Base de dados : MEDLINE
Pesquisa : C04.557.470.200.025 [Categoria DeCS]
Referências encontradas : 138671 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 13868 ir para página                         

  1 / 138671 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29505548
[Au] Autor:Xu M; Zhou F; Huang L
[Ad] Endereço:Department of Pathology.
[Ti] Título:Concomitant endometrial and cervical adenocarcinoma: A case report and literature review.
[So] Source:Medicine (Baltimore);97(1):e9596, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Concomitant malignancy of the endometrium and cervix is extremely rare. PATIENT CONCERNS: A 56-year-old female presented to the Women's Hospital, School of Medicine, Zhejiang University, complaining of irregular vaginal bleeding. The human papillomavirus test (type 18/45) was positive. We performed dilation and curettage; pathology revealed moderately differentiated endometrial carcinoma exhibiting squamous differentiation. The epithelium of the cervical uterus was atypical upon biopsy. DIAGNOSES: Histological and immunochemical tests confirmed a diagnosis of endometrial carcinoma concomitant with cervical adenocarcinoma. INTERVENTIONS: She underwent laparoscopic staging surgery. OUTCOMES: The patient fully recovered with only surgery. LESSONS: Endometrial carcinoma concomitant with cervical adenocarcinoma is very rare. It is imperative to schedule adequate examination, and to perform careful preoperative diagnosis and appropriate treatment to minimize relapse.
[Mh] Termos MeSH primário: Adenocarcinoma/patologia
Neoplasias do Endométrio/patologia
Neoplasias Primárias Múltiplas/patologia
Neoplasias do Colo do Útero/patologia
Útero/patologia
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[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.0000000000009596


  2 / 138671 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29505541
[Au] Autor:Noh HM; Yoo JH; Jeong JY; Park YS
[Ad] Endereço:Department of Family Medicine, Hallym University Sacred Heart Hospital, Hallym University College of Medicine, Anyang.
[Ti] Título:Bone mineral density after treatment for gastric cancer: Endoscopic treatment versus gastrectomy.
[So] Source:Medicine (Baltimore);97(1):e9582, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Changes in bone metabolism among gastric cancer survivors have long been recognized. The aim of our study was to clarify the changes of bone mineral density (BMD) among gastric cancer survivors who underwent endoscopic resection or gastrectomy. Forty-nine patients diagnosed with tumor, node, and metastasis (TNM) stage 1 gastric cancer with pathologic confirmation, who underwent BMD measurement just before the procedure, and had no prior osteoporosis treatment, were studied. BMD was measured with dual energy x-ray absorptiometry before and after treatment. Laboratory tests were performed using fresh serum, and serum levels of alkaline phosphatase, albumin, calcium, and phosphorus were measured. We used a nested case-control design to compare groups. Of the 49 patients, 34 underwent gastrectomy and 15 underwent endoscopic treatment. There were no differences in baseline clinical characteristics, including BMD, and biochemical data between groups. The mean and median follow-up intervals for BMD measurement were 32.6 months (standard deviation, 16.5) and 31.0 months (interquartile range: 21.5, 41.0), respectively. The follow-up BMDs of the femoral neck and total hip were lower in the gastrectomy group (P = .010 and .011, respectively). The percentage changes in BMD for the lumbar spine, femoral neck, and total hip were -3.30%, -1.52%, and 0.40%, respectively, in the endoscopic treatment group, and -7.17%, -6.30%, and -3.49%, respectively, in the gastrectomy group. Bone loss of the lumbar spine and femoral neck were greater in the gastrectomy group (P = .028 and .022, respectively). BMD is lower after gastrectomy than after endoscopic treatment among early stage gastric cancer survivors.
[Mh] Termos MeSH primário: Adenocarcinoma/cirurgia
Densidade Óssea
Gastrectomia
Gastroscopia
Neoplasias Gástricas/cirurgia
[Mh] Termos MeSH secundário: Adenocarcinoma/metabolismo
Adulto
Idoso
Osso e Ossos/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Retrospectivos
Neoplasias Gástricas/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; OBSERVATIONAL STUDY
[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.0000000000009582


  3 / 138671 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[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


