Base de dados : MEDLINE
Pesquisa : D12.776.320 [Categoria DeCS]
Referências encontradas : 3160 [refinar]
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[PMID]:28740134
[Au] Autor:Zhang Y; Qin W; Lu X; Xu J; Huang H; Bai H; Li S; Lin S
[Ad] Endereço:Laboratory of Chemical Genomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen, 518055, China.
[Ti] Título:Programmable base editing of zebrafish genome using a modified CRISPR-Cas9 system.
[So] Source:Nat Commun;8(1):118, 2017 07 25.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Precise genetic modifications in model animals are essential for biomedical research. Here, we report a programmable "base editing" system to induce precise base conversion with high efficiency in zebrafish. Using cytidine deaminase fused to Cas9 nickase, up to 28% of site-specific single-base mutations are achieved in multiple gene loci. In addition, an engineered Cas9-VQR variant with 5'-NGA PAM specificities is used to induce base conversion in zebrafish. This shows that Cas9 variants can be used to expand the utility of this technology. Collectively, the targeted base editing system represents a strategy for precise and effective genome editing in zebrafish.The use of base editing enables precise genetic modifications in model animals. Here the authors show high efficient single-base editing in zebrafish using modified Cas9 and its VQR variant with an altered PAM specificity.
[Mh] Termos MeSH primário: Sistemas CRISPR-Cas/genética
Edição de Genes/métodos
Mutagênese Sítio-Dirigida/métodos
Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência de Bases
Proteínas Fetais/genética
Engenharia Genética/métodos
Fator 6 de Diferenciação de Crescimento/genética
Mutação Puntual
Reprodutibilidade dos Testes
Homologia de Sequência de Aminoácidos
Homologia de Sequência do Ácido Nucleico
Proteínas com Domínio T-Box/genética
Proteínas de Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Brachyury protein); 0 (Fetal Proteins); 0 (Growth Differentiation Factor 6); 0 (T-Box Domain Proteins); 0 (Zebrafish Proteins); 0 (gdf6a protein, zebrafish)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-00175-6


  2 / 3160 MEDLINE  
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[PMID]:28982779
[Au] Autor:Parisis N; Krasinska L; Harker B; Urbach S; Rossignol M; Camasses A; Dewar J; Morin N; Fisher D
[Ad] Endereço:IGMM, CNRS Univ. Montpellier, Montpellier, France.
[Ti] Título:Initiation of DNA replication requires actin dynamics and formin activity.
[So] Source:EMBO J;36(21):3212-3231, 2017 Nov 02.
[Is] ISSN:1460-2075
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nuclear actin regulates transcriptional programmes in a manner dependent on its levels and polymerisation state. This dynamics is determined by the balance of nucleocytoplasmic shuttling, formin- and redox-dependent filament polymerisation. Here, using egg extracts and human somatic cells, we show that actin dynamics and formins are essential for DNA replication. In proliferating cells, formin inhibition abolishes nuclear transport and initiation of DNA replication, as well as general transcription. In replicating nuclei from transcriptionally silent egg extracts, we identified numerous actin regulators, and disruption of actin dynamics abrogates nuclear transport, preventing NLS (nuclear localisation signal)-cargo release from RanGTP-importin complexes. Nuclear formin activity is further required to promote loading of cyclin-dependent kinase (CDK) and proliferating cell nuclear antigen (PCNA) onto chromatin, as well as initiation and elongation of DNA replication. Therefore, actin dynamics and formins control DNA replication by multiple direct and indirect mechanisms.
