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[PMID]:29385191
[Au] Autor:Chuerduangphui J; Ekalaksananan T; Chaiyarit P; Patarapadungkit N; Chotiyano A; Kongyingyoes B; Promthet S; Pientong C
[Ad] Endereço:Department of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
[Ti] Título:Effects of arecoline on proliferation of oral squamous cell carcinoma cells by dysregulating c-Myc and miR-22, directly targeting oncostatin M.
[So] Source:PLoS One;13(1):e0192009, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arecoline, the major alkaloid of areca nut, is known to induce oral carcinogenesis, however, its mechanism is still needed to elucidate. This study investigated the effects of arecoline on cell viability and cell-cycle progression of oral squamous cell carcinoma (OSCC) cells as well as a relevant cellular gene expression. The results showed that a low concentration of arecoline (0.025 µg/ml) increased OSCC cell viability, proportion of cells in G2/M phase and cell proliferation. Simultaneously, it induced IL-6, STAT3 and c-Myc expression. Interestingly, c-myc promoter activity was also induced by arecoline. MiR-22 expression in arecoline-treated OSCC cells was suppressed and comparable to an upregulated c-Myc expression. In arecoline-treated OSCC cells, oncostatin M (OSM) expression was significantly upregulated and inversely correlated with miR-22 expression. Likewise, OSM expression and its post-transcriptional activity were significantly decreased in miR-22-transfected OSCC and 293FT cells. This result demonstrated that miR-22 directly targeted OSM. Interestingly, miR-22 played an important role as a tumor suppresser on suppressing cell proliferation, migration and cell-cycle progression of OSCC cells. This result suggested the effect of arecoline to promote cell proliferation and cell-cycle progression of OSCC cells might be involved in induction of c-Myc expression and reduction of miR-22 resulting in OSM upregulation.
[Mh] Termos MeSH primário: Arecolina/farmacologia
Carcinoma de Células Escamosas/patologia
Proliferação Celular/efeitos dos fármacos
MicroRNAs/metabolismo
Neoplasias Bucais/patologia
Proteínas Proto-Oncogênicas c-myc/metabolismo
[Mh] Termos MeSH secundário: Carcinoma de Células Escamosas/metabolismo
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Seres Humanos
Interleucina-6/biossíntese
MicroRNAs/genética
Neoplasias Bucais/metabolismo
Regiões Promotoras Genéticas
Proteínas Proto-Oncogênicas c-myc/genética
Fator de Transcrição STAT3/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-6); 0 (MIRN22 microRNA, human); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins c-myc); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 4ALN5933BH (Arecoline)
[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:180201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0192009


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[PMID]:29381751
[Au] Autor:Chea C; Miyauchi M; Inubushi T; Febriyanti Ayuningtyas N; Subarnbhesaj A; Nguyen PT; Shrestha M; Haing S; Ohta K; Takata T
[Ad] Endereço:Department of Oral & Maxillofacial Pathobiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
[Ti] Título:Molecular mechanism of inhibitory effects of bovine lactoferrin on the growth of oral squamous cell carcinoma.
[So] Source:PLoS One;13(1):e0191683, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Lactoferrin (LF), a member of the transferrin family, recently has been demonstrated to have anticancer effects on various cancers including oral squamous cell carcinoma (OSCC). However, little is known about the underlying mechanisms of its effects on OSCC. Therefore, we aimed to investigate the mechanism of the suppressive effects of bovine LF (bLF) on the growth of OSCC cells. METHODS: In the current study, HSC2, HSC3, HSC4 and normal human oral keratinocytes (RT7) cell lines were tested with bLF 1, 10, and 100 µg/ml. The effects and detail mechanisms of bLF on proliferation and apoptosis of cells were investigated using flow cytometry and western blotting. RESULTS: We found that bLF (1, 10, and 100 µg/ml) induced activation of p53, a tumor suppressor gene, is associated with the induction of cell cycle arrest in G1/S phase and apoptosis in OSCC. Moreover, bLF downregulated the phosphorylation of Akt and activated suppressor of cytokine signaling 3 (SOCS3), thereby attenuating multiple signaling pathways including mTOR/S6K and JAK/STAT3. Interestingly, we revealed that bLF exerted its effect selectively against HSC3 but not on RT7 via different effects on the phosphorylation status of NF-κB and Akt. CONCLUSION: This is the first report showing that bLF selectively suppresses proliferation through mTOR/S6K and JAK/STAT3 pathways and induction of apoptosis in OSCC. This study provides important new findings, which might be useful in the prevention and treatment of OSCC.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/patologia
Lactoferrina/farmacologia
Neoplasias Bucais/patologia
[Mh] Termos MeSH secundário: Animais
Bovinos
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Transformada
Proliferação Celular/efeitos dos fármacos
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.4.21.- (Lactoferrin)
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191683


