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[PMID]:29343684
[Au] Autor:Howson LJ; Napolitani G; Shepherd D; Ghadbane H; Kurupati P; Preciado-Llanes L; Rei M; Dobinson HC; Gibani MM; Teng KWW; Newell EW; Veerapen N; Besra GS; Pollard AJ; Cerundolo V
[Ad] Endereço:Medical Research Council (MRC) Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, OX3 9DS, UK.
[Ti] Título:MAIT cell clonal expansion and TCR repertoire shaping in human volunteers challenged with Salmonella Paratyphi A.
[So] Source:Nat Commun;9(1):253, 2018 01 17.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mucosal-associated invariant T (MAIT) cells are innate-like T cells that can detect bacteria-derived metabolites presented on MR1. Here we show, using a controlled infection of humans with live Salmonella enterica serovar Paratyphi A, that MAIT cells are activated during infection, an effect maintained even after antibiotic treatment. At the peak of infection MAIT cell T-cell receptor (TCR)ß clonotypes that are over-represented prior to infection transiently contract. Select MAIT cell TCRß clonotypes that expand after infection have stronger TCR-dependent activation than do contracted clonotypes. Our results demonstrate that host exposure to antigen may drive clonal expansion of MAIT cells with increased functional avidity, suggesting a role for specific vaccination strategies to increase the frequency and potency of MAIT cells to optimize effector function.
[Mh] Termos MeSH primário: Proliferação Celular
Células T Invariáveis Associadas à Mucosa/imunologia
Febre Paratifoide/imunologia
Receptores de Antígenos de Linfócitos T alfa-beta/imunologia
Salmonella paratyphi A/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Linhagem Celular Tumoral
Células Clonais/imunologia
Células Clonais/metabolismo
Células Clonais/microbiologia
Voluntários Saudáveis
Interações Hospedeiro-Patógeno/imunologia
Seres Humanos
Células Jurkat
Leucócitos Mononucleares/imunologia
Leucócitos Mononucleares/metabolismo
Leucócitos Mononucleares/microbiologia
Meia-Idade
Células T Invariáveis Associadas à Mucosa/metabolismo
Células T Invariáveis Associadas à Mucosa/microbiologia
Febre Paratifoide/metabolismo
Febre Paratifoide/microbiologia
Receptores de Antígenos de Linfócitos T alfa-beta/genética
Receptores de Antígenos de Linfócitos T alfa-beta/metabolismo
Salmonella paratyphi A/fisiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Antigen, T-Cell, alpha-beta)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180119
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02540-x


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[PMID]:29186352
[Au] Autor:Karayazi Atici Ö; Urbanska A; Gopinathan SG; Boutillon F; Goffin V; Shemanko CS
[Ad] Endereço:Department of Biological Sciences, University of Calgary, Calgary, Alberta, Canada.
[Ti] Título:ATM Is Required for the Prolactin-Induced HSP90-Mediated Increase in Cellular Viability and Clonogenic Growth After DNA Damage.
[So] Source:Endocrinology;159(2):907-930, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prolactin (PRL) acts as a survival factor for breast cancer cells, but the PRL signaling pathway and the mechanism are unknown. Previously, we identified the master chaperone, heat shock protein 90 (HSP90) α, as a prolactin-Janus kinase 2 (JAK2)-signal transducer and activator of transcription 5 (STAT5) target gene involved in survival, and here we investigated the role of HSP90 in the mechanism of PRL-induced viability in response to DNA damage. The ataxia-telangiectasia mutated kinase (ATM) protein plays a critical role in the cellular response to double-strand DNA damage. We observed that PRL increased viability of breast cancer cells treated with doxorubicin or etoposide. The increase in cellular resistance is specific to the PRL receptor, because the PRL receptor antagonist, Δ1-9-G129R-hPRL, prevented the increase in viability. Two different HSP90 inhibitors, 17-allylamino-17-demethoxygeldanamycin and BIIB021, reduced the PRL-mediated increase in cell viability of doxorubicin-treated cells and led to a decrease in JAK2, ATM, and phosphorylated ATM protein levels. Inhibitors of JAK2 (G6) and ATM (KU55933) abolished the PRL-mediated increase in cell viability of DNA-damaged cells, supporting the involvement of each, as well as the crosstalk of ATM with the PRL pathway in the context of DNA damage. Drug synergism was detected between the ATM inhibitor (KU55933) and doxorubicin and between the HSP90 inhibitor (BIIB021) and doxorubicin. Short interfering RNA directed against ATM prevented the PRL-mediated increase in cell survival in two-dimensional cell culture, three-dimensional collagen gel cultures, and clonogenic cell survival, after doxorubicin treatment. Our results indicate that ATM contributes to the PRL-JAK2-STAT5-HSP90 pathway in mediating cellular resistance to DNA-damaging agents.
[Mh] Termos MeSH primário: Proteínas Mutadas de Ataxia Telangiectasia/fisiologia
Proliferação Celular/efeitos dos fármacos
Dano ao DNA/efeitos dos fármacos
Proteínas de Choque Térmico HSP90/metabolismo
Prolactina/farmacologia
[Mh] Termos MeSH secundário: Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Células Clonais/efeitos dos fármacos
Células Clonais/fisiologia
Dano ao DNA/genética
Feminino
Seres Humanos
Células MCF-7
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (HSP90 Heat-Shock Proteins); 9002-62-4 (Prolactin); EC 2.7.11.1 (ATM protein, human); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00652


