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[PMID]:28469098
[Au] Autor:Fang XJ; Yu M; Wu Y; Zhang ZH; Wang WW; Wang ZX; Yuan Y
[Ad] Endereço:Department of Neurology, Peking University First Hospital, Beijing 100034, China.
[Ti] Título:Study of Enhanced Depth Imaging Optical Coherence Tomography in Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy.
[So] Source:Chin Med J (Engl);130(9):1042-1048, 2017 May 05.
[Is] ISSN:0366-6999
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary small artery disease caused by NOTCH3 gene mutation. We performed enhanced depth imaging optical coherence tomography (EDI-OCT) to evaluate the retinal vessel changes in CADASIL patients and assessed their consonance with brain magnetic resonance imaging (MRI) findings. METHODS: Of 27 genetically confirmed patients and an equal number of controls were recruited at the Peking University First Hospital from January 2015 to August 2016. All patients underwent 7T-MRI of the brain. Fazekas score, number of small infarcts and microbleeds were evaluated. All patients and controls underwent EDI-OCT to measure subfoveal choroidal thickness (SFCT), inner and outer diameters as well as arterial and venous wall thickness, and arterial venous ratio of the inner (AVRin) and outer diameters (AVRout). The relation between retinal vessel changes and Fazekas scores, numbers of small infarcts, or microbleeds was analyzed. Paired t-test was used to compare the SFCT and retinal vessel measurement data between patients and controls. Spearman's correlation was used to investigate the correlation between retinal vessel changes and MRI lesions. RESULTS: In CADASIL patients, mean SFCT (268.37 ± 46.50 µm) and mean arterial inner diameter (93.46 ± 9.70 µm) were significantly lower than that in controls (P < 0.001,P = 0.048, respectively). Mean arterial outer diameter (131.74 ± 10.87 µm), venous inner (128.99 ± 13.62 µm) and outer diameter (164.82 ± 14.77 µm), and mean arterial (19.13 ± 1.85 µm) and venous (17.91 ± 2.76 µm) wall thickness were significantly higher than that in controls (P = 0.023,P = 0.004,P < 0.001,P < 0.001, respectively). Arterial inner diameter (rs= -0.39, P= 0.044), AVRin (rs= -0.65,P < 0.001), and AVRout (rs= -0.56, P= 0.002) showed a negative correlation with the number of small infarcts. Venous inner diameter (rs = 0.46, P= 0.016) showed a positive correlation with the number of small infarcts. Venous inner diameter (rs = 0.59, P= 0.002), outer diameter (rs = 0.47, P= 0.017), showed a positive correlation with the number of cerebral microbleeds (CMBs). AVRin (rs= -0.52, P= 0.007) and AVRout (rs= -0.40, P= 0.048) showed a negative correlation with the number of CMBs. CONCLUSIONS: Measurement of retinal vessels using EDI-OCT correlates moderately well with MRI parameters. EDI-OCT might be a useful evaluation tool for CADASIL patients.
[Mh] Termos MeSH primário: Leucoencefalopatias/patologia
Imagem por Ressonância Magnética/métodos
Tomografia de Coerência Óptica/métodos
[Mh] Termos MeSH secundário: Adulto
Encéfalo/metabolismo
CADASIL
Infarto Cerebral/patologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Mutação
Receptor Notch3/genética
Vasos Retinianos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptor, Notch3)
[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:10.4103/0366-6999.204935


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[PMID]:29194448
[Au] Autor:Nagata Y; Kiyono T; Okamura K; Goto YI; Matsuo M; Ikemoto-Uezumi M; Hashimoto N
[Ad] Endereço:Department of Regenerative Medicine, National Center for Geriatrics and Gerontology, Morioka, Oobu, Aichi, Japan.
[Ti] Título:Interleukin-1beta (IL-1ß)-induced Notch ligand Jagged1 suppresses mitogenic action of IL-1ß on human dystrophic myogenic cells.
