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[PMID]:29446294
[Au] Autor:Efimova NV; Rukavishnikov VS; Pankov VA; Perezhogin AN; Shayakhmetov SF; Meshchakova NM; Lisetskaya LG
[Ti] Título:[Assessment of carcinogenic risks to workers of the main enterprises of the Irkutsk region].
[So] Source:Gig Sanit;95(12):1163-7, 2016.
[Is] ISSN:0016-9900
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The purpose of research is the assessment of the individual cancer risk (ICR) for workers of the basic occupations in key branches of industry of the Irkutsk region. There was executed the calculation of ICR levels for workers of the basic occupations of the aircraft industry, aluminum smelters and vinyl chloride production plants. The estimation of the exposure for workers was carried out according to long-term time-weighted average concentrations in the air of the working area, for the population - on annual average concentrations in the ambient air. To assess the risk that is not associated with the profession, the dose was calculated for the period of life (70 years). When calculating the toxicant doses in the working area there were used the "standard" indices ofpulmonary ventilation for adults, body weight, the work experience in the contact with carcinogens of 30 years, the number of days in the contact of 240, the duration of the working time 8 or 12 hours (in accordance with the working hours) duration. ICR for the Irkutsk population amounted of 3.08E-04, in Shelekhov - 4.8E-05, Sayansk - 1.1E-05. The amount of risk depends on the content offormaldehyde in all territories and chromium VI in cities of Irkutsk and Shelekhov. ICR for workers of basic occupations of studied plants in dozens of times are higher than for the urban population. Priority carcinogens are: chromium VI, nickel, formaldehyde, silicon dioxide -for the aircraft plant employees; 1,2-dichloretan, vinyl chloride - for the workers of vinyl chloride production plant; benzopyrene - for the aluminum smelter workers.
[Mh] Termos MeSH primário: Poluentes Ocupacionais do Ar
Carcinogênese/induzido quimicamente
Cromo
Formaldeído
Indústria Manufatureira
Cloreto de Vinil
[Mh] Termos MeSH secundário: Poluentes Ocupacionais do Ar/análise
Poluentes Ocupacionais do Ar/toxicidade
Carcinógenos Ambientais/análise
Carcinógenos Ambientais/toxicidade
Cromo/análise
Cromo/toxicidade
Formaldeído/análise
Formaldeído/toxicidade
Seres Humanos
Indústria Manufatureira/métodos
Indústria Manufatureira/normas
Exposição Ocupacional/efeitos adversos
Exposição Ocupacional/análise
Exposição Ocupacional/prevenção & controle
Medição de Risco/métodos
Medição de Risco/estatística & dados numéricos
Fatores de Risco
Sibéria/epidemiologia
Tempo
Cloreto de Vinil/análise
Cloreto de Vinil/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Air Pollutants, Occupational); 0 (Carcinogens, Environmental); 0R0008Q3JB (Chromium); 18540-29-9 (chromium hexavalent ion); 1HG84L3525 (Formaldehyde); WD06X94M2D (Vinyl Chloride)
[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:180216
[St] Status:MEDLINE