  4 / 138671 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28465312
[Au] Autor:Noorani A; Bornschein J; Lynch AG; Secrier M; Achilleos A; Eldridge M; Bower L; Weaver JMJ; Crawte J; Ong CA; Shannon N; MacRae S; Grehan N; Nutzinger B; O'Donovan M; Hardwick R; Tavaré S; Fitzgerald RC; Oesophageal Cancer Clinical and Molecular Stratification (OCCAMS) Consortium
[Ad] Endereço:Medical Research Council Cancer Unit, Hutchison/Medical Research Council Research Centre, University of Cambridge, Cambridge CB2 0XZ, United Kingdom.
[Ti] Título:A comparative analysis of whole genome sequencing of esophageal adenocarcinoma pre- and post-chemotherapy.
[So] Source:Genome Res;27(6):902-912, 2017 06.
[Is] ISSN:1549-5469
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The scientific community has avoided using tissue samples from patients that have been exposed to systemic chemotherapy to infer the genomic landscape of a given cancer. Esophageal adenocarcinoma is a heterogeneous, chemoresistant tumor for which the availability and size of pretreatment endoscopic samples are limiting. This study compares whole-genome sequencing data obtained from chemo-naive and chemo-treated samples. The quality of whole-genomic sequencing data is comparable across all samples regardless of chemotherapy status. Inclusion of samples collected post-chemotherapy increased the proportion of late-stage tumors. When comparing matched pre- and post-chemotherapy samples from 10 cases, the mutational signatures, copy number, and SNV mutational profiles reflect the expected heterogeneity in this disease. Analysis of SNVs in relation to allele-specific copy-number changes pinpoints the common ancestor to a point prior to chemotherapy. For cases in which pre- and post-chemotherapy samples do show substantial differences, the timing of the divergence is near-synchronous with endoreduplication. Comparison across a large prospective cohort (62 treatment-naive, 58 chemotherapy-treated samples) reveals no significant differences in the overall mutation rate, mutation signatures, specific recurrent point mutations, or copy-number events in respect to chemotherapy status. In conclusion, whole-genome sequencing of samples obtained following neoadjuvant chemotherapy is representative of the genomic landscape of esophageal adenocarcinoma. Excluding these samples reduces the material available for cataloging and introduces a bias toward the earlier stages of cancer.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Antineoplásicos/uso terapêutico
Neoplasias Esofágicas/genética
Regulação Neoplásica da Expressão Gênica
Genoma Humano
Taxa de Mutação
Proteínas de Neoplasias/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/tratamento farmacológico
Adenocarcinoma/metabolismo
Adenocarcinoma/patologia
Idoso
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/metabolismo
Transformação Celular Neoplásica/patologia
Biologia Computacional
Variações do Número de Cópias de DNA
Neoplasias Esofágicas/tratamento farmacológico
Neoplasias Esofágicas/metabolismo
Neoplasias Esofágicas/patologia
Esôfago/metabolismo
Esôfago/patologia
Feminino
Perfilação da Expressão Gênica
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Masculino
Meia-Idade
Terapia Neoadjuvante/métodos
Proteínas de Neoplasias/metabolismo
Mutação Puntual
Polimorfismo de Nucleotídeo Único
Estudos Prospectivos
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Neoplasm Proteins)
[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:170504
[St] Status:MEDLINE
[do] DOI:10.1101/gr.214296.116