[So] Source:PLoS One;12(12):e0188821, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Duchenne muscular dystrophy (DMD) is a severe X-linked recessive muscle disorder caused by mutations in the dystrophin gene. Nonetheless, secondary processes involving perturbation of muscle regeneration probably exacerbate disease progression, resulting in the fatal loss of muscle in DMD patients. A dysfunction of undifferentiated myogenic cells is the most likely cause for the reduction of regenerative capacity of muscle. To clarify molecular mechanisms in perturbation of the regenerative capacity of DMD muscle, we have established several NCAM (CD56)-positive immortalized human dystrophic and non-dystrophic myogenic cell lines from DMD and healthy muscles. A pro-inflammatory cytokine, IL-1ß, promoted cell cycle progression of non-dystrophic myogenic cells but not DMD myogenic cells. In contrast, IL-1ß upregulated the Notch ligand Jagged1 gene in DMD myogenic cells but not in non-dystrophic myogenic cells. Knockdown of Jagged1 in DMD myogenic cells restored the IL-1ß-promoted cell cycle progression. Conversely, enforced expression of Jagged1-blocked IL-1ß promoted proliferation of non-dystrophic myogenic cells. In addition, IL-1ß prevented myogenic differentiation of DMD myogenic cells depending on Jagged1 but not of non-dystrophic myogenic cells. These results demonstrate that Jagged1 induced by IL-1ß in DMD myogenic cells modified the action of IL-1ß and reduced the ability to proliferate and differentiate. IL-1ß induced Jagged1 gene expression may be a feedback response to excess stimulation with this cytokine because high IL-1ß (200-1000 pg/ml) induced Jagged1 gene expression even in non-dystrophic myogenic cells. DMD myogenic cells are likely to acquire the susceptibility of the Jagged1 gene to IL-1ß under the microcircumstances in DMD muscles. The present results suggest that Jagged1 induced by IL-1ß plays a crucial role in the loss of muscle regeneration capacity of DMD muscles. The IL-1ß/Jagged1 pathway may be a new therapeutic target to ameliorate exacerbation of muscular dystrophy in a dystrophin-independent manner.
[Mh] Termos MeSH primário: Interleucina-1beta/metabolismo
Proteína Jagged-1/metabolismo
Distrofia Muscular de Duchenne/metabolismo
Receptor Notch3/metabolismo
[Mh] Termos MeSH secundário: Diferenciação Celular
Células Cultivadas
Seres Humanos
Desenvolvimento Muscular
Distrofia Muscular de Duchenne/patologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Jagged-1 Protein); 0 (NOTCH3 protein, human); 0 (Receptor, Notch3)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188821


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[PMID]:29023469
[Au] Autor:Choi SH; Severson E; Pear WS; Liu XS; Aster JC; Blacklow SC
[Ad] Endereço:Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, United States of America.
[Ti] Título:The common oncogenomic program of NOTCH1 and NOTCH3 signaling in T-cell acute lymphoblastic leukemia.
[So] Source:PLoS One;12(10):e0185762, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Notch is a major oncogenic driver in T cell acute lymphoblastic leukemia (T-ALL), in part because it binds to an enhancer that increases expression of MYC. Here, we exploit the capacity of activated NOTCH1 and NOTCH3 to induce T-ALL, despite substantial divergence in their intracellular regions, as a means to elucidate a broad, common Notch-dependent oncogenomic program through systematic comparison of the transcriptomes and Notch-bound genomic regulatory elements of NOTCH1- and NOTCH3-dependent T-ALL cells. ChIP-seq studies show a high concordance of functional NOTCH1 and NOTCH3 genomic binding sites that are enriched in binding motifs for RBPJ, the transcription factor that recruits activated Notch to DNA. The interchangeability of NOTCH1 and NOTCH3 was confirmed by rescue of NOTCH1-dependent T-ALL cells with activated NOTCH3 and vice versa. Despite remarkable overall similarity, there are nuanced differences in chromatin landscapes near critical common Notch target genes, most notably at a Notch-dependent enhancer that regulates MYC, which correlates with responsiveness to Notch pathway inhibitors. Overall, a common oncogenomic program driven by binding of either Notch is sufficient to maintain T-ALL cell growth, whereas cell-context specific differences appear to influence the response of T-ALL cells to Notch inhibition.