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[PMID]:28456786
[Au] Autor:Moon S; Kim DK; Kim J
[Ad] Endereço:Department of Dental Hygiene, College of Nursing Healthcare, Sorabol College, Gyeongju 38063, Republic of Korea.
[Ti] Título:Apoptosis-related microRNA-145-5p enhances the effects of pheophorbide a-based photodynamic therapy in oral cancer.
[So] Source:Oncotarget;8(21):35184-35192, 2017 May 23.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MicroRNAs (miRNAs) regulate key biological processes, and their aberrant expression has been related to cancer development. Photodynamic therapy (PDT) has emerged as one of the most promising modalities for cancer treatment. However, the application of PDT has been limited to superficially localized human cancerous and precancerous lesions. To increase the usefulness of both PDT and miRNAs in cancer therapy, this study investigated whether apoptosis-related miRNA expression is influenced by PDT in oral cancer and whether miRNAs can enhance PDT efficacy. To achieve this goal, we performed a miRNA array-based comparison of apoptosis-related miRNA expression patterns following PDT using pheophorbide a (Pa) as a photosensitizer. After Pa-PDT, 13.1% of the miRNAs were down-regulated, and 16.7% of the miRNAs were up-regulated. Representative miRNAs were selected according to expression difference: miR-9-5p, miR-32-5p, miR-143-3p, miR-145-5p, miR-192-5p, miR-193a-5p, miR-204-5p, miR-212-3p, miR-338-3p, and miR-451a. Among them, only miR-145-5p showed the consistent reduction repeatedly in all cell lines after Pa-PDT. Further, the combined treatment of a miR-145-5p mimic and Pa-PDT increased phototoxicity, reactive oxygen species generation, and apoptotic cell death, suggesting that miRNAs expression could be a useful marker for enhancing the therapeutic effect of Pa-PDT. This study will provide a promising strategy for introducing miRNA as cancer therapy.
[Mh] Termos MeSH primário: Clorofila/análogos & derivados
MicroRNAs/genética
Neoplasias Bucais/genética
Fármacos Fotossensibilizantes/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Clorofila/farmacologia
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Neoplasias Bucais/tratamento farmacológico
Neoplasias Bucais/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos
Fotoquimioterapia
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN145 microRNA, human); 0 (MicroRNAs); 0 (Photosensitizing Agents); 0 (Reactive Oxygen Species); 1406-65-1 (Chlorophyll); IA2WNI2HO2 (pheophorbide a)
[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:170501
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.17059