  5 / 138671 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28453388
[Au] Autor:Ayars M; Eshleman J; Goggins M
[Ad] Endereço:a Department of Pathology , The Johns Hopkins University School of Medicine , Baltimore , MD, USA.
[Ti] Título:Susceptibility of ATM-deficient pancreatic cancer cells to radiation.
[So] Source:Cell Cycle;16(10):991-998, 2017 May 19.
[Is] ISSN:1551-4005
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ataxia telangiectasia mutated (ATM) is inactivated in a significant minority of pancreatic ductal adenocarcinomas and may be predictor of treatment response. We determined if ATM deficiency renders pancreatic cancer cells more sensitive to fractionated radiation or commonly used chemotherapeutics. ATM expression was knocked down in three pancreatic cancer cell lines using ATM-targeting shRNA. Isogenic cell lines were tested for sensitivity to several chemotherapeutic agents and radiation. DNA repair kinetics were analyzed in irradiated cells using the comet assay. We find that while rendering pancreatic cancer cells ATM-deficient did not significantly change their sensitivity to several chemotherapeutics, it did render them exquisitely sensitized to radiation. Pancreatic cancer ATM status may help predict response to radiotherapy.
[Mh] Termos MeSH primário: Adenocarcinoma/radioterapia
Proteínas Mutadas de Ataxia Telangiectasia/genética
Carcinoma Ductal Pancreático/radioterapia
Tolerância a Radiação/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Adenocarcinoma/patologia
Carcinoma Ductal Pancreático/genética
Carcinoma Ductal Pancreático/patologia
Linhagem Celular Tumoral
Quebras de DNA de Cadeia Dupla
Dano ao DNA/efeitos da radiação
Reparo do DNA/efeitos da radiação
Regulação Neoplásica da Expressão Gênica/efeitos da radiação
Seres Humanos
Fosforilação/efeitos da radiação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.11.1 (ATM protein, human); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.1080/15384101.2017.1312236


  6 / 138671 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29191879
[Au] Autor:Engblom C; Pfirschke C; Zilionis R; Da Silva Martins J; Bos SA; Courties G; Rickelt S; Severe N; Baryawno N; Faget J; Savova V; Zemmour D; Kline J; Siwicki M; Garris C; Pucci F; Liao HW; Lin YJ; Newton A; Yaghi OK; Iwamoto Y; Tricot B; Wojtkiewicz GR; Nahrendorf M; Cortez-Retamozo V; Meylan E; Hynes RO; Demay M; Klein A; Bredella MA; Scadden DT; Weissleder R; Pittet MJ
[Ad] Endereço:Center for Systems Biology, Massachusetts General Hospital Research Institute and Harvard Medical School, Boston, MA 02114, USA.
[Ti] Título:Osteoblasts remotely supply lung tumors with cancer-promoting SiglecF neutrophils.
[So] Source:Science;358(6367), 2017 12 01.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone marrow-derived myeloid cells can accumulate within tumors and foster cancer outgrowth. Local immune-neoplastic interactions have been intensively investigated, but the contribution of the systemic host environment to tumor growth remains poorly understood. Here, we show in mice and cancer patients ( = 70) that lung adenocarcinomas increase bone stromal activity in the absence of bone metastasis. Animal studies reveal that the cancer-induced bone phenotype involves bone-resident osteocalcin-expressing (Ocn ) osteoblastic cells. These cells promote cancer by remotely supplying a distinct subset of tumor-infiltrating SiglecF neutrophils, which exhibit cancer-promoting properties. Experimentally reducing Ocn cell numbers suppresses the neutrophil response and lung tumor outgrowth. These observations posit osteoblasts as remote regulators of lung cancer and identify SiglecF neutrophils as myeloid cell effectors of the osteoblast-driven protumoral response.
[Mh] Termos MeSH primário: Adenocarcinoma/patologia
Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/metabolismo
Osso e Ossos/patologia
Lectinas/metabolismo
Neoplasias Pulmonares/patologia
Infiltração de Neutrófilos
Neutrófilos/metabolismo
Neutrófilos/patologia
Osteoblastos/patologia
[Mh] Termos MeSH secundário: Animais
Densidade Óssea
Células da Medula Óssea/patologia
Osso e Ossos/metabolismo
Linhagem Celular Tumoral
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Células Mieloides/patologia
Neoplasias Experimentais/patologia
Osteocalcina/metabolismo
Receptor para Produtos Finais de Glicação Avançada/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (Lectins); 0 (Receptor for Advanced Glycation End Products); 0 (SIGLEC5 protein, human); 0 (sRAGE protein, human); 104982-03-8 (Osteocalcin)
[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