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[PMID]:29408622
[Au] Autor:Zeng Y; Shen Z; Gu W; Wu M
[Ad] Endereço:Department of Medical Oncology, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu 210009, China; The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, China. Ele
[Ti] Título:Inhibition of hepatocellular carcinoma tumorigenesis by curcumin may be associated with CDKN1A and CTGF.
[So] Source:Gene;651:183-193, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:This study aimed to explore crucial genes, transcription factors (TFs), and microRNAs (miRNAs) associated with the effects of curcumin against hepatocellular carcinoma (HCC). We downloaded data (GSE59713) from Gene Expression Omnibus to analyze differentially expressed genes (DEGs) between curcumin-treated and untreated HCC cell lines. Then, we identified the disease ontology (DO) and functional enrichment analysis of these DEGs and analyzed their protein-protein interactions (PPIs). Additionally, we constructed TF-target gene and miRNA-target gene regulatory networks and explored the potential functions of these DEGs. Finally, we detected the expression of CDKN1A, CTGF, LEF1 TF and MIR-19A regulated by curcumin in PLC/PRF/5 cells using RT-PCR. In total, 345 upregulated and 212 downregulated genes were identified. The main enriched pathway of upregulated genes was the TNF signaling pathway. The downregulated genes were significantly enriched in TGF-beta signaling pathway. In addition, most DEGs were significantly enriched in DO terms such as liver cirrhosis, hepatitis, hepatitis C and cholestasis (eg., CTGF). In the constructed PPI network, CDKN1A and CTGF were the key proteins. Moreover, LEF1, CDKN1A, and miR-19A that regulated CTGF were highlighted in the regulatory networks. Furthermore, the expression of CDKN1A, CTGF, LEF1 TF and miR-19A regulated by curcumin in PLC/PRF/5 cells was consistent with the aforementioned bioinformatics analysis results. To conclude, curcumin might exert its protective effects against HCC tumorigenesis by downregulating LEF1 and downregulating CTGF regulated by MIR-19A and upregulating CDKN1A expression.
[Mh] Termos MeSH primário: Carcinogênese/efeitos dos fármacos
Carcinoma Hepatocelular/tratamento farmacológico
Fator de Crescimento do Tecido Conjuntivo/genética
Curcumina/uso terapêutico
Inibidor de Quinase Dependente de Ciclina p21/genética
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/genética
Linhagem Celular Tumoral
Bases de Dados Genéticas
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Neoplasias Hepáticas/genética
Fator 1 de Ligação ao Facilitador Linfoide/genética
MicroRNAs/genética
Proteínas de Neoplasias/genética
Mapas de Interação de Proteínas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDKN1A protein, human); 0 (CTGF protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (LEF1 protein, human); 0 (Lymphoid Enhancer-Binding Factor 1); 0 (MIRN19 microRNA, human); 0 (MicroRNAs); 0 (Neoplasm Proteins); 139568-91-5 (Connective Tissue Growth Factor); IT942ZTH98 (Curcumin)
[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:180207
[St] Status:MEDLINE


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[PMID]:29339161
[Au] Autor:El Nagar S; Zindy F; Moens C; Martin L; Plassard D; Roussel MF; Lamonerie T; Billon N
[Ad] Endereço:Université Côte d'Azur, CNRS, Inserm, iBV, Nice, France.
[Ti] Título:A new genetically engineered mouse model of choroid plexus carcinoma.
[So] Source:Biochem Biophys Res Commun;496(2):568-574, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Choroid plexus carcinomas (CPCs) are highly malignant brain tumours predominantly found in children and associated to poor prognosis. Improved therapy for these cancers would benefit from the generation of animal models. Here we have created a novel mouse CPC model by expressing a stabilised form of c-Myc (MycT58A) and inactivating Trp53 in the choroid plexus of newborn mice. This induced aberrant proliferation of choroid plexus epithelial cells, leading to aggressive tumour development and death within 150 days. Choroid plexus tumours occurred with a complete penetrance in all brain ventricles, with prevalence in the lateral and fourth ventricles. Histological and cellular analysis indicated that these tumours were CPCs resembling their human counterparts. Comparison of gene expression profiles of CPCs and non-neoplastic tissues revealed profound alterations in cell cycle regulation and DNA damage responses, suggesting that dysregulation of cell division and DNA checkpoint pathways may represent key vulnerabilities. This novel animal model of CPC provides an invaluable tool to elucidate the mechanism of CPC formation and to develop successful therapies against this devastating paediatric cancer.
[Mh] Termos MeSH primário: Carcinoma/genética
Carcinoma/patologia
Neoplasias do Plexo Corióideo/genética
Neoplasias do Plexo Corióideo/patologia
Plexo Corióideo/patologia
Proteínas Proto-Oncogênicas c-myc/genética
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Animais
Carcinogênese/genética
Carcinogênese/patologia
Proliferação Celular
Dano ao DNA
Modelos Animais de Doenças
Seres Humanos
Camundongos
Camundongos Transgênicos
Mutação
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-myc); 0 (Tumor Suppressor Protein p53)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE


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[PMID]:29181576
[Au] Autor:Araújo R; Santos JMO; Fernandes M; Dias F; Sousa H; Ribeiro J; Bastos MMSM; Oliveira PA; Carmo D; Casaca F; Silva S; Medeiros R; Gil da Costa RM
[Ad] Endereço:Molecular Oncology and Viral Pathology Group, IPO Porto Research Center (CI-IPOP), Portuguese Oncology Institute of Porto (IPO Porto), Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
[Ti] Título:Expression profile of microRNA-146a along HPV-induced multistep carcinogenesis: a study in HPV16 transgenic mice.
[So] Source:J Cancer Res Clin Oncol;144(2):241-248, 2018 Feb.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Persistent human papillomavirus (HPV) infection is associated with the development of certain types of cancer and the dysregulation of microRNAs has been implicated in HPV-associated carcinogenesis. This is the case of microRNA-146a (miR-146a), which is thought to regulate tumor-associated inflammation. We sought to investigate the expression levels of miR-146a during HPV16-mediated carcinogenesis using skin samples from K14-HPV16 transgenic mice which develop the consecutive phases of the carcinogenesis process. METHODS: Female transgenic (HPV ) and wild-type (HPV ) mice were sacrificed at 24-26 weeks-old or 28-30 weeks-old. Chest and ear skin samples from HPV and HPV mice were histologically classified and used for microRNA extraction and quantification by qPCR. RESULTS: Chest skin samples from 24 to 26 weeks-old HPV mice presented diffuse epidermal hyperplasia and only 22.5% showed multifocal dysplasia, while at 28-30 weeks-old all (100.0%) HPV animals showed epidermal dysplasia. All HPV ear skin samples showed carcinoma in situ (CIS). MiR-146a expression levels were higher in HPV compared to HPV mice (p = 0.006). There was also an increase in miR-146a expression in dysplastic skin lesions compared with hyperplasic lesions (p = 0.011). Samples showing CIS had a significant decrease in miR-146a expression when compared to samples showing epidermal hyperplasia (p = 0.018) and epidermal dysplasia (p = 0.009). CONCLUSIONS: These results suggest that HPV16 induces the overexpression of miR-146a in the initial stages of carcinogenesis (hyperplasia and dysplasia), whereas decreases its expression at later stages (CIS). Taken together, these data implicate and suggest different roles of miR-146a in HPV-mediated carcinogenesis.
[Mh] Termos MeSH primário: Carcinogênese/genética
Papillomavirus Humano 16/genética
MicroRNAs/biossíntese
[Mh] Termos MeSH secundário: Animais
Carcinogênese/metabolismo
Carcinogênese/patologia
Feminino
Hiperplasia/virologia
Camundongos
Camundongos Transgênicos
MicroRNAs/genética
Infecções por Papillomavirus/genética
Infecções por Papillomavirus/metabolismo
Infecções por Papillomavirus/virologia
Pele/patologia
Pele/virologia
Neoplasias Cutâneas/genética
Neoplasias Cutâneas/metabolismo
Neoplasias Cutâneas/patologia
Neoplasias Cutâneas/virologia
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (Mirn146 microRNA, mouse)
[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:171129
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2549-5


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[PMID]:28467999
[Au] Autor:Thorgeirsson SS
[Ad] Endereço:Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA.
[Ti] Título:Stemness in Liver Cancer.
[So] Source:Dig Dis;35(4):387-389, 2017.
[Is] ISSN:1421-9875
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Cancer cells possessing "stemness," or stem-cell properties, are referred to as cancer stem cells (CSC) or cancer-initiating cells. The concept that these cells rest at the apex of the cancer hierarchy is an evolving theme in cancer research. These cells are by definition primarily responsible for the initiation and propagation of tumors as well as relapse after therapy, and they are therefore of major scientific interest. Several studies indicate that hepatocellular carcinomas that harbor phenotypic features of stem cells and progenitor cells constitute a subclass of therapeutically challenging cancers that are associated with a particularly poor prognosis. We recently demonstrated that any cell type in the mouse hepatic lineage can undergo oncogenic reprogramming into a CSC by activating different cell type-specific pathways [1]. Identification of common and cell of origin-specific phenotypic and genetic changes could provide new therapeutic targets for liver cancer.
[Mh] Termos MeSH primário: Neoplasias Hepáticas/patologia
Células-Tronco Neoplásicas/patologia
[Mh] Termos MeSH secundário: Animais
Carcinogênese/patologia
Carcinoma Hepatocelular/patologia
Seres Humanos
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[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:10.1159/000456592