[Mh] Termos MeSH primário: Leucemia-Linfoma Linfoblástico de Células T Precursoras/metabolismo
Receptor Notch1/metabolismo
Receptor Notch3/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Regulação Leucêmica da Expressão Gênica
Seres Humanos
Proteína de Ligação a Sequências Sinal de Recombinação J de Imunoglobina/biossíntese
Proteína de Ligação a Sequências Sinal de Recombinação J de Imunoglobina/genética
Leucemia-Linfoma Linfoblástico de Células T Precursoras/genética
Proteínas Proto-Oncogênicas c-myc/biossíntese
Proteínas Proto-Oncogênicas c-myc/genética
Receptor Notch1/genética
Receptor Notch3/genética
Elementos de Resposta
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulin J Recombination Signal Sequence-Binding Protein); 0 (MYC protein, human); 0 (NOTCH1 protein, human); 0 (NOTCH3 protein, human); 0 (Proto-Oncogene Proteins c-myc); 0 (RBPJ protein, human); 0 (Receptor, Notch1); 0 (Receptor, Notch3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171022
[Lr] Data última revisão:
171022
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185762


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[PMID]:28968839
[Au] Autor:Xie K; Ye Y; Zeng Y; Gu J; Yang H; Wu X
[Ad] Endereço:Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
[Ti] Título:Polymorphisms in genes related to epithelial-mesenchymal transition and risk of non-small cell lung cancer.
[So] Source:Carcinogenesis;38(10):1029-1035, 2017 Oct 01.
[Is] ISSN:1460-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The epithelial-mesenchymal transition (EMT) process is a crucial step for tumor invasion and metastasis. Previous research investigating EMT has mostly focused on its role in cancer progression. Recent studies showed that EMT and EMT-driving transcription factor (EMT-TF) expression are early events in lung cancer pathogenesis, implying a potential association between EMT and lung cancer risk. In this study, we examined whether genetic variants in EMT-related genes are associated with risk of non-small cell lung cancer (NSCLC). We used data from a genome-wide association study of 1482 NSCLC cases and 1544 healthy controls as the discovery phase, in which we analyzed 1602 single-nucleotide polymorphisms (SNPs) within 159 EMT-related genes. We then validated the significant SNPs in another 5699 cases and 5815 controls from the National Cancer Institute lung cancer genome-wide association study. Cumulative effects were evaluated for validated SNPs, and a gene-based test was performed to explore gene-level association with disease risk. In the discovery phase, 174 SNPs demonstrated significant associations with NSCLC risk. In the validation phase, seven SNPs mapped to EGFR, NOTCH3, ADGRF1 and SMAD3 were confirmed. Cumulative effect analysis of the significant SNPs demonstrated increasing risk with the number of unfavorable genotypes in the discovery and validation datasets. Gene-based analysis implicated ADGRF1, NOTCH3 and CDH1 as significant for NSCLC risk. Functional prediction revealed several potential mechanisms underlying these associations. Our results suggest that EMT-related gene variants may be involved in susceptibility to NSCLC; if confirmed, they might help identify higher-risk individuals.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/genética
Transição Epitelial-Mesenquimal/genética
Neoplasias Pulmonares/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Caderinas/genética
Estudos de Casos e Controles
Simulação por Computador
Feminino
Regulação Neoplásica da Expressão Gênica
Predisposição Genética para Doença
Seres Humanos
Masculino
Meia-Idade
Proteínas Oncogênicas/genética
Receptor do Fator de Crescimento Epidérmico/genética
Receptor Notch3/genética
Receptores Acoplados a Proteínas-G/genética
Proteína Smad3/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDH1 protein, human); 0 (Cadherins); 0 (GPR110 protein, human); 0 (NOTCH3 protein, human); 0 (Oncogene Proteins); 0 (Receptor, Notch3); 0 (Receptors, G-Protein-Coupled); 0 (SMAD3 protein, human); 0 (Smad3 Protein); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171003
[St] Status:MEDLINE
[do] DOI:10.1093/carcin/bgx079


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[PMID]:28889086
[Au] Autor:Inder S; O'Rourke S; McDermott N; Manecksha R; Finn S; Lynch T; Marignol L
[Ad] Endereço:Translational Radiobiology and Molecular Oncology, Applied Radiation Therapy Trinity, Trinity College Dublin, Dublin, Ireland; Department of Urology, St James's Hospital, Dublin, Ireland.
[Ti] Título:The Notch-3 receptor: A molecular switch to tumorigenesis?