[Mh] Termos MeSH primário: Actinas/genética
Cromatina/metabolismo
Replicação do DNA
Proteínas Fetais/genética
Proteínas dos Microfilamentos/genética
Proteínas Nucleares/genética
Transcrição Genética
[Mh] Termos MeSH secundário: Actinas/metabolismo
Transporte Ativo do Núcleo Celular/genética
Animais
Linhagem Celular Tumoral
Núcleo Celular/metabolismo
Cromatina/química
Misturas Complexas/química
Citoplasma/metabolismo
Células Epiteliais/citologia
Células Epiteliais/metabolismo
Proteínas Fetais/metabolismo
Regulação da Expressão Gênica
Células HeLa
Seres Humanos
Carioferinas/genética
Carioferinas/metabolismo
Proteínas dos Microfilamentos/metabolismo
Sinais de Localização Nuclear
Proteínas Nucleares/metabolismo
Antígeno Nuclear de Célula em Proliferação/genética
Antígeno Nuclear de Célula em Proliferação/metabolismo
Transdução de Sinais
Xenopus laevis
Zigoto/química
Proteína ran de Ligação ao GTP/genética
Proteína ran de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Chromatin); 0 (Complex Mixtures); 0 (Fetal Proteins); 0 (Karyopherins); 0 (Microfilament Proteins); 0 (Nuclear Localization Signals); 0 (Nuclear Proteins); 0 (Proliferating Cell Nuclear Antigen); 147336-47-8 (formin 1); EC 3.6.5.2 (ran GTP-Binding Protein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE
[do] DOI:10.15252/embj.201796585


  3 / 3160 MEDLINE  
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[PMID]:28953967
[Au] Autor:Obeng-Adjei N; Portugal S; Holla P; Li S; Sohn H; Ambegaonkar A; Skinner J; Bowyer G; Doumbo OK; Traore B; Pierce SK; Crompton PD
[Ad] Endereço:Malaria Infection Biology and Immunity Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.
[Ti] Título:Malaria-induced interferon-γ drives the expansion of Tbethi atypical memory B cells.
[So] Source:PLoS Pathog;13(9):e1006576, 2017 Sep.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many chronic infections, including malaria and HIV, are associated with a large expansion of CD21-CD27- 'atypical' memory B cells (MBCs) that exhibit reduced B cell receptor (BCR) signaling and effector functions. Little is known about the conditions or transcriptional regulators driving atypical MBC differentiation. Here we show that atypical MBCs in malaria-exposed individuals highly express the transcription factor T-bet, and that T-bet expression correlates inversely with BCR signaling and skews toward IgG3 class switching. Moreover, a longitudinal analysis of a subset of children suggested a correlation between the incidence of febrile malaria and the expansion of T-bethi B cells. The Th1-cytokine containing supernatants of malaria-stimulated PBMCs plus BCR cross linking induced T-bet expression in naïve B cells that was abrogated by neutralizing IFN-γ or blocking the IFN-γ receptor on B cells. Accordingly, recombinant IFN-γ plus BCR cross-linking drove T-bet expression in peripheral and tonsillar B cells. Consistent with this, Th1-polarized Tfh (Tfh-1) cells more efficiently induced T-bet expression in naïve B cells. These data provide new insight into the mechanisms underlying atypical MBC differentiation.
[Mh] Termos MeSH primário: Linfócitos B/citologia
Linfócitos B/imunologia
Diferenciação Celular/imunologia
Regulação da Expressão Gênica/imunologia
Memória Imunológica/imunologia
Interferon gama/biossíntese
Malária/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Pré-Escolar
Feminino
Proteínas Fetais/metabolismo
Seres Humanos
Lactente
Malária/metabolismo
Masculino
Receptores de Antígenos de Linfócitos B/metabolismo
Proteínas com Domínio T-Box/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brachyury protein); 0 (Fetal Proteins); 0 (Receptors, Antigen, B-Cell); 0 (T-Box Domain Proteins); 82115-62-6 (Interferon-gamma)
[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:170928
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006576


  4 / 3160 MEDLINE  
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[PMID]:28928284
[Au] Autor:Reeves WM; Wu Y; Harder MJ; Veeman MT
[Ad] Endereço:Division of Biology, Kansas State University, Manhattan, KS 66506, USA.
[Ti] Título:Functional and evolutionary insights from the notochord transcriptome.
[So] Source:Development;144(18):3375-3387, 2017 09 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The notochord of the ascidian consists of only 40 cells, and is a longstanding model for studying organogenesis in a small, simple embryo. Here, we perform RNAseq on flow-sorted notochord cells from multiple stages to define a comprehensive notochord transcriptome. We identify 1364 genes with enriched expression and extensively validate the results by hybridization. These genes are highly enriched for Gene Ontology terms related to the extracellular matrix, cell adhesion and cytoskeleton. Orthologs of 112 of the notochord genes have known notochord expression in vertebrates, more than twice as many as predicted by chance alone. This set of putative effector genes with notochord expression conserved from tunicates to vertebrates will be invaluable for testing hypotheses about notochord evolution. The full set of notochord genes provides a foundation for systems-level studies of notochord gene regulation and morphogenesis. We find only modest overlap between this set of notochord-enriched transcripts and the genes upregulated by ectopic expression of the key notochord transcription factor Brachyury, indicating that Brachyury is not a notochord master regulator gene as strictly defined.