  7 / 138671 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29442032
[Au] Autor:Jiang JF; Zhai J; Liu ZR; Chao L; Zhao YF; Wu YJ; Cui MX
[Ti] Título:Ampelopsin sodium induces mitochondrial-mediated apoptosis in human lung adenocarcinoma SPC-A-1 cell line.
[So] Source:Pharmazie;71(8):455-459, 2016 08 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Ampelopsin is a well-known flavonoid which has variety of biological and pharmacological actions including anticancer effects and induction of apoptosis on the several cancer cell lines. The present study aimed to evaluate the role of ampelopsin sodium (Amp-Na) in the mitochondrial-mediated apoptosis of human lung adenocarcionma SPC-A-1 cells. The analysis of cell proliferation and ultrastructure were performed. Furthermore, to clarify its action mechanism by determining the mitochondrial membrane potential (Δψm), intracellular calcium (Ca2+) concentration, mitochondrial nitric oxide (NO) level and total ATPase activity. The results showed that Amp-Na markedly inhibited the SPC-A-1 cell proliferation and caused ultrastructural apoptosis feature in SPC-A-1 cells in a dose-dependent manner. Amp-Na led to a rapid and sustained Ca2+ elevation and Δψm reduction, and induced the mitochondrial NO production and decreased the total ATPase activity in SPC-A-1 cells. The results enhance the potential of Amp-Na as a therapeutic drug for treating lung cancer, and provide new information for mechanism of Amp-Na which induces mitochondrial-mediated apoptosis in tumor cells.
[Mh] Termos MeSH primário: Adenocarcinoma/tratamento farmacológico
Antineoplásicos Fitogênicos/farmacologia
Apoptose/efeitos dos fármacos
Flavonoides/farmacologia
Neoplasias Pulmonares/tratamento farmacológico
Mitocôndrias/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenocarcinoma/patologia
Adenocarcinoma/ultraestrutura
Adenosina Trifosfatases/metabolismo
Cálcio/metabolismo
Linhagem Celular Tumoral
Proliferação Celular
Relação Dose-Resposta a Droga
Seres Humanos
Neoplasias Pulmonares/patologia
Neoplasias Pulmonares/ultraestrutura
Potencial da Membrana Mitocondrial/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Flavonoids); 27200-12-0 (ampelopsin); EC 3.6.1.- (Adenosine Triphosphatases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6571