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[PMID]:29300727
[Au] Autor:Risques RA; Kennedy SR
[Ad] Endereço:Department of Pathology, University of Washington, Seattle, Washington, United States of America.
[Ti] Título:Aging and the rise of somatic cancer-associated mutations in normal tissues.
[So] Source:PLoS Genet;14(1):e1007108, 2018 01.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA mutations are inevitable. Despite proficient DNA repair mechanisms, somatic cells accumulate mutations during development and aging, generating cells with different genotypes within the same individual, a phenomenon known as somatic mosaicism. While the existence of somatic mosaicism has long been recognized, in the last five years, advances in sequencing have provided unprecedented resolution to characterize the extent and nature of somatic genetic variation. Collectively, these new studies are revealing a previously uncharacterized aging phenotype: the accumulation of clones with cancer driver mutations. Here, we summarize the most recent findings, which converge in the novel notion that cancer-associated mutations are prevalent in normal tissue and accumulate with aging.
[Mh] Termos MeSH primário: Envelhecimento/genética
Neoplasias/genética
[Mh] Termos MeSH secundário: Células Clonais
Reparo do DNA/genética
Bases de Dados Genéticas
Seres Humanos
Mosaicismo
Mutação/genética
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180105
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007108


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[PMID]:29227594
[Au] Autor:Bazalii AV; Horak IR; Pasi chn yk GV; Komisarenko SV; Drobot LB
[Ti] Título:Transcriptional regulation of NOX genes express ion in human breast adenocarcinoma MCF-7 cells is modulated by adaptor protein Ruk/CIN 85.
[So] Source:Ukr Biochem J;88(1):119-25, 2016 Jan-Feb.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:NADPH oxidases are key components of redox-dependent signaling networks involved in the control of cancer cell proliferation, survival and invasion. The data have been accumulated that demonstrate specific expression patterns and levels of NADPH oxidase homologues (NOXs) and accessory genes in human cancer cell lines and primary tumors as well as modulation of these parameters by extracellular cues. Our previous studies revealed that ROS production by human colorectal adenocarcinoma HT-29 cells is positively correlated with adaptor protein Ruk/CIN85 expression while increased levels of Ruk/CIN85 in weakly invasive human breast adenocarcinoma MC F-7 cells contribute to their malignant phenotype through the constitutive activation of Src/Akt pathway. In this study, to investigate whether overexpression of Ruk/CIN85 in MC F-7 cells can influence transcriptional regulation of NOXs genes, the subclones of MCF-7 cells with different levels of Ruk/CIN85 were screened for NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1 and DUOX2 as well as for regulatory subunit p22Phox mRNA contents by quantitative RT-PCR (qPCR). Systemic multidirectional changes in mRNA levels for NOX1, NOX2, NOX5, DUOX2 and p22Phox were revealed in Ruk/CIN85 overexpressing cells in comparison to control WT cells. Knocking down of Ruk/CIN85 using technology of RNA-interference resulted in the reversion of these changes. Further studies are necessary to elucidate, by which molecular mechanisms Ruk/CIN85 could affect transcriptional regulation of NOXs genes.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/genética
Regulação Neoplásica da Expressão Gênica
NADPH Oxidase 1/genética
Espécies Reativas de Oxigênio/metabolismo
Transcrição Genética
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/antagonistas & inibidores
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Células Clonais
Oxidases Duais/genética
Oxidases Duais/metabolismo
Seres Humanos
Isoenzimas/genética
Isoenzimas/metabolismo
Células MCF-7
NADPH Oxidase 1/metabolismo
NADPH Oxidases/genética
NADPH Oxidases/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Isoenzymes); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); 0 (SH3KBP1 protein, human); EC 1.11.1.- (Dual Oxidases); EC 1.6.3.- (NADPH Oxidase 1); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.- (NOX1 protein, human); EC 1.6.3.1 (CYBA protein, human); EC 1.6.3.1 (DUOX1 protein, human); EC 1.6.3.1 (DUOX2 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.01.119