[So] Source:Cancer Treat Rev;60:69-76, 2017 Nov.
[Is] ISSN:1532-1967
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The Notch pathway is a highly conserved pathway increasingly implicated with the progression of human cancers. Of the four existing receptors associated with the pathway, the deregulation in the expression of the Notch-3 receptor is associated with more aggressive disease and poor prognosis. Selective targeting of this receptor has the potential to enhance current anti-cancer treatments. Molecular profiling strategies are increasingly incorporated into clinical decision making. This review aims to evaluate the clinical potential of Notch-3 within this new era of personalised medicine.
[Mh] Termos MeSH primário: Carcinogênese
Neoplasias/metabolismo
Receptor Notch3/metabolismo
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/metabolismo
Transformação Celular Neoplásica
Progressão da Doença
Seres Humanos
Neoplasias/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Receptor, Notch3)
[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:170911
[St] Status:MEDLINE


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[PMID]:28775167
[Au] Autor:Chan CHT; Munusamy P; Loke SY; Koh GL; Wong ESY; Law HY; Yoon CS; Tan MH; Yap YS; Ang P; Lee ASG
[Ad] Endereço:Division of Medical Sciences, Humphrey Oei Institute of Cancer Research, National Cancer Centre, Singapore.
[Ti] Título:Identification of Novel Breast Cancer Risk Loci.
[So] Source:Cancer Res;77(19):5428-5437, 2017 Oct 01.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It has been estimated that >1,000 genetic loci have yet to be identified for breast cancer risk. Here we report the first study utilizing targeted next-generation sequencing to identify single-nucleotide polymorphisms (SNP) associated with breast cancer risk. Targeted sequencing of 283 genes was performed in 240 women with early-onset breast cancer (≤40 years) or a family history of breast and/or ovarian cancer. Common coding variants with minor allele frequencies (MAF) >1% that were identified were presumed initially to be SNPs, but further database inspections revealed variants had MAF of ≤1% in the general population. Through prioritization and stringent selection criteria, we selected 24 SNPs for further genotyping in 1,516 breast cancer cases and 1,189 noncancer controls. Overall, we identified the SNP rs56118985 to be significantly associated with overall breast cancer risk. Subtype analysis performed for patient subgroups defined by ER, PR, and HER2 status suggested additional associations of the SNP rs200504060 and the SNP rs142179458 with breast cancer risk. analysis indicated that coding amino acids encoded at these three SNP sites were conserved evolutionarily and associated with decreased protein stability, suggesting a likely impact on protein function. Our results offer proof of concept for identifying novel cancer risk loci from next-generation sequencing data, with iterative data analysis from targeted, whole-exome, or whole-genome sequencing a wellspring to identify new SNPs associated with cancer risk. .
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Neoplasias da Mama/genética
Carcinoma Ductal de Mama/genética
Carcinoma Lobular/genética
Loci Gênicos
Polimorfismo de Nucleotídeo Único/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais/metabolismo
Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Carcinoma Ductal de Mama/metabolismo
Carcinoma Ductal de Mama/patologia
Carcinoma Lobular/metabolismo
Carcinoma Lobular/patologia
Estudos de Casos e Controles
Feminino
Seguimentos
Predisposição Genética para Doença
Genótipo
Sequenciamento de Nucleotídeos em Larga Escala/métodos
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/química
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Janus Quinase 2/química
Janus Quinase 2/genética
Janus Quinase 2/metabolismo
Meia-Idade
Gradação de Tumores
Estadiamento de Neoplasias
Prognóstico
Conformação Proteica
Estabilidade Proteica
Receptor ErbB-2/metabolismo
Receptor Notch3/química
Receptor Notch3/genética
Receptor Notch3/metabolismo
Receptores Estrogênicos/metabolismo
Receptores de Progesterona/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (NOTCH3 protein, human); 0 (Receptor, Notch3); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2); EC 2.7.10.2 (JAK2 protein, human); EC 2.7.10.2 (Janus Kinase 2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170805
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-17-0992


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[PMID]:28698285
[Au] Autor:Machuca-Parra AI; Bigger-Allen AA; Sanchez AV; Boutabla A; Cardona-Vélez J; Amarnani D; Saint-Geniez M; Siebel CW; Kim LA; D'Amore PA; Arboleda-Velasquez JF
[Ad] Endereço:Schepens Eye Research Institute of Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA.