[Mh] Termos MeSH primário: Evolução Biológica
Ciona intestinalis/embriologia
Ciona intestinalis/genética
Notocorda/embriologia
Notocorda/metabolismo
Transcriptoma/genética
[Mh] Termos MeSH secundário: Animais
Citoesqueleto/genética
Embrião não Mamífero/metabolismo
Matriz Extracelular/metabolismo
Proteínas Fetais/genética
Proteínas Fetais/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Ontologia Genética
Hibridização In Situ
Camundongos
Reprodutibilidade dos Testes
Análise de Sequência de RNA
Proteínas com Domínio T-Box/genética
Proteínas com Domínio T-Box/metabolismo
Peixe-Zebra/embriologia
Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Brachyury protein); 0 (Fetal Proteins); 0 (T-Box Domain Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1242/dev.156174


  5 / 3160 MEDLINE  
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[PMID]:28826820
[Au] Autor:Koch F; Scholze M; Wittler L; Schifferl D; Sudheer S; Grote P; Timmermann B; Macura K; Herrmann BG
[Ad] Endereço:Department of Developmental Genetics, Max Planck Institute for Molecular Genetics, Ihnestr. 63-73, 14195 Berlin, Germany.
[Ti] Título:Antagonistic Activities of Sox2 and Brachyury Control the Fate Choice of Neuro-Mesodermal Progenitors.
[So] Source:Dev Cell;42(5):514-526.e7, 2017 Sep 11.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The spinal cord and mesodermal tissues of the trunk such as the vertebral column and skeletal musculature derive from neuro-mesodermal progenitors (NMPs). Sox2, Brachyury (T), and Tbx6 have been correlated with NMP potency and lineage choice; however, their exact role and interaction in these processes have not yet been revealed. Here we present a global analysis of NMPs and their descending lineages performed on purified cells from embryonic day 8.5 wild-type and mutant embryos. We show that T, cooperatively with WNT signaling, controls the progenitor state and the switch toward the mesodermal fate. Sox2 acts antagonistically and promotes neural development. T is also involved in remodeling the chromatin for mesodermal development. Tbx6 reinforces the mesodermal fate choice, represses the progenitor state, and confers paraxial fate commitment. Our findings refine previous models and establish molecular principles underlying mammalian trunk development, comprising NMP maintenance, lineage choice, and mesoderm formation.
[Mh] Termos MeSH primário: Linhagem da Célula/genética
Proteínas Fetais/metabolismo
Mesoderma/citologia
Neurônios/citologia
Fatores de Transcrição SOXB1/metabolismo
Células-Tronco/citologia
Proteínas com Domínio T-Box/metabolismo
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Cromatina/metabolismo
Montagem e Desmontagem da Cromatina/genética
Proteínas Fetais/genética
Perfilação da Expressão Gênica
Regulação da Expressão Gênica no Desenvolvimento
Camundongos
Modelos Biológicos
Neurônios/metabolismo
Fatores de Transcrição SOXB1/genética
Análise de Célula Única
Células-Tronco/metabolismo
Proteínas com Domínio T-Box/genética
Fatores de Transcrição/metabolismo
Via de Sinalização Wnt/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brachyury protein); 0 (Chromatin); 0 (Fetal Proteins); 0 (SOXB1 Transcription Factors); 0 (T-Box Domain Proteins); 0 (Tbx6 protein, mouse); 0 (Transcription Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE


  6 / 3160 MEDLINE  
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[PMID]:28807491
[Au] Autor:Ahmad SF; Ansari MA; Nadeem A; Bakheet SA; Almutairi MM; Attia SM
[Ad] Endereço:Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia. Electronic address: fashaikh@ksu.edu.sa.
[Ti] Título:Adenosine A2A receptor signaling affects IL-21/IL-22 cytokines and GATA3/T-bet transcription factor expression in CD4 T cells from a BTBR T Itpr3tf/J mouse model of autism.
