Base de dados : MEDLINE
Pesquisa : G03.197.300.500 [Categoria DeCS]
Referências encontradas : 146 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 15 ir para página                         

  1 / 146 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
[PMID]:29267502
[Au] Autor:Liu C; Shui CL; Wang Q; Luo H; Gu CG
[Ad] Endereço:Department of Urology, The Second People's Hospital of Deyang City, Deyang, Sichuan Province, China.
[Ti] Título:Mechanism of hif-1α mediated hypoxia-induced permeability changes in bladder endothelial cells.
[So] Source:Braz J Med Biol Res;51(2):e6768, 2017 Dec 18.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:This study aimed to investigate the mechanism of hypoxia-inducible factor-1 alpha (HIF-1α) mediated hypoxia-induced permeability changes in bladder endothelial cells. Models of in vitro hypoxic cell culture of bladder cancer, bladder cancer cells with low HIF-1α expression and HIF-1α RNA interference (RNAi) expression vector were established. Western blot and reverse transcription polymerase chain reaction (RT-PCR) were used to detect the expression of HIF-1α and vascular endothelial growth factor (VEGF) in each group. Bladder cell permeability was determined. Results showed that protein and mRNA expression of HIF-1α and VEGF at 3 and 12 h of hypoxia were significantly higher than normal control (P<0.05), and peaked at 12 h. HIF-1α and VEGF expression in the hypoxic group and hypoxic+3-(5'-hydroxymethyl-2'-furyl)-1-benzyl indazole (YC-1) group were significantly higher than normal control (P<0.05), while expression in the hypoxic+YC-1 group was significantly lower than the hypoxic group (P<0.05). Bladder cell permeability in the hypoxic and hypoxic+YC-1 group were significantly increased compared to normal control (P<0.05), while in the hypoxic+YC-1 group was significantly decreased compared to the hypoxic group (P<0.05). Most of the cells in the stably transfected HIF-1α RNAi expression vector pcDNA6.2-GW/EmGFP-miR-siHIF-1α expressed green fluorescence protein (GFP) under fluorescence microscope. pcDNA6.2-GW/EmGFP-miR-siHIF-1α could significantly inhibit HIF-1α gene expression (P<0.05). HIF-1α and VEGF expression in the hypoxic group and siHIF-1α hypoxic group were significantly higher than normal group (P<0.05), while expression in the siHIF-1α hypoxic group was significantly lower than the hypoxic group (P<0.05). Findings suggest that HIF-1α is an important factor in the increase of bladder cancer cell permeability.
[Mh] Termos MeSH primário: Células Endoteliais/fisiologia
Subunidade alfa do Fator 1 Induzível por Hipóxia/fisiologia
Hipóxia Tumoral/fisiologia
Neoplasias da Bexiga Urinária/metabolismo
Fator A de Crescimento do Endotélio Vascular/fisiologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linhagem Celular Tumoral
Células Endoteliais/patologia
Regulação Neoplásica da Expressão Gênica/fisiologia
Subunidade alfa do Fator 1 Induzível por Hipóxia/análise
Permeabilidade
Interferência de RNA
Coelhos
Reação em Cadeia da Polimerase em Tempo Real
Neoplasias da Bexiga Urinária/genética
Neoplasias da Bexiga Urinária/patologia
Fator A de Crescimento do Endotélio Vascular/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Vascular Endothelial Growth Factor A)
[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