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[PMID]:28464892
[Au] Autor:Li B; Gale RP; Xu Z; Qin T; Song Z; Zhang P; Bai J; Zhang L; Zhang Y; Liu J; Huang G; Xiao Z
[Ad] Endereço:MDS and MPN Centre, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, 288 Nanjing Road, Tianjin, 300020, China.
[Ti] Título:Non-driver mutations in myeloproliferative neoplasm-associated myelofibrosis.
[So] Source:J Hematol Oncol;10(1):99, 2017 May 02.
[Is] ISSN:1756-8722
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We studied non-driver mutations in 62 subjects with myeloproliferative neoplasm (MPN)-associated myelofibrosis upon diagnosis, including 45 subjects with primary myelofibrosis (PMF) and 17 with post-polycythemia vera or post-essential thrombocythemia myelofibrosis (post-PV/ET MF). Fifty-eight subjects had ≥1 non-driver mutation upon diagnosis. Mutations in mRNA splicing genes, especially in U2AF1, were significantly more frequent in PMF than in post-PV/ET MF (33 vs. 6%; P = 0.015). There were also striking differences in clonal architecture. These data indicate different genomic spectrums between PMF and post-PV/ET MF.
[Mh] Termos MeSH primário: Mutação
Policitemia Vera/genética
Mielofibrose Primária/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Apoptose/genética
Adesão Celular/genética
Ciclo Celular/genética
Montagem e Desmontagem da Cromatina/genética
Células Clonais
Metilação de DNA/genética
Reparo do DNA/genética
Feminino
Seres Humanos
Masculino
Meia-Idade
Policitemia Vera/complicações
Mielofibrose Primária/etiologia
Processamento de RNA/genética
Transdução de Sinais/genética
Fator de Processamento U2AF/genética
Trombocitemia Essencial/complicações
Trombocitemia Essencial/genética
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; LETTER
[Nm] Nome de substância:
0 (Splicing Factor U2AF); 0 (U2AF1 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s13045-017-0472-5


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[PMID]:29253888
[Au] Autor:Norris MH; Heacock-Kang Y; Zarzycki-Siek J; Bluhm AP; McMillan IA; Schweizer HP; Hoang TT
[Ad] Endereço:Department of Microbiology, University of Hawaii at Manoa, Honolulu, HI, United States of America.
[Ti] Título:Burkholderia pseudomallei natural competency and DNA catabolism: Identification and characterization of relevant genes from a constructed fosmid library.
[So] Source:PLoS One;12(12):e0189018, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Burkholderia spp. are genetically and physiologically diverse. Some strains are naturally transformable and capable of DNA catabolism. Burkholderia pseudomallei (Bp) strains 1026b and K96243 and B. thailandensis strain E264 are able to utilize DNA as a sole carbon source for growth, while only strains 1026b and E264 are naturally transformable. In this study, we constructed low-copy broad-host-range fosmid library, containing Bp strain 1026b chromosomal DNA fragments, and employed a novel positive selection approach to identify genes responsible for DNA uptake and DNA catabolism. The library was transferred to non-competent Bp K96243 and B. cenocepacia (Bc) K56-2, harboring chromosomally-inserted FRT-flanked sacB and pheS counter-selection markers. The library was incubated with DNA encoding Flp recombinase, followed by counter-selection on sucrose and chlorinated phenylalanine, to select for clones that took up flp-DNA, transiently expressed Flp, and excised the sacB-pheS cassette. Putative clones that survived the counter-selection were subsequently incubated with gfp-DNA and bacteria were visualized via fluorescent microscopy to confirm natural competency. Fosmid sequencing identified several 1026b genes implicated in DNA uptake, which were validated using chromosomal mutants. One of the naturally competent clones selected in Bc K56-2 enabled Bc, Bp and B. mallei to utilize DNA as a sole carbon source, and all fosmids were used to successfully create mutations in non-naturally-competent B. mallei and Bp strains.
[Mh] Termos MeSH primário: Burkholderia pseudomallei/genética
DNA Bacteriano/metabolismo
Biblioteca Gênica
Genes Bacterianos
Plasmídeos/genética
[Mh] Termos MeSH secundário: Alelos
Cromossomos Bacterianos/genética
Células Clonais
Reprodutibilidade dos Testes
Especificidade da Espécie
Transformação Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Bacterial)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189018