[So] Source:J Neuroimmunol;311:59-67, 2017 Oct 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Autism is a complex heterogeneous neurodevelopmental disorder; previous studies have identified altered immune responses among individuals diagnosed with autism. An imbalance in the production of pro- and anti-inflammatory cytokines and transcription factors plays a role in neurodevelopmental behavioral and autism disorders. BTBR T Itpr3tf/J (BTBR) mice are used as a model for autism, as they exhibit social deficits, communication deficits, and repetitive behaviors compared with C57BL/6J (B6) mice. The adenosine A2A receptor (A2AR) appears to be a potential target for the improvement of behavioral, inflammatory, immune, and neurological disorders. We investigated the effects of the A2AR antagonist SCH 5826 (SCH) and agonist CGS 21680 (CGS) on IL-21, IL-22, T-bet, T-box transcription factor (T-bet), GATA3 (GATA Binding Protein 3), and CD152 (CTLA-4) expression in BTBR mice. Our results showed that BTBR mice treated with SCH had increased CD4 IL-21 , CD4 IL-22 , CD4 GATA3 , and CD4 T-bet and decreased CD4 CTLA-4 expression in spleen cells compared with BTBR control mice. Moreover, CGS efficiently decreased CD4 IL-21 , CD4 IL-22 , CD4 GATA3 , and CD4 T-bet and increased CD4 CTLA-4 production in spleen cells compared with SCH-treated and BTBR control mice. Additionally, SCH treatment significantly increased the mRNA and protein expression levels of IL-21, IL-22, GATA3, and T-bet in brain tissue compared with CGS-treated and BTBR control mice. The augmented levels of IL-21/IL-22 and GATA3/T-bet could be due to altered A2AR signaling. Our results indicate that A2AR agonists may represent a new class of compounds that can be developed for use in the treatment of autistic and neuroimmune dysfunctions.
[Mh] Termos MeSH primário: Transtorno Autístico/patologia
Linfócitos T CD4-Positivos/metabolismo
Citocinas/metabolismo
Fator de Transcrição GATA3/metabolismo
Receptor A2A de Adenosina/metabolismo
Transdução de Sinais/genética
[Mh] Termos MeSH secundário: Adenosina/análogos & derivados
Adenosina/farmacologia
Agonistas do Receptor A2 de Adenosina/farmacologia
Antagonistas do Receptor A2 de Adenosina/farmacologia
Animais
Transtorno Autístico/genética
Transtorno Autístico/imunologia
Encéfalo/metabolismo
Linfócitos T CD4-Positivos/efeitos dos fármacos
Modelos Animais de Doenças
Proteínas Fetais/genética
Proteínas Fetais/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Receptores de Inositol 1,4,5-Trifosfato/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Mutantes Neurológicos
Proteínas do Tecido Nervoso/deficiência
Proteínas do Tecido Nervoso/genética
Fenetilaminas/farmacologia
Pirimidinas/farmacologia
Transdução de Sinais/efeitos dos fármacos
Baço/patologia
Proteínas com Domínio T-Box/genética
Proteínas com Domínio T-Box/metabolismo
Triazóis/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-amino-7-(2-phenylethyl)-2-(2-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidine); 0 (Adenosine A2 Receptor Agonists); 0 (Adenosine A2 Receptor Antagonists); 0 (Brachyury protein); 0 (Cytokines); 0 (Disc1 protein, mouse); 0 (Fetal Proteins); 0 (GATA3 Transcription Factor); 0 (ITPR3 protein, mouse); 0 (Inositol 1,4,5-Trisphosphate Receptors); 0 (Nerve Tissue Proteins); 0 (Phenethylamines); 0 (Pyrimidines); 0 (Receptor, Adenosine A2A); 0 (T-Box Domain Proteins); 0 (Triazoles); 120225-54-9 (2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE


  7 / 3160 MEDLINE  
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[PMID]:28705897
[Au] Autor:Servetnick MD; Steinworth B; Babonis LS; Simmons D; Salinas-Saavedra M; Martindale MQ
[Ad] Endereço:Division of Biological Sciences, University of Washington Bothell, Bothell, WA 98011, USA mds56@uw.edu.
[Ti] Título:Cas9-mediated excision of disrupts endoderm development, pharynx formation and oral-aboral patterning.
[So] Source:Development;144(16):2951-2960, 2017 08 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The mesoderm is a key novelty in animal evolution, although we understand little of how the mesoderm arose. , the founding member of the T-box gene family, is a key gene in chordate mesoderm development. However, the gene was present in the common ancestor of fungi and animals long before mesoderm appeared. To explore ancestral roles of prior to the evolution of definitive mesoderm, we excised the gene using CRISPR/Cas9 in the diploblastic cnidarian is normally expressed in precursors of the pharynx, which separates endoderm from ectoderm. In knockout embryos, the pharynx does not form, embryos fail to elongate, and endoderm organization, ectodermal cell polarity and patterning along the oral-aboral axis are disrupted. Expression of many genes both inside and outside the expression domain is affected, including downregulation of Wnt genes at the oral pole. Our results point to an ancient role for in morphogenesis, cell polarity and the patterning of both ectodermal and endodermal derivatives along the primary body axis.