  2 / 146 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28463025
[Au] Autor:Chen X; Wang P; Guo F; Wang X; Wang J; Xu J; Yuan D; Zhang J; Shao C
[Ad] Endereço:a Institute of Radiation Medicine , Fudan University , Shanghai , China.
[Ti] Título:Autophagy enhanced the radioresistance of non-small cell lung cancer by regulating ROS level under hypoxia condition.
[So] Source:Int J Radiat Biol;93(8):764-770, 2017 08.
[Is] ISSN:1362-3095
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Tumor resistance towards radiation has been a big obstacle in the poor prognosis of lung cancer. It has been reported that hypoxia and autophagy partly contribute to this resistance. However, there is controversy over whether autophagy plays a positive role in cancer therapy or not. We aim to find out the specific mechanism of radiation resistance. MATERIALS AND METHODS: A549 cells were treated with conditioned medium (CM) under 12 h hypoxia or normoxia before irradiation, followed by the measurement of clonogenic survival, reactive oxygen species (ROS), signal of mitochondria and autophagy flux. In some experiments, the A549 cells were respectively transfected with LC3 small interfering RNA (siRNA), or treated with Earle's Balanced Salt Solution (EBSS). RESULTS: We found that hypoxia enhanced cell radioresistance by increasing the induction of autophagy. And after hypoxia stress, the number of mitochondria was reduced but the cellular ROS level was enhanced. It was significant that autophagy may enhance cell radioresistance by reducing ROS during hypoxic treatment. CONCLUSIONS: We elucidated the possible mechanisms of autophagy in regulating cancer cell death or survival. These results supply a new opinion about the intrinsic factor of radioresistance of hypoxia tumors.
[Mh] Termos MeSH primário: Autofagia/efeitos da radiação
Carcinoma Pulmonar de Células não Pequenas/patologia
Neoplasias Pulmonares/patologia
Tolerância a Radiação/efeitos da radiação
Espécies Reativas de Oxigênio/metabolismo
Hipóxia Tumoral/efeitos da radiação
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Seres Humanos
Tamanho Mitocondrial/efeitos da radiação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Reactive Oxygen Species)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180111
[Lr] Data última revisão:
180111
[Sb] Subgrupo de revista:IM; S
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1080/09553002.2017.1325025


  3 / 146 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29196263
[Au] Autor:Bousquet PA; Sandvik JA; Jeppesen Edin NF; Krengel U
[Ad] Endereço:Department of Chemistry, University of Oslo, P.O. Box 1033 Blindern, NO-0315 Oslo, Norway. Electronic address: paula.bousquet@kjemi.uio.no.
[Ti] Título:Hypothesis: Hypoxia induces de novo synthesis of NeuGc gangliosides in humans through CMAH domain substitute.
[So] Source:Biochem Biophys Res Commun;495(1):1562-1566, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Immunotherapy is a growing field in cancer research. A privileged tumor-associated antigen that has received much attention is N-glycolyl (NeuGc) GM3. This ganglioside is present in several types of cancer, but is almost undetectable in human healthy tissues. However, its non-hydroxylated variant, NeuAc GM3, is abundant in all mammals. Due to a deletion in the human gene encoding the key enzyme for synthesis of NeuGc, humans, in contrast to other mammals, cannot synthesize NeuGc GM3. Therefore the presence of this ganglioside in human cancer cells represents an enigma. It has been shown that hypoxic conditions trigger the expression of NeuGc gangliosides, which not only serve as attractive targets for cancer therapy, but also as diagnostic and prognostic tumor marker. Here, we confirm hypoxia-induced expression of the NeuGc GM3 ganglioside also in HeLa cells and reveal several candidate proteins, in particular GM3 synthase and subunit B of respiratory complex II (SDHB), that may be involved in the generation of NeuGc GM3 by SILAC-based proteome analysis. These findings have the potential to significantly advance our understanding of how this enigmatic tumor-associated antigen is produced in humans, and also suggest a possible mechanism of action of anti-tumor antibodies that recognize hypoxia markers, such as 14F7.
[Mh] Termos MeSH primário: Gangliosídeo G(M3)/metabolismo
Oxigenases de Função Mista/metabolismo
Modelos Biológicos
Oxigênio/metabolismo
Hipóxia Tumoral/fisiologia
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Células HeLa
Seres Humanos
Domínios Proteicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (G(M3) Ganglioside); EC 1.- (Mixed Function Oxygenases); EC 1.14.18.2 (CMPacetylneuraminate monooxygenase); S88TT14065 (Oxygen)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171203
[St] Status:MEDLINE