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[PMID]:29253018
[Au] Autor:Dittmann K; Mayer C; Czemmel S; Huber SM; Rodemann HP
[Ad] Endereço:Division of Radiobiology and Molecular Environmental Research, University of Tuebingen, Tuebingen, Germany.
[Ti] Título:New roles for nuclear EGFR in regulating the stability and translation of mRNAs associated with VEGF signaling.
[So] Source:PLoS One;12(12):e0189087, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell membrane-associated epidermal growth factor receptor (EGFR) translocates into a perinuclear/nuclear location upon stimulation, where it complexes with mRNAs. Treatment with radiation and cisplatin decreases the amounts of mRNAs present within this complex. Gene array analyses of mRNAs in complex with immunoprecipitated nEGFR revealed significant enrichment of different mRNA species compared to the control immunoprecipitation. Functional annotation with help of DAVID Gene Ontology Analysis identified under other terms the HIF-1A/VEGF signaling pathway as one of the top scoring KEGG pathways. RT-PCR and western blots revealed the radiation-induced expression of mRNAs and proteins involved in HIF-1A/VEGF signaling. Simultaneously, the levels of the corresponding validated miRNAs within the complex containing nEGFR and mRNAs were decreased. This finding argues that an mRNA/miRNA/nEGFR complex regulates protein expression. Indeed, we detected the GW182, AGO2, PABPC1 and cNOT1 proteins, which belong to the deadenylase complex, in a complex with nuclear EGFR. Erlotinib-mediated inhibition of EGFR kinase reduced the radiation-induced increase in mRNA expression. In this context, erlotinib reduced AGO2 phosphorylation by the EGFR kinase at residue Y393, which was associated with increased cNOT1 deadenylase activity and reduced mRNA stability. To prove the roles of miRNAs in this context, we transfected cells with an inhibitor of Hsa-mir-1180p5, which targets the NFATC4 mRNA, an mRNA associated with VEGF signaling, or pretreated cells with erlotinib. Indeed, Hsa-mir-1180p5 knockdown increased and the erlotinib treatment decreased the expression of the NFATC4 protein. The expression of the NFATC4 protein controlled the cloning efficiency and radiosensitivity of A549 and FaDu tumor cells. Thus, this study is the first to show that a membrane-located tyrosine kinase receptor, such as EGFR, is internalized to a nuclear/perinuclear location upon exposure to stress and modulates the stability and translation of miRNA-selected mRNAs. This mechanism enables cells to directly express proteins in response to EGFR activation and may contribute to treatment resistance in EGFR-overexpressing tumors.
[Mh] Termos MeSH primário: Núcleo Celular/metabolismo
Biossíntese de Proteínas
Estabilidade de RNA
Receptor do Fator de Crescimento Epidérmico/metabolismo
Transdução de Sinais
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Mh] Termos MeSH secundário: Células A549
Trifosfato de Adenosina/metabolismo
Sobrevivência Celular
Células Clonais
DNA Complementar/genética
Seres Humanos
Fatores de Transcrição NFATC/metabolismo
Ligação Proteica
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Complexo de Inativação Induzido por RNA/metabolismo
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CNOT1 protein, human); 0 (DNA, Complementary); 0 (NFATC Transcription Factors); 0 (RNA, Messenger); 0 (RNA-Induced Silencing Complex); 0 (Transcription Factors); 0 (Vascular Endothelial Growth Factor A); 8L70Q75FXE (Adenosine Triphosphate); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189087