  8 / 138671 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28922779
[Au] Autor:Hanley CJ; Mellone M; Ford K; Thirdborough SM; Mellows T; Frampton SJ; Smith DM; Harden E; Szyndralewiez C; Bullock M; Noble F; Moutasim KA; King EV; Vijayanand P; Mirnezami AH; Underwood TJ; Ottensmeier CH; Thomas GJ
[Ad] Endereço:Cancer Sciences Unit, University of Southampton Faculty of Medicine, Southampton, UK; Genkyotex SA, Plan-les-Ouates, Switzerland; La Jolla Institute for Allergy and Immunology, La Jolla, CA.
[Ti] Título:Targeting the Myofibroblastic Cancer-Associated Fibroblast Phenotype Through Inhibition of NOX4.
[So] Source:J Natl Cancer Inst;110(1), 2018 Jan 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Cancer-associated fibroblasts (CAFs) are tumor-promoting and correlate with poor survival in many cancers, which has led to their emergence as potential therapeutic targets. However, effective methods to manipulate these cells clinically have yet to be developed. Methods: CAF accumulation and prognostic significance in head and neck cancer (oral, n = 260; oropharyngeal, n = 271), and colorectal cancer (n = 56) was analyzed using immunohistochemistry. Mechanisms regulating fibroblast-to-myofibroblast transdifferentiation were investigated in vitro using RNA interference/pharmacological inhibitors followed by polymerase chain reaction (PCR), immunoblotting, immunofluorescence, and functional assays. RNA sequencing/bioinformatics and immunohistochemistry were used to analyze NAD(P)H Oxidase-4 (NOX4) expression in different human tumors. NOX4's role in CAF-mediated tumor progression was assessed in vitro, using CAFs from multiple tissues in Transwell and organotypic culture assays, and in vivo, using xenograft (n = 9-15 per group) and isograft (n = 6 per group) tumor models. All statistical tests were two-sided. Results: Patients with moderate/high levels of myofibroblastic-CAF had a statistically significant decrease in cancer-specific survival rates in each cancer type analyzed (hazard ratios [HRs] = 1.69-7.25, 95% confidence intervals [CIs] = 1.11 to 31.30, log-rank P ≤ .01). Fibroblast-to-myofibroblast transdifferentiation was dependent on a delayed phase of intracellular reactive oxygen species, generated by NOX4, across different anatomical sites and differentiation stimuli. A statistically significant upregulation of NOX4 expression was found in multiple human cancers (P < .001), strongly correlating with myofibroblastic-CAFs (r = 0.65-0.91, adjusted P < .001). Genetic/pharmacological inhibition of NOX4 was found to revert the myofibroblastic-CAF phenotype ex vivo (54.3% decrease in α-smooth muscle actin [α-SMA], 95% CI = 10.6% to 80.9%, P = .009), prevent myofibroblastic-CAF accumulation in vivo (53.2%-79.0% decrease in α-SMA across different models, P ≤ .02) and slow tumor growth (30.6%-64.0% decrease across different models, P ≤ .04). Conclusions: These data suggest that pharmacological inhibition of NOX4 may have broad applicability for stromal targeting across cancer types.
[Mh] Termos MeSH primário: Adenocarcinoma/tratamento farmacológico
Fibroblastos Associados a Câncer/patologia
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Carcinoma de Células Escamosas/tratamento farmacológico
Neoplasias Colorretais/química
Neoplasias Esofágicas/tratamento farmacológico
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Bucais/química
Miofibroblastos/patologia
NADPH Oxidases/antagonistas & inibidores
Neoplasias Orofaríngeas/química
[Mh] Termos MeSH secundário: Actinas/análise
Adenocarcinoma/química
Adenocarcinoma/genética
Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Fibroblastos Associados a Câncer/química
Fibroblastos Associados a Câncer/fisiologia
Carcinoma Pulmonar de Células não Pequenas/química
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma de Células Escamosas/química
Carcinoma de Células Escamosas/genética
Contagem de Células
Transdiferenciação Celular/efeitos dos fármacos
Transdiferenciação Celular/genética
Neoplasias Colorretais/patologia
Progressão da Doença
Neoplasias Esofágicas/química
Neoplasias Esofágicas/genética
Feminino
Neoplasias de Cabeça e Pescoço/química
Neoplasias de Cabeça e Pescoço/tratamento farmacológico
Neoplasias de Cabeça e Pescoço/genética
Seres Humanos
Neoplasias Pulmonares/química
Neoplasias Pulmonares/genética
Masculino
Camundongos
Meia-Idade
Neoplasias Bucais/patologia
Miofibroblastos/química
NADPH Oxidase 4
NADPH Oxidases/análise
NADPH Oxidases/genética
Transplante de Neoplasias
Neoplasias Orofaríngeas/patologia
Fenótipo
Pirazóis/uso terapêutico
Piridinas/uso terapêutico
Interferência de RNA
Espécies Reativas de Oxigênio/metabolismo
Taxa de Sobrevida
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (GKT137831); 0 (Pyrazoles); 0 (Pyridines); 0 (Reactive Oxygen Species); EC 1.6.3.- (NADPH Oxidase 4); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.- (NOX4 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx121


