCormick A; Earp E; Elliot K; Cuthbert G; O'Donnell R; Wilson BT; Sutton R; Leeson C; Thomas HD; Blair H; Fordham S; Lunec J; Allan J; Edmondson RJ
[Ad] Endereço:Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, UK.
[Ti] Título:Functional characterisation of a novel ovarian cancer cell line, NUOC-1.
[So] Source:Oncotarget;8(16):26832-26844, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cell lines provide a powerful model to study cancer and here we describe a new spontaneously immortalised epithelial ovarian cancer cell line (NUOC-1) derived from the ascites collected at a time of primary debulking surgery for a mixed endometrioid / clear cell / High Grade Serous (HGS) histology. RESULTS: This spontaneously immortalised cell line was found to maintain morphology and epithelial markers throughout long-term culture. NUOC-1 cells grow as an adherent monolayer with a doubling time of 58 hours. The cells are TP53 wildtype, positive for PTEN, HER2 and HER3 expression but negative for oestrogen, progesterone and androgen receptor expression. NUOC-1 cells are competent in homologous recombination and non-homologous end joining, but base excision repair defective. Karyotype analysis demonstrated a complex tetraploid karyotype. SNP array analysis of parent and derived subpopulations (NUOC-1-A1 and NUOC-1-A2) cells demonstrated heterogeneous cell populations with numerous copy number alterations and a pro-amplification phenotype. The characteristics of this new cell line lends it to be an excellent model for investigation of a number of the identified targets. MATERIALS AND METHODS: The cell line has been characterised for growth, drug sensitivity, expression of common ovarian markers and mutations, clonogenic potential and ability to form xenografts in SCID mice. Copy number changes and clonal evolution were assessed by SNP arrays.
[Mh] Termos MeSH primário: Linhagem Celular Tumoral
Neoplasias Ovarianas/genética
Neoplasias Ovarianas/patologia
[Mh] Termos MeSH secundário: Animais
Bandeamento Cromossômico
Evolução Clonal/genética
Variações do Número de Cópias de DNA
Reparo do DNA
Modelos Animais de Doenças
Feminino
Amplificação de Genes
Genes myc
Xenoenxertos
Seres Humanos
Hibridização in Situ Fluorescente
Camundongos
Camundongos SCID
Meia-Idade
Mutação
Gradação de Tumores
Células-Tronco Neoplásicas/metabolismo
Proteína Supressora de Tumor p53/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tumor Suppressor Protein p53)
[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.15821


  8 / 14096 MEDLINE  
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[PMID]:28460462
[Au] Autor:Ness N; Andersen S; Khanehkenari MR; Nordbakken CV; Valkov A; Paulsen EE; Nordby Y; Bremnes RM; Donnem T; Busund LT; Richardsen E
[Ad] Endereço:Department of Medical Biology, UiT The Arctic University of Norway, N-9037 Tromso, Norway.
[Ti] Título:The prognostic role of immune checkpoint markers programmed cell death protein 1 (PD-1) and programmed death ligand 1 (PD-L1) in a large, multicenter prostate cancer cohort.
[So] Source:Oncotarget;8(16):26789-26801, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Programmed cell death protein 1 (PD-1) and its ligand Programmed death ligand 1 (PD-L1) have gained massive attention in cancer research due to recent availability and their targeted antitumor effects. Their role in prostate cancer is still undetermined. We constructed tissue microarrays from prostatectomy specimens from 535 prostate cancer patients. Following validation of antibodies, immunohistochemistry was used to evaluate the expression of PD-1 in lymphocytes and PD-L1 in epithelial and stromal cells of primary tumors. PD-L1 expression was commonly seen in tumor epithelial cells (92% of cases). Univariate survival analysis revealed a positive association between a high density of PD-1+ lymphocytes and worse clinical failure-free survival, limited to a trend (p = 0.084). In subgroups known to indicate unfavorable prostate cancer prognosis (Gleason grade 9, age < 65, preoperative PSA > 10, pT3) patients with high density of PD-1+ lymphocytes had a significantly higher risk of clinical failure (p = < 0.001, p = 0.025, p = 0.039 and p = 0.011, respectively). In the multivariate analysis, high density of PD-1+ lymphocytes was a significant negative independent prognostic factor for clinical failure-free survival (HR = 2.48, CI 95% 1.12-5.48, p = 0.025).
[Mh] Termos MeSH primário: Antígeno B7-H1/metabolismo
Biomarcadores Tumorais
Imunomodulação
Receptor de Morte Celular Programada 1/metabolismo
Neoplasias da Próstata/imunologia
Neoplasias da Próstata/metabolismo
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Fibroblastos Associados a Câncer/metabolismo
Seres Humanos
Imuno-Histoquímica
Imunofenotipagem
Linfócitos do Interstício Tumoral/imunologia
Linfócitos do Interstício Tumoral/metabolismo
Masculino
Meia-Idade
Gradação de Tumores
Estadiamento de Neoplasias
Prognóstico
Neoplasias da Próstata/mortalidade
Neoplasias da Próstata/patologia
Reprodutibilidade dos Testes
Análise Serial de Tecidos
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (B7-H1 Antigen); 0 (Biomarkers, Tumor); 0 (CD274 protein, human); 0 (Programmed Cell Death 1 Receptor)
[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.15817