  4 / 146 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29100962
[Au] Autor:Na YR; Je S; Seok SH
[Ad] Endereço:Macrophage Lab, Department of Microbiology and Immunology, and Institute of Endemic Disease, Seoul National University College of Medicine, 103 Daehak-ro, Chongno-gu, Seoul 110-799, South Korea.
[Ti] Título:Metabolic features of macrophages in inflammatory diseases and cancer.
[So] Source:Cancer Lett;413:46-58, 2018 Jan 28.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Macrophages are now considered to be important players in various inflammatory diseases as well as tumor progression. Emerging evidence reveals that macrophage metabolic features are deeply associated with their immune functions. Understanding the interaction between cellular metabolism and immune signaling pathways in macrophages can help us to develop appropriate therapeutic approaches for inflammatory diseases. In this review, we briefly summarize key metabolic features of M1 and M2 macrophages as well as signaling interactions between major metabolic molecules with TLRs and NLRs. Current knowledges of cellular metabolism are focused on macrophages in various disease situations including sepsis, atherosclerosis, obesity, tuberculosis and cancer. Novel insights and present targets for regulating macrophage metabolism are also discussed.
[Mh] Termos MeSH primário: Metabolismo Energético
Inflamação/metabolismo
Macrófagos/metabolismo
Neoplasias/metabolismo
[Mh] Termos MeSH secundário: Animais
Doenças Transmissíveis/imunologia
Doenças Transmissíveis/metabolismo
Doenças Transmissíveis/patologia
Citocinas/metabolismo
Seres Humanos
Inflamação/imunologia
Inflamação/patologia
Mediadores da Inflamação/metabolismo
Macrófagos/imunologia
Macrófagos/patologia
Neoplasias/imunologia
Neoplasias/patologia
Fenótipo
Transdução de Sinais
Hipóxia Tumoral
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammation Mediators)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171105
[St] Status:MEDLINE


  5 / 146 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28961236
[Au] Autor:Brady LK; Wang H; Radens CM; Bi Y; Radovich M; Maity A; Ivan C; Ivan M; Barash Y; Koumenis C
[Ad] Endereço:Department of Radiation Oncology Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
[Ti] Título:Transcriptome analysis of hypoxic cancer cells uncovers intron retention in EIF2B5 as a mechanism to inhibit translation.
[So] Source:PLoS Biol;15(9):e2002623, 2017 Sep.
[Is] ISSN:1545-7885
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cells adjust to hypoxic stress within the tumor microenvironment by downregulating energy-consuming processes including translation. To delineate mechanisms of cellular adaptation to hypoxia, we performed RNA-Seq of normoxic and hypoxic head and neck cancer cells. These data revealed a significant down regulation of genes known to regulate RNA processing and splicing. Exon-level analyses classified > 1,000 mRNAs as alternatively spliced under hypoxia and uncovered a unique retained intron (RI) in the master regulator of translation initiation, EIF2B5. Notably, this intron was expressed in solid tumors in a stage-dependent manner. We investigated the biological consequence of this RI and demonstrate that its inclusion creates a premature termination codon (PTC), that leads to a 65kDa truncated protein isoform that opposes full-length eIF2Bε to inhibit global translation. Furthermore, expression of 65kDa eIF2Bε led to increased survival of head and neck cancer cells under hypoxia, providing evidence that this isoform enables cells to adapt to conditions of low oxygen. Additional work to uncover -cis and -trans regulators of EIF2B5 splicing identified several factors that influence intron retention in EIF2B5: a weak splicing potential at the RI, hypoxia-induced expression and binding of the splicing factor SRSF3, and increased binding of total and phospho-Ser2 RNA polymerase II specifically at the intron retained under hypoxia. Altogether, these data reveal differential splicing as a previously uncharacterized mode of translational control under hypoxia and are supported by a model in which hypoxia-induced changes to cotranscriptional processing lead to selective retention of a PTC-containing intron in EIF2B5.
[Mh] Termos MeSH primário: Fator de Iniciação 2B em Eucariotos/genética
Perfilação da Expressão Gênica/métodos
Íntrons/genética
Biossíntese de Proteínas/genética
Hipóxia Tumoral/genética
[Mh] Termos MeSH secundário: Processamento Alternativo/genética
Sequência de Bases
Linhagem Celular Tumoral
Regulação Neoplásica da Expressão Gênica
Loci Gênicos
Neoplasias de Cabeça e Pescoço/genética
Neoplasias de Cabeça e Pescoço/patologia
Seres Humanos
Modelos Biológicos
Motivos de Nucleotídeos/genética
Fosforilação
Reação em Cadeia da Polimerase
Ligação Proteica
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
RNA Polimerase II/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Sequências Reguladoras de Ácido Nucleico/genética
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EIF2B5 protein, human); 0 (Eukaryotic Initiation Factor-2B); 0 (Protein Isoforms); 0 (RNA, Messenger); EC 2.7.7.- (RNA Polymerase II)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170930
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pbio.2002623