  9 / 138671 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28453696
[Au] Autor:Böger C; Krüger S; Behrens HM; Bock S; Haag J; Kalthoff H; Röcken C
[Ad] Endereço:Department of Pathology, Christian-Albrechts-University, Kiel, Germany
[Ti] Título:Epstein-Barr virus-associated gastric cancer reveals intratumoral heterogeneity of PIK3CA mutations.
[So] Source:Ann Oncol;28(5):1005-1014, 2017 05 01.
[Is] ISSN:1569-8041
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background: Recent whole-genome sequencing identified four molecular subtypes of gastric cancer (GC), of which the subgroup of Epstein-Barr virus-associated GC (EBVaGC) showed a significant enrichment of PIK3CA mutations. We here aimed to validate independently the enrichment of PIK3CA mutations in EBVaGC of a Central European GC cohort, to correlate EBV status with clinico-pathological patient characteristics and to test for a major issue of GC, intratumoral heterogeneity. Patients and methods: In a first step, 484 GCs were screened for EBV and PIK3CA hot spot mutations of exon 9/20 using EBER in situ hybridization and pyrosequencing, respectively. Secondly, an extended sequencing of PIK3CA also utilizing next generation sequencing was carried out in all EBVaGCs and 96 corresponding lymph node metastases. Results: Twenty-two GCs were EBER-positive, all being of latency type I. Intratumoral heterogeneity of EBER-positivity was found in 18% of EBVaGCs. Twenty-three GCs held PIK3CA mutations in hot spot regions of exon 9 or 20, being significantly more common in EBVaGCs (P < 0.001). Subsequent extended sequencing of PIK3CA of EBVaGCs showed that 14% harvested three to five different PIK3CA genotypes (including wildtype) in the same primary tumor, albeit in histologically and spatially distinct tumor areas, and that intratumoral heterogeneity of PIK3CA was also present in the corresponding lymph node metastases. Conclusions: Our findings unravel issues of tumor heterogeneity and illustrate that the assessment of the EBV status in tissue biopsies might carry the risk of sampling errors, which may significantly hamper adequate molecular tumor classification in a more clinical setting. Moreover, this is the first report of intratumoral heterogeneity of PIK3CA mutations in GC, and our findings lead to the conclusion that PIK3CA mutant and -wildtype tumor subclones are skilled to metastasize independently to different regional lymph nodes.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Classe I de Fosfatidilinositol 3-Quinases/genética
Infecções por Vírus Epstein-Barr/genética
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/mortalidade
Adenocarcinoma/secundário
Adenocarcinoma/virologia
Idoso
Infecções por Vírus Epstein-Barr/mortalidade
Infecções por Vírus Epstein-Barr/patologia
Infecções por Vírus Epstein-Barr/virologia
Feminino
Frequência do Gene
Estudos de Associação Genética
Heterogeneidade Genética
Predisposição Genética para Doença
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Estimativa de Kaplan-Meier
Metástase Linfática
Masculino
Técnicas de Diagnóstico Molecular
Mutação
Neoplasias Gástricas/mortalidade
Neoplasias Gástricas/patologia
Neoplasias Gástricas/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.1.137 (Class I Phosphatidylinositol 3-Kinases); EC 2.7.1.137 (PIK3CA protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/annonc/mdx047


  10 / 138671 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28449064
[Au] Autor:Hou Y; Tozbikian G; Zynger DL; Li Z
[Ad] Endereço:From the Department of Pathology, The Ohio State University Wexner Medical Center, Columbus.
[Ti] Título:Using the Modified Magee Equation to Identify Patients Unlikely to Benefit From the 21-Gene Recurrence Score Assay (Oncotype DX Assay).
[So] Source:Am J Clin Pathol;147(6):541-548, 2017 Jun 01.
[Is] ISSN:1943-7722
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Objectives: This study aimed to compare a modified Magee equation with Oncotype DX (Genomic Health, Redwood City, CA) recurrence score (RS) and identify patients who are unlikely to benefit from Oncotype DX. Methods: Magee equation RS was calculated in 438 cases and correlated with Oncotype DX RS. Results: The Pearson correlation coefficient ( r ) for the Magee equation and Oncotype DX RS was 0.6645 ( P < .00001), and the overall agreement was 66.4%. All cases (11.6%) with a Magee equation RS greater than 30 or 11 or less had been correctly predicted to have either high Oncotype DX RS or low Oncotype DX RS, respectively. Conclusions: The modified Magee equation is able to identify up to 12% patients who are unlikely to benefit from Oncotype DX testing. Using the modified Magee equation RS on these patients would be an alternative to Oncotype DX, leading to cost savings.
[Mh] Termos MeSH primário: Adenocarcinoma Mucinoso/diagnóstico
Adenocarcinoma/diagnóstico
Biomarcadores Tumorais/genética
Neoplasias da Mama/diagnóstico
Carcinoma Ductal de Mama/diagnóstico
Carcinoma Lobular/diagnóstico
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Adenocarcinoma/patologia
Adenocarcinoma Mucinoso/genética
Adenocarcinoma Mucinoso/patologia
Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais/metabolismo
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Carcinoma Ductal de Mama/genética
Carcinoma Ductal de Mama/patologia
Carcinoma Lobular/genética
Carcinoma Lobular/patologia
Feminino
Genômica
Seres Humanos
Meia-Idade
Técnicas de Diagnóstico Molecular/métodos
Medição de Risco
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1093/ajcp/aqx008



página 1 de 13868 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