[Mh] Termos MeSH primário: Endoderma/embriologia
Faringe/embriologia
Anêmonas-do-Mar/embriologia
Anêmonas-do-Mar/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas Fetais/genética
Proteínas Fetais/metabolismo
Imuno-Histoquímica
Hibridização In Situ
RNA Guia/metabolismo
Proteínas com Domínio T-Box/genética
Proteínas com Domínio T-Box/metabolismo
Proteínas Wnt/genética
Proteínas Wnt/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Brachyury protein); 0 (Fetal Proteins); 0 (RNA, Guide); 0 (T-Box Domain Proteins); 0 (Wnt Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1242/dev.145839


  8 / 3160 MEDLINE  
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[PMID]:28621227
[Au] Autor:Lee KH; Kim EY; Park YL; Do SI; Chae SW; Park CH
[Ad] Endereço:1 Department of Surgery, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea.
[Ti] Título:Expression of epithelial-mesenchymal transition driver brachyury and status of tumor-infiltrating CD8+ and FOXP3+ lymphocytes in predicting treatment responses to neoadjuvant chemotherapy of breast cancer.
[So] Source:Tumour Biol;39(6):1010428317710575, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brachyury has been characterized as a driver of epithelial-mesenchymal transition process which is regarded as an important mechanism of cancer cell invasion and metastatic progression. The status of tumor-infiltrating lymphocytes has been proposed to predict response to neoadjuvant chemotherapy in breast cancer. We investigated the clinical significance and value of tumor-infiltrating lymphocytes and brachyury as biomarkers to predict treatment responses to neoadjuvant chemotherapy in breast cancer. We also examined the correlation of the Neo-Bioscore with tumor-infiltrating lymphocytes and brachyury to indirectly predict long-term outcome. This retrospective study included a series of 44 consecutive patients treated between January 2011 and December 2015. All patient samples were obtained using core needle biopsy before neoadjuvant chemotherapy. The relationship of expression of Brachyury and tumor-infiltrating lymphocyte subsets (CD8+, forkhead box protein 3 tumor-infiltrating lymphocytes) with clinicopathological factors was assessed to identify its predictive role with respect to tumor response to neoadjuvant chemotherapy and the outcome. Of 44 patients, 6 showed no response, 31 had partial response, and 7 demonstrated pathological complete response. Forkhead box protein 3 was significantly higher in the response group than in the no response group (no response = 2.6, partial response = 7.0, complete response = 9.7, p = 0.020). Brachyury expression was inversely associated with response to neoadjuvant chemotherapy, but the difference was not statistically significant ( p = 0.62). We also observed a significant association between forkhead box protein 3 ( p = 0.001) and the Neo-Bioscore, while only a marginal difference was observed with CD8+ expression ( p = 0.074). This study demonstrated that forkhead box protein 3 expression has value as the only independent marker that predicts a good response to neoadjuvant chemotherapy and that it is related with a good prognosis according to the Neo-Bioscore. Brachyury was significantly associated with estrogen receptor positive and human epidermal growth factor receptor 2 negative status; further study would be needed to clarify how it affects treatment prognosis.
[Mh] Termos MeSH primário: Neoplasias da Mama/tratamento farmacológico
Linfócitos T CD8-Positivos/metabolismo
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Proteínas Fetais/biossíntese
Fatores de Transcrição Forkhead/genética
Proteínas com Domínio T-Box/biossíntese
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores Tumorais/genética
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Feminino
Proteínas Fetais/genética
Seres Humanos
Linfócitos do Interstício Tumoral/metabolismo
Linfócitos do Interstício Tumoral/patologia
Meia-Idade
Terapia Neoadjuvante
Prognóstico
Receptor ErbB-2/genética
Proteínas com Domínio T-Box/genética
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Brachyury protein); 0 (FOXP3 protein, human); 0 (Fetal Proteins); 0 (Forkhead Transcription Factors); 0 (T-Box Domain Proteins); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170622
[Lr] Data última revisão:
170622
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317710575


  9 / 3160 MEDLINE  
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[PMID]:28527698
[Au] Autor:Dutta P; Das S; Maiti S
[Ad] Endereço:Department of Biological Sciences, Indian Institute of Science Education and Research, Kolkata, India; Department of Biology, Indian Institute of Science Education and Research, Pune, India.