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[PMID]:29416026
[Au] Autor:Wang YQ; Wang HL; Xu J; Tan J; Fu LN; Wang JL; Zou TH; Sun DF; Gao QY; Chen YX; Fang JY
[Ad] Endereço:Division of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 145 Middle Shandong Road, Shanghai, 200001, China.
[Ti] Título:Sirtuin5 contributes to colorectal carcinogenesis by enhancing glutaminolysis in a deglutarylation-dependent manner.
[So] Source:Nat Commun;9(1):545, 2018 02 07.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Reversible post-translational modifications represent a mechanism to control tumor metabolism. Here we show that mitochondrial Sirtuin5 (SIRT5), which mediates lysine desuccinylation, deglutarylation, and demalonylation, plays a role in colorectal cancer (CRC) glutamine metabolic rewiring. Metabolic profiling identifies that deletion of SIRT5 causes a marked decrease in C-glutamine incorporation into tricarboxylic-acid (TCA) cycle intermediates and glutamine-derived non-essential amino acids. This reduces the building blocks required for rapid growth. Mechanistically, the direct interaction between SIRT5 and glutamate dehydrogenase 1 (GLUD1) causes deglutarylation and functional activation of GLUD1, a critical regulator of cellular glutaminolysis. Consistently, GLUD1 knockdown diminishes SIRT5-induced proliferation, both in vivo and in vitro. Clinically, overexpression of SIRT5 is significantly correlated with poor prognosis in CRC. Thus, SIRT5 supports the anaplerotic entry of glutamine into the TCA cycle in malignant phenotypes of CRC via activating GLUD1.
[Mh] Termos MeSH primário: Carcinogênese/metabolismo
Neoplasias Colorretais/metabolismo
Regulação Neoplásica da Expressão Gênica/fisiologia
Glutamato Desidrogenase/metabolismo
Glutamina/metabolismo
Sirtuínas/metabolismo
[Mh] Termos MeSH secundário: Proliferação Celular
Ciclo do Ácido Cítrico/fisiologia
Regulação Enzimológica da Expressão Gênica/fisiologia
Glutamato Desidrogenase/genética
Células HCT116
Seres Humanos
Interferência de RNA
Sirtuínas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0RH81L854J (Glutamine); EC 1.4.1.2 (Glutamate Dehydrogenase); EC 1.4.1.3 (GLUD1 protein, human); EC 3.5.1.- (SIRT5 protein, human); EC 3.5.1.- (Sirtuins)
[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:180209
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-018-02951-4


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[PMID]:29381398
[Au] Autor:Orywal K; Jelski W; Werel T; Szmitkowski M
[Ad] Endereço:a Department of Biochemical Diagnostics , Medical University , Bialystok , Podlaskie , Poland.
[Ti] Título:The Activity of Class I-IV Alcohol Dehydrogenase Isoenzymes and Aldehyde Dehydrogenase in Bladder Cancer Cells.
[So] Source:Cancer Invest;36(1):66-72, 2018 Jan 02.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: The aim of this study was to determine the differences in the activity of Alcohol Dehydrogenase (ADH) isoenzymes and Aldehyde Dehydrogenase (ALDH) in normal and cancerous bladder cells. METHODS: Class III, IV of ADH and total ADH activity were measured by the photometric method and class I, II ADH and ALDH activity by the fluorometric method. RESULTS: Significantly higher total activity of ADH was found in both, low-grade and high-grade bladder cancer, in comparison to healthy tissues. CONCLUSION: The increased activity of total ADH in bladder cancer cells may be the cause of metabolic disorders in cancer cells, which may intensify carcinogenesis.
[Mh] Termos MeSH primário: Álcool Desidrogenase/metabolismo
Aldeído Desidrogenase/metabolismo
Isoenzimas/metabolismo
Neoplasias da Bexiga Urinária/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Carcinogênese/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
Bexiga Urinária/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Isoenzymes); EC 1.1.1.1 (Alcohol Dehydrogenase); EC 1.2.1.3 (Aldehyde Dehydrogenase)
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2017.1422511