  4 / 29683 MEDLINE  
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[PMID]:29267666
[Au] Autor:Iriya PMO; Romaniszen LW; Fernandes TMF; Poleti ML
[Ad] Endereço:Universidade Estadual do Norte do Paraná - Unopar, Londrina, PR, Brazil.
[Ti] Título:Health-related quality of life of patients with squamous cell carcinoma: a comparison according to tumor location.
[So] Source:Braz Oral Res;31:e105, 2017 Dec 18.
[Is] ISSN:1807-3107
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to evaluate the health-related quality of life (QOL) of patients with squamous cell carcinoma (SCC) according to tumor location. The sample consisted of 27 patients with primary SCC in the oral cavity (n = 15), pharynx (n = 7), and larynx (n = 5) who were undergoing cancer treatment at the Cancer Hospital of Londrina, regardless of age, sex, clinical stage, and type of antineoplastic treatment. Health-related QOL was evaluated using the 30-item Cancer-Quality of Life Questionnaire (QLQ-C30), the 35-item Head and Neck Cancer-Quality of Life Questionnaire (QLQ-HN35), and the University of Washington Quality of Life Questionnaire (UW-QOL). These questionnaires were administered individually to each patient before ambulatory care. Sociodemographic data (age and sex) and clinical data (T stage, tumor location, and type of antineoplastic treatment) were collected from the patients' medical records. Scores were compared according to tumor location using the chi-squared test and one-way analysis of variance (p < 0.05). No score differed significantly according to tumor location. It can be concluded that the health-related QOL of patients with SCC was not influenced by tumor location.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas
Neoplasias Laríngeas
Neoplasias Bucais
Neoplasias Faríngeas
Qualidade de Vida
[Mh] Termos MeSH secundário: Fatores Etários
Idoso
Análise de Variância
Antineoplásicos/uso terapêutico
Carcinoma de Células Escamosas/tratamento farmacológico
Carcinoma de Células Escamosas/patologia
Estudos Transversais
Feminino
Seres Humanos
Neoplasias Laríngeas/tratamento farmacológico
Neoplasias Laríngeas/patologia
Masculino
Meia-Idade
Neoplasias Bucais/tratamento farmacológico
Neoplasias Bucais/patologia
Estadiamento de Neoplasias
Neoplasias Faríngeas/tratamento farmacológico
Neoplasias Faríngeas/patologia
Fatores Sexuais
Inquéritos e Questionários
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Antineoplastic Agents)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


  5 / 29683 MEDLINE  
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[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


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[PMID]:28453233
[Au] Autor:Huang YP; Chang NW
[Ad] Endereço:Department of Physiology, College of Medicine, China Medical University, Taichung, Taiwan.
[Ti] Título:Proteomic analysis of oral cancer reveals new potential therapeutic targets involved in the Warburg effect.
[So] Source:Clin Exp Pharmacol Physiol;44(8):880-887, 2017 Aug.
[Is] ISSN:1440-1681
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Activation of peroxisome proliferator-activated receptor alpha (PPARα) has been reported to disrupt tumour metabolism and to promote anticancer activity through interfering with the Warburg effect. This study is to investigate whether Warburg effect-related proteins also could be identified in oral tumour lesions and to explore the functional significance of PPARα in metabolic shift. Five pairs of tongue tumour tissues and adjacent reference tissues obtained from 4-NQO/arecoline induced mouse model were analyzed by 2-d-gel-electrophoresis and LC-MS. Further, the hexokinase II level, pyruvate dehydrogenase (PDH) activity, and metabolites of glycolysis and TCA cycle were all examined in order to validate the effect of PPARα on metabolic shift. Changes in protein expression levels revealed that seven proteins, which were involved in glycolysis, the tricarboxylic acid cycle, and the respiratory chain, were down-regulated in tumour tissues. We found that activation of PPARα through fenofibrate could inhibit oral cancer cell growth and switch the way of energy production from the Warburg effect to oxidative phosphorylation. Fenofibrate induced a reduction of hexokinase II protein levels, increases in PDH activity and metabolites of the TCA cycle, and an impairment of ATP production. These findings suggested that activation of the PPARα to reprogram the metabolic pathway might impair the Warburg effect and trigger cancer cell death. The study provides a novel view of changes in protein expression profiles involved in the Warburg effect during oral tumourigenesis. Activation of the PPARα to impair the Warburg effect might offer a new strategy for oral cancer treatment.
[Mh] Termos MeSH primário: Terapia de Alvo Molecular
Neoplasias Bucais/tratamento farmacológico
Neoplasias Bucais/metabolismo
Proteômica
[Mh] Termos MeSH secundário: Animais
Ciclo do Ácido Cítrico/efeitos dos fármacos
Glicólise/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Neoplasias Bucais/patologia
Fosforilação Oxidativa/efeitos dos fármacos
PPAR alfa/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PPAR alpha)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1111/1440-1681.12774