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[PMID]:29212853
[Au] Autor:Simon S; Vignard V; Varey E; Parrot T; Knol AC; Khammari A; Gervois N; Lang F; Dreno B; Labarriere N
[Ad] Endereço:CRCINA, INSERM, Université d'Angers, Université de Nantes, Nantes, France.
[Ti] Título:Emergence of High-Avidity Melan-A-Specific Clonotypes as a Reflection of Anti-PD-1 Clinical Efficacy.
[So] Source:Cancer Res;77(24):7083-7093, 2017 Dec 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Therapeutic strategies using anti-PD-1-blocking antibodies reported unparalleled effectiveness for melanoma immunotherapy, but deciphering immune responses modulated by anti-PD-1 treatment remains a crucial issue. Here, we analyzed the composition and functions of the large Melan-A-specific T-cell repertoire in the peripheral blood of 9 melanoma patients before and after 2 months of treatment with anti-PD-1. We observed amplification of Melan-A-specific Vß subfamilies undetectable before therapy (thereafter called emerging Vß subfamilies) in responding patients, with a predominant expansion in patients with a complete response. These emerging Vß subfamilies displayed a higher functional avidity for their cognate antigen than Vß subfamilies not amplified upon anti-PD-1 therapy and could be identified by a sustained coexpression of PD-1 and TIGIT receptors. Thus, in addition to the emergence of neoantigen-specific T cells previously documented upon anti-PD-1 therapy, our work describes the emergence of high-avidity Melan-A-specific clonotypes as a surrogate marker of treatment efficacy. .
[Mh] Termos MeSH primário: Anticorpos Monoclonais/uso terapêutico
Afinidade de Anticorpos
Imunoterapia/métodos
Antígeno MART-1/imunologia
Melanoma/terapia
Receptor de Morte Celular Programada 1/imunologia
[Mh] Termos MeSH secundário: Formação de Anticorpos
Antígenos de Neoplasias/imunologia
Células Cultivadas
Células Clonais
Seres Humanos
Antígeno MART-1/metabolismo
Melanoma/imunologia
Melanoma/patologia
Especificidade por Substrato
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antigens, Neoplasm); 0 (MART-1 Antigen); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-17-1856


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[PMID]:29183944
[Au] Autor:Tsugawa S; Hervieux N; Kierzkowski D; Routier-Kierzkowska AL; Sapala A; Hamant O; Smith RS; Roeder AHK; Boudaoud A; Li CB
[Ad] Endereço:Theoretical Biology Laboratory, RIKEN, Wako 351-0198, Japan.
[Ti] Título:Clones of cells switch from reduction to enhancement of size variability in sepals.
[So] Source:Development;144(23):4398-4405, 2017 Dec 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Organs form with remarkably consistent sizes and shapes during development, whereas a high variability in growth is observed at the cell level. Given this contrast, it is unclear how such consistency in organ scale can emerge from cellular behavior. Here, we examine an intermediate scale, the growth of clones of cells in sepals. Each clone consists of the progeny of a single progenitor cell. At early stages, we find that clones derived from a small progenitor cell grow faster than those derived from a large progenitor cell. This results in a reduction in clone size variability, a phenomenon we refer to as size uniformization. By contrast, at later stages of clone growth, clones change their growth pattern to enhance size variability, when clones derived from larger progenitor cells grow faster than those derived from smaller progenitor cells. Finally, we find that, at early stages, fast growing clones exhibit greater cell growth heterogeneity. Thus, cellular variability in growth might contribute to a decrease in the variability of clones throughout the sepal.
[Mh] Termos MeSH primário: Arabidopsis/citologia
Arabidopsis/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Diferenciação Celular
Divisão Celular
Tamanho Celular
Células Clonais/citologia
Flores/citologia
Flores/crescimento & desenvolvimento
Modelos Biológicos
Desenvolvimento Vegetal/fisiologia
Células-Tronco/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[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:171130
[St] Status:MEDLINE
[do] DOI:10.1242/dev.153999


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[PMID]:29074950
[Au] Autor:Villacorta-Martin C; Craig AJ; Villanueva A
[Ad] Endereço:Liver Cancer Research Program, Division of Liver Diseases, Tisch Cancer Institute, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
[Ti] Título:Divergent evolutionary trajectories in transplanted tumor models.
[So] Source:Nat Genet;49(11):1565-1566, 2017 Oct 27.
[Is] ISSN:1546-1718
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human-derived tumor models are becoming popular in the context of personalized medicine, but a new study shows that these models could be less representative of primary tumors than previously thought, particularly when using late passages.
[Mh] Termos MeSH primário: Evolução Clonal
DNA de Neoplasias/imunologia
Xenoenxertos/imunologia
Hospedeiro Imunocomprometido
Neoplasias/imunologia
[Mh] Termos MeSH secundário: Animais
Células Clonais
Variações do Número de Cópias de DNA
DNA de Neoplasias/genética
Modelos Animais de Doenças
Xenoenxertos/patologia
Seres Humanos
Camundongos
Neoplasias/genética
Neoplasias/metabolismo
Neoplasias/patologia
Medicina de Precisão
Especificidade da Espécie
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Neoplasm)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171028
[St] Status:MEDLINE
[do] DOI:10.1038/ng.3983



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