  6 / 146 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28928094
[Au] Autor:Zong S; Li W; Li H; Han S; Liu S; Shi Q; Hou F
[Ad] Endereço:Department of Geriatrics, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200071, China. Electronic address: vigilucky@126.com.
[Ti] Título:Identification of hypoxia-regulated angiogenic genes in colorectal cancer.
[So] Source:Biochem Biophys Res Commun;493(1):461-467, 2017 Nov 04.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The tumour hypoxia would trigger the angiogenesis switch for survival, and increase the ability of cancer cells to invade and metastasis. However, hypoxia regulated genes that invovled in angiogenesis in colorectal cancer (CRC) have not been explored in detail. The aim of this study was to explore angiogenic genes under hypoxia condition in CRC. Here, we found that endothelial cells tube formation and cancer cells invasion ability were promoted even under chronic hypoxia condition (72 h) in colon adenocarcinoma HCT-116 cells. Then, we explored the differentially expressed genes (DEGs) under chronic hypoxia condition by microarray from Gene Expression Omnibus (GEO) database. Subsequent bioinformatic analysis identified 17 genes that invovled in angiogenesis, blood vessel development, blood vessel morphgensis, vascular development. of these genes, VEGF-A, Smad7, Jun, IL-8, CXCR-4, PDGF-A, TGF-A, ANGPTL-4 expression levels up-regulated under hypoxia condition. Additionally, the gene expression level in acute hypoxia (24 h) was significantly higher than chronic condition (72 h). Finally, knockdown of hypoxia inducible factor (HIF-1α) by shRNA reversed the role of Smad7, CXCR-4, PDGF-A, TGF-A and ANGPTL-4 overexpression in HCT-116 cells, these findings provide the potential angiogenic targets for the treatment of colorectal cancer.
[Mh] Termos MeSH primário: Proteínas Angiogênicas/metabolismo
Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/patologia
Proteínas de Neoplasias/metabolismo
Neovascularização Patológica/metabolismo
Neovascularização Patológica/patologia
Hipóxia Tumoral
[Mh] Termos MeSH secundário: Doença Aguda
Doença Crônica
Neoplasias Colorretais/complicações
Perfilação da Expressão Gênica
Genes Neoplásicos
Seres Humanos
Invasividade Neoplásica
Neovascularização Patológica/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenic Proteins); 0 (Neoplasm Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE


  7 / 146 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28920955
[Au] Autor:Wu MZ; Cheng WC; Chen SF; Nieh S; O'Connor C; Liu CL; Tsai WW; Wu CJ; Martin L; Lin YS; Wu KJ; Lu LF; Izpisua Belmonte JC
[Ad] Endereço:Gene Expression Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.
[Ti] Título:miR-25/93 mediates hypoxia-induced immunosuppression by repressing cGAS.
[So] Source:Nat Cell Biol;19(10):1286-1296, 2017 Oct.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The mechanisms by which hypoxic tumours evade immunological pressure and anti-tumour immunity remain elusive. Here, we report that two hypoxia-responsive microRNAs, miR-25 and miR-93, are important for establishing an immunosuppressive tumour microenvironment by downregulating expression of the DNA sensor cGAS. Mechanistically, miR-25/93 targets NCOA3, an epigenetic factor that maintains basal levels of cGAS expression, leading to repression of cGAS during hypoxia. This allows hypoxic tumour cells to escape immunological responses induced by damage-associated molecular pattern molecules, specifically the release of mitochondrial DNA. Moreover, restoring cGAS expression results in an anti-tumour immune response. Clinically, decreased levels of cGAS are associated with poor prognosis for patients with breast cancer harbouring high levels of miR-25/93. Together, these data suggest that inactivation of the cGAS pathway plays a critical role in tumour progression, and reveal a direct link between hypoxia-responsive miRNAs and adaptive immune responses to the hypoxic tumour microenvironment, thus unveiling potential new therapeutic strategies.
[Mh] Termos MeSH primário: Neoplasias da Mama/enzimologia
MicroRNAs/metabolismo
Nucleotidiltransferases/metabolismo
Evasão Tumoral
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Animais
Neoplasias da Mama/genética
Neoplasias da Mama/imunologia
Neoplasias da Mama/patologia
DNA Mitocondrial/genética
DNA Mitocondrial/metabolismo
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Progressão da Doença
Epigênese Genética
Feminino
Regulação Enzimológica da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Células MCF-7
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
MicroRNAs/genética
Oxigenases de Função Mista/genética
Oxigenases de Função Mista/metabolismo
Coativador 3 de Receptor Nuclear/genética
Coativador 3 de Receptor Nuclear/metabolismo
Nucleotidiltransferases/genética
Proteínas Proto-Oncogênicas/genética
Proteínas Proto-Oncogênicas/metabolismo
Interferência de RNA
Receptor de Interferon alfa e beta/deficiência
Receptor de Interferon alfa e beta/genética
Transdução de Sinais
Fatores de Tempo
Transfecção
Hipóxia Tumoral
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Mitochondrial); 0 (DNA-Binding Proteins); 0 (MIRN25 microRNA, human); 0 (MIRN25 microRNA, mouse); 0 (MIRN93 microRNA, human); 0 (MicroRNAs); 0 (Mirn93 microRNA, mouse); 0 (Proto-Oncogene Proteins); 0 (TET1 protein, mouse); 156986-95-7 (Receptor, Interferon alpha-beta); EC 1.- (Mixed Function Oxygenases); EC 1.- (TET1 protein, human); EC 2.3.1.48 (NCOA3 protein, human); EC 2.3.1.48 (Ncoa3 protein, mouse); EC 2.3.1.48 (Nuclear Receptor Coactivator 3); EC 2.7.7.- (MB21D1 protein, human); EC 2.7.7.- (MB21D1 protein, mouse); EC 2.7.7.- (Nucleotidyltransferases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3615