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[PMID]:28467300
[Au] Autor:Ku AT; Shaver TM; Rao AS; Howard JM; Rodriguez CN; Miao Q; Garcia G; Le D; Yang D; Borowiak M; Cohen DN; Chitsazzadeh V; Diwan AH; Tsai KY; Nguyen H
[Ad] Endereço:Stem Cell and Regenerative Medicine Center, Baylor College of Medicine, Houston, United States.
[Ti] Título:TCF7L1 promotes skin tumorigenesis independently of ß-catenin through induction of LCN2.
[So] Source:Elife;6, 2017 05 03.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The transcription factor is an embryonic stem cell signature gene that is upregulated in multiple aggressive cancer types, but its role in skin tumorigenesis has not yet been defined. Here we document TCF7L1 upregulation in skin squamous cell carcinoma (SCC) and demonstrate that TCF7L1 overexpression increases tumor incidence, tumor multiplicity, and malignant progression in the chemically induced mouse model of skin SCC. Additionally, we show that downregulation of TCF7L1 and its paralogue TCF7L2 reduces tumor growth in a xenograft model of human skin SCC. Using separation-of-function mutants, we show that TCF7L1 promotes tumor growth, enhances cell migration, and overrides oncogenic RAS-induced senescence independently of its interaction with ß-catenin. Through transcriptome profiling and combined gain- and loss-of-function studies, we identified LCN2 as a major downstream effector of TCF7L1 that drives tumor growth. Our findings establish a tumor-promoting role for TCF7L1 in skin and elucidate the mechanisms underlying its tumorigenic capacity.
[Mh] Termos MeSH primário: Carcinogênese
Carcinoma de Células Escamosas/fisiopatologia
Lipocalina-2/metabolismo
Neoplasias Cutâneas/fisiopatologia
Proteína 1 Semelhante ao Fator 7 de Transcrição/metabolismo
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Perfilação da Expressão Gênica
Xenoenxertos
Seres Humanos
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (CTNNB1 protein, human); 0 (LCN2 protein, human); 0 (Lipocalin-2); 0 (TCF7L1 protein, human); 0 (Transcription Factor 7-Like 1 Protein); 0 (beta Catenin)
[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:170504
[St] Status:MEDLINE


  9 / 6412 MEDLINE  
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[PMID]:29421992
[Au] Autor:Lopes-Coelho F; Gouveia-Fernandes S; Serpa J
[Ad] Endereço:1 Centro de Estudos de Doenças Crónicas (CEDOC), NOVA Medical School/Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Lisbon, Portugal.
[Ti] Título:Metabolic cooperation between cancer and non-cancerous stromal cells is pivotal in cancer progression.
[So] Source:Tumour Biol;40(2):1010428318756203, 2018 Feb.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The way cancer cells adapt to microenvironment is crucial for the success of carcinogenesis, and metabolic fitness is essential for a cancer cell to survive and proliferate in a certain organ/tissue. The metabolic remodeling in a tumor niche is endured not only by cancer cells but also by non-cancerous cells that share the same microenvironment. For this reason, tumor cells and stromal cells constitute a complex network of signal and organic compound transfer that supports cellular viability and proliferation. The intensive dual-address cooperation of all components of a tumor sustains disease progression and metastasis. Herein, we will detail the role of cancer-associated fibroblasts, cancer-associated adipocytes, and inflammatory cells, mainly monocytes/macrophages (tumor-associated macrophages), in the remodeling and metabolic adaptation of tumors.
[Mh] Termos MeSH primário: Carcinogênese/metabolismo
Neoplasias/metabolismo
Células Estromais/metabolismo
Microambiente Tumoral
[Mh] Termos MeSH secundário: Fibroblastos Associados a Câncer/metabolismo
Carcinogênese/patologia
Proliferação Celular
Sobrevivência Celular
Progressão da Doença
Seres Humanos
Macrófagos/metabolismo
Neoplasias/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180210
[St] Status:MEDLINE
[do] DOI:10.1177/1010428318756203


  10 / 6412 MEDLINE  
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[PMID]:28471108
[Au] Autor:Zhang MW; Fujiwara K; Che X; Zheng S; Zheng L
[Ad] Endereço:The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.
[Ti] Título:DNA methylation in the tumor microenvironment.
[So] Source:J Zhejiang Univ Sci B;18(5):365-372, 2017 May.
[Is] ISSN:1862-1783
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:The tumor microenvironment (TME) plays an important role in supporting cancer progression. The TME is composed of tumor cells, the surrounding tumor-associated stromal cells, and the extracellular matrix (ECM). Crosstalk between the TME components contributes to tumorigenesis. Recently, one of our studies showed that pancreatic ductal adenocarcinoma (PDAC) cells can induce DNA methylation in cancer-associated fibroblasts (CAFs), thereby modifying tumor-stromal interactions in the TME, and subsequently creating a TME that supports tumor growth. Here we summarize recent studies about how DNA methylation affects tumorigenesis through regulating tumor-associated stromal components including fibroblasts and immune cells. We also discuss the potential for targeting DNA methylation for the treatment of cancers.
[Mh] Termos MeSH primário: Carcinogênese/genética
Metilação de DNA/genética
DNA de Neoplasias/genética
Regulação Neoplásica da Expressão Gênica/genética
Neoplasias/genética
Neoplasias/patologia
Microambiente Tumoral/genética
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Modelos Genéticos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (DNA, Neoplasm)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1631/jzus.B1600579



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