  9 / 14096 MEDLINE  
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[PMID]:28460460
[Au] Autor:Valdés-Mora F; Locke WJ; Bandrés E; Gallego-Ortega D; Cejas P; García-Cabezas MA; Colino-Sanguino Y; Feliú J; Del Pulgar TG; Lacal JC
[Ad] Endereço:Histone Variants Group, Epigenetics Research Program, Genomics and Epigenetics Division, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.
[Ti] Título:Clinical relevance of the transcriptional signature regulated by CDC42 in colorectal cancer.
[So] Source:Oncotarget;8(16):26755-26770, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CDC42 is an oncogenic Rho GTPase overexpressed in colorectal cancer (CRC). Although CDC42 has been shown to regulate gene transcription, the specific molecular mechanisms regulating the oncogenic ability of CDC42 remain unknown. Here, we have characterized the transcriptional networks governed by CDC42 in the CRC SW620 cell line using gene expression analysis. Our results establish that several cancer-related signaling pathways, including cell migration and cell proliferation, are regulated by CDC42. This transcriptional signature was validated in two large cohorts of CRC patients and its clinical relevance was also studied. We demonstrate that three CDC42-regulated genes offered a better prognostic value when combined with CDC42 compared to CDC42 alone. In particular, the concordant overexpression of CDC42 and silencing of the putative tumor suppressor gene CACNA2D2 dramatically improved the prognostic value. The CACNA2D2/CDC42 prognostic classifier was further validated in a third CRC cohort as well as in vitro and in vivo CRC models. Altogether, we show that CDC42 has an active oncogenic role in CRC via the transcriptional regulation of multiple cancer-related pathways and that CDC42-mediated silencing of CACNA2D2 is clinically relevant. Our results further support the use of CDC42 specific inhibitors for the treatment of the most aggressive types of CRC.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Regulação Neoplásica da Expressão Gênica
Transcriptoma
Proteína cdc42 de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Animais
Canais de Cálcio/genética
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Neoplasias Colorretais/diagnóstico
Neoplasias Colorretais/mortalidade
Modelos Animais de Doenças
Feminino
Perfilação da Expressão Gênica
Redes Reguladoras de Genes
Genes Supressores de Tumor
Xenoenxertos
Seres Humanos
Camundongos
Gradação de Tumores
Metástase Neoplásica
Estadiamento de Neoplasias
Prognóstico
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CACNA2D2 protein, human); 0 (Calcium Channels); EC 3.6.5.2 (cdc42 GTP-Binding Protein)
[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.15815


  10 / 14096 MEDLINE  
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[PMID]:28460455
[Au] Autor:Zhang X; Zheng Q; Wang C; Zhou H; Jiang G; Miao Y; Zhang Y; Liu Y; Li Q; Qiu X; Wang E
[Ad] Endereço:Department of Pathology, College of Basic Medical Sciences, China Medical University, Shenyang, China.
[Ti] Título:CCDC106 promotes non-small cell lung cancer cell proliferation.
[So] Source:Oncotarget;8(16):26662-26670, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Coiled-coil domain containing (CCDC) family members enhance tumor cell proliferation, and high CCDC protein levels correlate with unfavorable prognoses. Limited research demonstrated that CCDC106 may promote the degradation of p53/TP53 protein and inhibit its transactivity. The present study demonstrated that CCDC106 expression correlates with advanced TNM stage (P = 0.008), positive regional lymph node metastasis (P < 0.001), and poor overall survival (P < 0.001) in 183 non-small cell lung cancer cases. A549 and H1299 cells were selected as representative of CCDC106-low and CCDC106-high expressing cell lines, respectively. CCDC106 overexpression promoted A549 cell proliferation and xenograft tumor growth in nude mice, while siRNA-mediated CCDC106 knockdown inhibited H1299 cell proliferation. CCDC106 promoted AKT phosphorylation and upregulated the cell cycle-regulating proteins Cyclin A2 and Cyclin B1. Cell proliferation promoted by CCDC106 via Cyclin A2 and Cyclin B1 was rescued by treatment with the AKT inhibitor, LY294002. Our studies revealed that CCDC106 is associated with non-small cell lung cancer progression and unfavorable prognosis. CCDC106 enhanced Cyclin A2 and Cyclin B1 expression and promoted A549 and H1299 cell proliferation, which depended on AKT signaling. These results suggest that CCDC106 may be a novel target for lung cancer treatment.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/genética
Proteínas de Transporte/genética
Expressão Gênica
Neoplasias Pulmonares/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Carcinoma Pulmonar de Células não Pequenas/mortalidade
Proteínas de Transporte/metabolismo
Linhagem Celular Tumoral
Proliferação Celular/genética
Ciclina A2/genética
Ciclina A2/metabolismo
Ciclina B1/genética
Ciclina B1/metabolismo
Feminino
Seres Humanos
Neoplasias Pulmonares/metabolismo
Neoplasias Pulmonares/mortalidade
Masculino
Meia-Idade
Gradação de Tumores
Metástase Neoplásica
Estadiamento de Neoplasias
Fosforilação
Prognóstico
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CCDC106 protein, human); 0 (Carrier Proteins); 0 (Cyclin A2); 0 (Cyclin B1); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[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.15792



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