[Ti] Título:Therapeutic antibody targeting of Notch3 signaling prevents mural cell loss in CADASIL.
[So] Source:J Exp Med;214(8):2271-2282, 2017 Aug 07.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a neurological syndrome characterized by small vessel disease (SVD), stroke, and vascular cognitive impairment and dementia caused by mutations in No therapies are available for this condition. Loss of mural cells, which encompass pericytes and vascular smooth muscle cells, is a hallmark of CADASIL and other SVDs, including diabetic retinopathy, resulting in vascular instability. Here, we showed that Notch3 signaling is both necessary and sufficient to support mural cell coverage in arteries using genetic rescue in Notch3 knockout mice. Furthermore, we show that systemic administration of an agonist Notch3 antibody prevents mural cell loss and modifies plasma proteins associated with Notch3 activity, including endostatin/collagen 18α1 and Notch3 extracellular domain in mice with the C455R mutation, a CADASIL variant associated with Notch3 loss of function. These findings open opportunities for the treatment of CADASIL and other SVDs by modulating Notch3 signaling.
[Mh] Termos MeSH primário: Anticorpos/uso terapêutico
CADASIL/terapia
Receptor Notch3/fisiologia
[Mh] Termos MeSH secundário: Animais
Anticorpos/imunologia
Modelos Animais de Doenças
Feminino
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Músculo Liso Vascular/citologia
Músculo Liso Vascular/fisiopatologia
Pericitos/fisiologia
Receptor Notch3/imunologia
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Notch3 protein, mouse); 0 (Receptor, Notch3)
[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:170713
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20161715


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[PMID]:28625320
[Au] Autor:Xue S; He L; Zhang X; Zhou J; Li F; Wang X
[Ad] Endereço:Department of Dermatology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
[Ti] Título:Expression of Jagged1/Notch3 Signaling Pathway and their Relationship with the Tumor Angiogenesis in TNBC.
[So] Source:Arch Med Res;48(2):169-179, 2017 Feb.
[Is] ISSN:1873-5487
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: Jagged1/Notch3 signaling pathway plays a key role in angiogenesis of breast cancer, but little is known in TNBC. This study was designed to investigate the expression of Jagged1/Notch3 mRNA and protein in TNBC, analyze their correlations with clinicopathological characteristics and prognosis. Moreover, the interrelationship among Jagged1/Notch3 and VEGF was initially evaluated. METHODS: Jagged1/Notch3 mRNA and protein expression levels were determined by Q-RT-PCR and Western blotting. Additionally, Immunohistochemistry for Jagged1/Notch3 was detected by Ventana platform, VEGF and CD34 was performed using the EnVision/HRP technique. RESULTS: mRNA transcriptionof Jagged1/Notch3 was in accord with protein expression. TNBC patients with positive Jagged1 expression had poorer DFS (p = 0.008) and OS (p = 0.004). Jagged1 expression was independent predictors of OS (p = 0.038). The expression of VEGF was positively correlative to MVD (p = 0.018), MVD was significantly associated with Jagged1 (p <0.0001) and Notch3 (p <0.0001). The expression of Jagged1/Notch3 has no correlation with VEGF, only in positive VEGF expression of TNBC patients Jagged1/Notch3 had influence on DFS and OS (p <0.05). CONCLUSION: Jagged1/Notch3 was -expressed at both the mRNA and protein levels, Jagged1 served as an independent predictor of poor prognosis. We speculate that there is a cross-talk between Jagged1/Notch3 and VEGF in TNBC angiogenesis. Jagged1/Notch3 is expected to be an important signaling pathway for TNBC progression and a potential target for TNBC neovascularization therapy.