  8 / 146 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28912577
[Au] Autor:Maley CC; Aktipis A; Graham TA; Sottoriva A; Boddy AM; Janiszewska M; Silva AS; Gerlinger M; Yuan Y; Pienta KJ; Anderson KS; Gatenby R; Swanton C; Posada D; Wu CI; Schiffman JD; Hwang ES; Polyak K; Anderson ARA; Brown JS; Greaves M; Shibata D
[Ad] Endereço:Virginia G. Piper Center for Personalized Diagnostics, Biodesign Institute, Arizona State University, 1001 S. McAllister Ave, Tempe, Arizona 85287, USA.
[Ti] Título:Classifying the evolutionary and ecological features of neoplasms.
[So] Source:Nat Rev Cancer;17(10):605-619, 2017 Oct.
[Is] ISSN:1474-1768
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Neoplasms change over time through a process of cell-level evolution, driven by genetic and epigenetic alterations. However, the ecology of the microenvironment of a neoplastic cell determines which changes provide adaptive benefits. There is widespread recognition of the importance of these evolutionary and ecological processes in cancer, but to date, no system has been proposed for drawing clinically relevant distinctions between how different tumours are evolving. On the basis of a consensus conference of experts in the fields of cancer evolution and cancer ecology, we propose a framework for classifying tumours that is based on four relevant components. These are the diversity of neoplastic cells (intratumoural heterogeneity) and changes over time in that diversity, which make up an evolutionary index (Evo-index), as well as the hazards to neoplastic cell survival and the resources available to neoplastic cells, which make up an ecological index (Eco-index). We review evidence demonstrating the importance of each of these factors and describe multiple methods that can be used to measure them. Development of this classification system holds promise for enabling clinicians to personalize optimal interventions based on the evolvability of the patient's tumour. The Evo- and Eco-indices provide a common lexicon for communicating about how neoplasms change in response to interventions, with potential implications for clinical trials, personalized medicine and basic cancer research.
[Mh] Termos MeSH primário: Evolução Biológica
Neoplasias/classificação
Neoplasias/fisiopatologia
[Mh] Termos MeSH secundário: Antígenos de Neoplasias/imunologia
Fenômenos Ecológicos e Ambientais
Expressão Gênica
Variação Genética
Seres Humanos
Microbiota
Neoplasias/genética
Neoplasias/patologia
Fenótipo
Espécies Reativas de Oxigênio
Fatores de Tempo
Hipóxia Tumoral
Microambiente Tumoral
[Pt] Tipo de publicação:CONSENSUS DEVELOPMENT CONFERENCE; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Reactive Oxygen Species)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1038/nrc.2017.69