[Ti] Título:Non diaphanous formin delphilin acts as a barbed end capping protein.
[So] Source:Exp Cell Res;357(2):163-169, 2017 Aug 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Formins are multi domain proteins present ubiquitously in all eukaryotes from lower fungi to higher vertebrates. Formins are characterized by the presence of formin homology domain-2 (FH2) and formin homology domain-1 (FH1). There are fifteen different formins present in mouse and human. Among these metazoan formins, Delphilin is a unique formin having two PDZ domains at the N-terminus and FH1, FH2 domain at the C-terminus respectively. In this study we observed that Delphilin binds to actin filaments, and Delphilin inhibits actin filament elongation like barbed end capping protein CapZ. In vitro, Delphilin stabilized actin filaments by inhibiting actin filament depolymerisation. Therefore, our study demonstrates Delphilin as an actin-filament capping protein.
[Mh] Termos MeSH primário: Citoesqueleto de Actina/metabolismo
Actinas/metabolismo
Proteínas Fetais/metabolismo
Proteínas dos Microfilamentos/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Proteínas Nucleares/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteína de Capeamento de Actina CapZ/metabolismo
Seres Humanos
Camundongos
Estrutura Terciária de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (CAPZA1 protein, human); 0 (CapZ Actin Capping Protein); 0 (Capza1 protein, mouse); 0 (Fetal Proteins); 0 (Microfilament Proteins); 0 (Nerve Tissue Proteins); 0 (Nuclear Proteins); 0 (delphilin); 147336-47-8 (formin 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170522
[St] Status:MEDLINE


  10 / 3160 MEDLINE  
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[PMID]:28432450
[Au] Autor:Kitamura Y; Sasaki H; Yoshida K
[Ad] Endereço:Department of Neurosurgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan. ykita@sc4.so-net.ne.jp.
[Ti] Título:Genetic aberrations and molecular biology of skull base chordoma and chondrosarcoma.
[So] Source:Brain Tumor Pathol;34(2):78-90, 2017 Apr.
[Is] ISSN:1861-387X
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Chordomas and chondrosarcomas are two major malignant bone neoplasms located at the skull base. These tumors are rarely metastatic, but can be locally invasive and resistant to conventional chemotherapies and radiotherapies. Accordingly, therapeutic approaches for the treatment of these tumors can be difficult. Additionally, their location at the skull base makes them problematic. Although accurate diagnosis of these tumors is important because of their distinct prognoses, distinguishing between these tumor types is difficult due to overlapping radiological and histopathological findings. However, recent accumulation of molecular and genetic studies, including extracranial location analysis, has provided us clues for accurate diagnosis. In this report, we review the genetic aberrations and molecular biology of these two tumor types. Among the abundant genetic features of these tumors, brachyury immunohistochemistry and direct sequencing of IDH1/2 are simple and useful techniques that can be used to distinguish between these tumors. Although it is still unclear why these tumors, which have such distinct genetic backgrounds, show similar histopathological findings, comparison of their genetic backgrounds could provide essential information.
[Mh] Termos MeSH primário: Condrossarcoma/genética
Cordoma/genética
Isocitrato Desidrogenase/genética
Mutação
Neoplasias da Base do Crânio/genética
[Mh] Termos MeSH secundário: Antígeno B7-H1
Condrossarcoma/diagnóstico
Condrossarcoma/imunologia
Condrossarcoma/terapia
Cordoma/diagnóstico por imagem
Cordoma/imunologia
Cordoma/terapia
Diagnóstico Diferencial
Proteínas Fetais/genética
Seres Humanos
Imuno-Histoquímica
Terapia de Alvo Molecular
Proteína 2 Ligante de Morte Celular Programada 1
Análise de Sequência de DNA
Neoplasias da Base do Crânio/diagnóstico
Neoplasias da Base do Crânio/imunologia
Neoplasias da Base do Crânio/terapia
Proteínas com Domínio T-Box/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (B7-H1 Antigen); 0 (Brachyury protein); 0 (CD274 protein, human); 0 (Fetal Proteins); 0 (PDCD1LG2 protein, human); 0 (Programmed Cell Death 1 Ligand 2 Protein); 0 (T-Box Domain Proteins); EC 1.1.1.41 (Isocitrate Dehydrogenase); EC 1.1.1.41 (isocitrate dehydrogenase 2, human); EC 1.1.1.42. (IDH1 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170423
[St] Status:MEDLINE
[do] DOI:10.1007/s10014-017-0283-y



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