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[PMID]:29241220
[Au] Autor:Yete S; D'Souza W; Saranath D
[Ad] Endereço:Department of Biological Sciences, Sunandan Divatia School of Science, NMIMS (deemed-to-be) University, Mumbai, India.
[Ti] Título:High-Risk Human Papillomavirus in Oral Cancer: Clinical Implications.
[So] Source:Oncology;94(3):133-141, 2018.
[Is] ISSN:1423-0232
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Oral cancer is the eleventh most common cancer globally, with well-established major risk factors of tobacco, areca nut, alcohol, and high-risk human papillomavirus (HR-HPV) types 16 and 18. HR-HPV16/18 are the etiologic agents of cervical cancers and a proportion of oropharyngeal cancers. HPV-associated oropharyngeal and oral cancers show better prognosis and response to therapy. However, the picture of HR-HPV16/18 and the clinical implications of oral cancers are not clear with the majority of reports combining oral cancer data with head and neck cancers. The current review compiles the global prevalence of HR-HPV16/18 in oral cancers, highlighting the unique clinical and molecular pathologic features, prognosis and therapeutic strategies in the prevention and management of HPV-positive oral cancers. The potential for the use of de-intensified therapy and prophylactic prevention in HPV-positive oral cancer patients is highlighted.
[Mh] Termos MeSH primário: Papillomavirus Humano 16/patogenicidade
Papillomavirus Humano 18/patogenicidade
Neoplasias Bucais/etiologia
Neoplasias Bucais/virologia
Infecções por Papillomavirus/complicações
[Mh] Termos MeSH secundário: Seres Humanos
Infecções por Papillomavirus/virologia
Prevalência
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1159/000485322


  8 / 29683 MEDLINE  
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[PMID]:28448645
[Au] Autor:Tam S; Araslanova R; Low TH; Warner A; Yoo J; Fung K; MacNeil SD; Palma DA; Nichols AC
[Ad] Endereço:Department of Otolaryngology-Head & Neck Surgery, Western University, London, Ontario, Canada.
[Ti] Título:Estimating Survival After Salvage Surgery for Recurrent Oral Cavity Cancer.
[So] Source:JAMA Otolaryngol Head Neck Surg;143(7):685-690, 2017 Jul 01.
[Is] ISSN:2168-619X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Locoregional recurrence of oral cavity squamous cell carcinoma (OCSCC) continues to be a life-threatening and difficult clinical situation. Salvage surgery can result in significant morbidities, and survival following recurrence is poor. Objective: To outline prognostic factors influencing overall survival (OS) following salvage surgery for OCSCC to guide management of treatment for patients with locoregionally recurrent disease. Design, Setting, and Participants: The medical records of 293 patients presenting to the London Health Sciences Center with locoregionally recurrent OCSCC between October 5, 1999, and May 2, 2011, were retrospectively reviewed. The primary outcome was OS from salvage treatment to last follow-up or death. Univariate analyses were carried out using the Cox proportional hazards regression model. A recursive partitioning analysis was used to create risk groups based on prognosis. Analysis was conducted from December 8, 2015, to February 26, 2016. Results: Of the 293 patients evaluated, 59 (20%) had recurrence identified after their initial OCSCC treatment; 39 (66%) were men, and the mean (SD) age at diagnosis was 62.2 (11.8) years. Thirty-nine (66%) of these patients underwent salvage surgery for locoregional recurrence with curative intent. Five-year OS from the time of salvage surgery was 43%. Recursive partitioning analysis identified 3 risk groups: (1) high risk (patients who received adjuvant chemoradiotherapy or radiotherapy after initial surgery) with 5-year OS rate of 10% (hazard ratio [HR], 9.41; 95% CI, 2.68-33.04), (2) intermediate risk (previous surgery alone, age ≥62 years) with a 5-year OS rate of 39% (HR, 2.95; 95% CI, 0.86-10.09), and (3) low risk (previous surgery alone, age <62 years) with 5-year OS rate of 74%. Conclusions and Relevance: This recursive partitioning analysis identified 3 prognostic groups in patients undergoing salvage surgery for recurrent OCSCC. The marked differences in survival between these groups should be taken into consideration when counselling and managing treatment for patients with locoregionally recurrent disease.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/patologia
Carcinoma de Células Escamosas/cirurgia
Neoplasias Bucais/patologia
Neoplasias Bucais/cirurgia
Recidiva Local de Neoplasia/patologia
Recidiva Local de Neoplasia/cirurgia
Terapia de Salvação
[Mh] Termos MeSH secundário: Idoso
Quimioterapia Adjuvante
Feminino
Seres Humanos
Masculino
Meia-Idade
Estadiamento de Neoplasias
Prognóstico
Radioterapia Adjuvante
Estudos Retrospectivos
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1001/jamaoto.2017.0001