  9 / 146 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28899657
[Au] Autor:Shang Y; Chen H; Ye J; Wei X; Liu S; Wang R
[Ad] Endereço:Department of Gastroenterology, Southwest Hospital, Third Military Medical University, Chongqing 400038, PR China.
[Ti] Título:HIF-1α/Ascl2/miR-200b regulatory feedback circuit modulated the epithelial-mesenchymal transition (EMT) in colorectal cancer cells.
[So] Source:Exp Cell Res;360(2):243-256, 2017 Nov 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have reported that Achaete scute-like 2 (Ascl2) transcriptionally repressed miR-200 family members and affected the epithelial-mesenchymal transition (EMT)-mesenchymal-epithelial transition (MET) plasticity in colorectal cancer (CRC) cells. However, little is known about the regulation of the Ascl2/miR-200 axis. Here, we found that hypoxia inducible factor-1α (HIF-1α) mRNA levels were positively correlated with Ascl2 mRNA levels and inversely correlated with miR-200b in CRC samples. Mechanistically, we showed that Ascl2 was a downstream target of HIF-1α and had a critical role in the EMT phenotype induced by hypoxia or HIF-1α over-expression. Hypoxia or HIF-1α over-expression activated Ascl2 expression in CRC cells in a direct transcriptional mechanism via binding with the hypoxia-response element (HRE) at the proximal Ascl2 promoter. HIF-1α-induced Ascl2 expression repressed miR-200b expression to induce EMT occurrence. Furthermore, we found HIF-1α was a direct target of miR-200b. MiR-200b bound with the 3'-UTR of HIF-1α in CRC cells. HIF-1α/Ascl2/miR-200b regulatory feedback circuit modulated the EMT-MET plasticity of CRC cells. Our results confirmed a novel HIF-1α/Ascl2/miR-200b regulatory feedback circuit in modulating EMT-MET plasticity of CRC cells, which could serve as a possible therapeutic target.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/fisiologia
Neoplasias Colorretais/genética
Neoplasias Colorretais/patologia
Transição Epitelial-Mesenquimal/genética
Retroalimentação Fisiológica/fisiologia
Subunidade alfa do Fator 1 Induzível por Hipóxia/fisiologia
MicroRNAs/fisiologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Plasticidade Celular/genética
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Transdução de Sinais/genética
Hipóxia Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ASCL2 protein, human); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (MIRN200 microRNA, human); 0 (MicroRNAs)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE


  10 / 146 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28873460
[Au] Autor:Feldman LA; Fabre MS; Grasso C; Reid D; Broaddus WC; Lanza GM; Spiess BD; Garbow JR; McConnell MJ; Herst PM
[Ad] Endereço:Department of Neurosurgery, Virginia Commonwealth University, Richmond, VA United States of America.
[Ti] Título:Perfluorocarbon emulsions radiosensitise brain tumors in carbogen breathing mice with orthotopic GL261 gliomas.
[So] Source:PLoS One;12(9):e0184250, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Tumour hypoxia limits the effectiveness of radiation therapy. Delivering normobaric or hyperbaric oxygen therapy elevates pO2 in both tumour and normal brain tissue. However, pO2 levels return to baseline within 15 minutes of stopping therapy. AIM: To investigate the effect of perfluorocarbon (PFC) emulsions on hypoxia in subcutaneous and intracranial mouse gliomas and their radiosensitising effect in orthotopic gliomas in mice breathing carbogen (95%O2 and 5%CO2). RESULTS: PFC emulsions completely abrogated hypoxia in both subcutaneous and intracranial GL261 models and conferred a significant survival advantage orthotopically (Mantel Cox: p = 0.048) in carbogen breathing mice injected intravenously (IV) with PFC emulsions before radiation versus mice receiving radiation alone. Carbogen alone decreased hypoxia levels substantially and conferred a smaller but not statistically significant survival advantage over and above radiation alone. CONCLUSION: IV injections of PFC emulsions followed by 1h carbogen breathing, radiosensitises GL261 intracranial tumors.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/tratamento farmacológico
Dióxido de Carbono/uso terapêutico
Fluorcarbonetos/uso terapêutico
Glioma/tratamento farmacológico
Oxigênio/uso terapêutico
Radiossensibilizantes/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Neoplasias Encefálicas/patologia
Dióxido de Carbono/farmacologia
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Emulsões
Fluorcarbonetos/farmacologia
Glioma/patologia
Camundongos Endogâmicos C57BL
Oxigênio/farmacologia
Radiossensibilizantes/farmacologia
Análise de Sobrevida
Hipóxia Tumoral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Emulsions); 0 (Fluorocarbons); 0 (Radiation-Sensitizing Agents); 142M471B3J (Carbon Dioxide); 8063-77-2 (carbogen); S88TT14065 (Oxygen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184250



página 1 de 15 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