[Mh] Termos MeSH primário: Proteína Jagged-1/metabolismo
Neovascularização Patológica/metabolismo
Receptor Notch3/metabolismo
Neoplasias de Mama Triplo Negativas/metabolismo
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Proteína Jagged-1/genética
Neovascularização Patológica/genética
Prognóstico
RNA Mensageiro/metabolismo
Transdução de Sinais
Neoplasias de Mama Triplo Negativas/irrigação sanguínea
Neoplasias de Mama Triplo Negativas/diagnóstico
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Jagged-1 Protein); 0 (RNA, Messenger); 0 (Receptor, Notch3); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE


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[PMID]:28476798
[Au] Autor:Strati TM; Kotoula V; Kostopoulos I; Manousou K; Papadimitriou C; Lazaridis G; Lakis S; Pentheroudakis G; Pectasides D; Pazarli E; Christodoulou C; Razis E; Pavlakis K; Magkou C; Chrisafi S; Aravantinos G; Bafaloukos D; Papakostas P; Gogas H; Kalogeras KT; Fountzilas G
[Ad] Endereço:Third Department of Surgery, AHEPA University Hospital, Aristotle University of Thessaloniki, School of Health Sciences, Faculty of Medicine, Thessaloniki, Greece Titika_marina_strati@mail.com.
[Ti] Título:Prognostic Subcellular Notch2, Notch3 and Jagged1 Localization Patterns in Early Triple-negative Breast Cancer.
[So] Source:Anticancer Res;37(5):2323-2334, 2017 05.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The Notch pathway has been implicated in triple-negative breast cancer (TNBC). Herein, we studied the subcellular localization of the less investigated Notch2 and Notch3 and that of the Jagged1 (Jag1) ligand in patients with operable TNBC. PATIENTS AND METHODS: We applied immunohistochemistry for Notch2, Notch3 and Jag1 in 333 tumors from TNBC patients treated with adjuvant anthracycline-based chemotherapy. We evaluated cytoplasmic (c), membranous (m) and nuclear (n) protein localization. RESULTS: c-Notch2 (35% positive tumors), c-Notch3 (63%), c-Jag1 (43%), m-Notch3 (23%) and n-Jag1 (17%) were analyzed individually and by using hierarchical clustering for prognostic evaluation. Upon multivariate analysis, compared to high m-Notch3 in the absence of n-Jag1 (cluster 4), all other marker combinations (clusters 1, 2, 3) conferred significantly higher risk for relapse (p<0.05). CONCLUSION: Specific Notch3 and Jag1 subcellular localization patterns may provide clues for the behavior of the tumors and potentially for Jag1 targeting in TNBC patients.
[Mh] Termos MeSH primário: Proteína Jagged-1/metabolismo
Receptor Notch2/metabolismo
Receptor Notch3/metabolismo
Neoplasias de Mama Triplo Negativas/metabolismo
[Mh] Termos MeSH secundário: Antraciclinas/uso terapêutico
Antineoplásicos/uso terapêutico
Membrana Celular/metabolismo
Núcleo Celular/metabolismo
Citoplasma/metabolismo
Feminino
Seres Humanos
Meia-Idade
Prognóstico
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracyclines); 0 (Antineoplastic Agents); 0 (JAG1 protein, human); 0 (Jagged-1 Protein); 0 (NOTCH2 protein, human); 0 (NOTCH3 protein, human); 0 (Receptor, Notch2); 0 (Receptor, Notch3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170810
[Lr] Data última revisão:
170810
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE


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[PMID]:28341077
[Au] Autor:You J; Liao S; Zhang F; Ma Z; Li G
[Ad] Endereço:Department of Neurology, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, People's Republic of China. Electronic address: youjs73@163.com.
[Ti] Título:First Report of Arg587Cys Mutation of Notch3 Gene in Two Chinese Families with CADASIL.
[So] Source:J Stroke Cerebrovasc Dis;26(1):e1-e4, 2017 Jan.
[Is] ISSN:1532-8511
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To explore Notch3 mutation sites of Chinese patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). METHODS: Direct sequencing of all exons in Notch3 gene was performed on 12 unrelated suspected CADASIL cases from mainland China. RESULT: A missense p.Arg587Cys (1759C>T) mutation in exon 11 was identified in 2 patients through genetic analysis. CONCLUSION: Chinese patients with CADASIL of R587C mutation in exon 11 was firstly reported.
[Mh] Termos MeSH primário: CADASIL/genética
Mutação de Sentido Incorreto
Receptor Notch3/genética
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático/genética
Encéfalo/diagnóstico por imagem
CADASIL/diagnóstico por imagem
China
Éxons
Família
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NOTCH3 protein, human); 0 (Receptor, Notch3)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170326
[St] Status:MEDLINE



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