  9 / 29683 MEDLINE  
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Texto completo SciELO Brasil
[PMID]:29211293
[Au] Autor:Rodini CO; Lopes NM; Lara VS; Mackenzie IC
[Ad] Endereço:Universidade de São Paulo, Faculdade de Odontologia de Bauru, Departamento de Ciências Biológicas, Bauru, SP, Brasil.
[Ti] Título:Oral cancer stem cells - properties and consequences.
[So] Source:J Appl Oral Sci;25(6):708-715, 2017 Nov-Dec.
[Is] ISSN:1678-7765
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Research on cancer stem cells (CSCs) has greatly increased in the field of medicine and pathology; however, some conceptual misunderstandings are still present among the public as well as within the general scientific community that is not yet familiar with the subject. The very first problem is the misinterpretation of CSCs as a synonym of their normal counterparts, the well-known stem cells (SCs). Particularly in Dentistry, another common mistake is the misinterpretation of oral CSCs as normal tooth-derived SCs. The present review aims to clarify important concepts related to normal SCs and CSCs, as well as discuss the relevance of CSCs to the development, metastasis and therapy resistance of oral squamous cell carcinoma.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/patologia
Neoplasias Bucais/patologia
Células-Tronco Neoplásicas/patologia
[Mh] Termos MeSH secundário: Diferenciação Celular
Transformação Celular Neoplásica
Transição Epitelial-Mesenquimal
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


  10 / 29683 MEDLINE  
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[PMID]:28448977
[Au] Autor:Aydemir L; Bireller ES; Avci H; Boy Metin Z; Deger K; Unur M; Cakmakoglu B
[Ad] Endereço:Department of Otolaryngology, Faculty of Medicine, Istanbul University, Istanbul, Turkey.
[Ti] Título:Is Human Oxoguanine Glycosylase 1 Genetic Variant Successful Even on Oral Squamous Cell Carcinoma?
[So] Source:Pathobiology;84(4):223-228, 2017.
[Is] ISSN:1423-0291
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Oral squamous cell carcinoma (OSCC) is one of the most widespread cancer types that arise from different sites of oral cavity and has a 5-year survival rate. This study is aimed at investigating the human oxoguanine glycosylase 1 (hOGG1)-Ser326Cys and APE-Asp148Glu polymorphisms of DNA repair genes in OSCC. MATERIALS AND METHODS: We investigated the hOGG1-Ser326Cys and APE-Asp148Glu polymorphisms of DNA repair genes in the oral cavity. Genotyping was conducted using polymerase chain reaction-restriction fragment length polymorphism analysis based on 132 patients who were diagnosed as having OSCC and 160 healthy subjects. RESULTS: Individuals with the genotype hOGG1-Ser326Cys, Cys allele carriers, were found significantly more frequently in the patient group compared to the control group as increase in risk (p < 0.001). Furthermore, it was observed that there were significantly more individuals with the Ser allele in the control group (p < 0.001). Individuals with genotype APE-Asp148Glu were not statistically significant; however, they were still more in the control group and provided protection against the disease. CONCLUSION: Our findings showed that hOGG1-Ser326Cys Cys allele is statistically important and relevant with respect to the development of oral squamous cancer. In view of our results, further studies including expression levels are required in which hOGG1-Ser326Cys should be investigated as molecular biomarkers for the early prediction of squamous cell carcinoma.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/genética
DNA Glicosilases/genética
Variação Genética
Neoplasias Bucais/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Alelos
Carcinoma de Células Escamosas/enzimologia
Carcinoma de Células Escamosas/patologia
Feminino
Genótipo
Seres Humanos
Masculino
Neoplasias Bucais/enzimologia
Neoplasias Bucais/patologia
Polimorfismo de Fragmento de Restrição
Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.2.2.- (DNA Glycosylases); EC 3.2.2.- (oxoguanine glycosylase 1, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1159/000466702



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