INT86370
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Our findings indicate that TP plant extract inhibits signaling pathways involved in regulating the E-cadherin/catenin complex and possibly other cell-cell adhesion genes via beta-catenin alteration, suggesting that this plant extract has therapeutic promise in the treatment of human metastatic prostate cancer. | |||||||||||||||
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Moreover, experiments were performed in order to evaluate whether COX-2 pharmacological inhibition may affect beta-catenin/E-cadherin signalling pathway. | |||||||||||||||
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Expression of several transcriptional repressors has been shown to down-regulate CDH1 transcription [3]. | |||||||||||||||
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The alterations of E-cadherin, p16, and HER2/neu seem to affect the progression from EIC to serous carcinoma [10]. | |||||||||||||||
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E-cadherin immunoreactivity was weakly present in their cytoplasm and beta-catenin was negative. | |||||||||||||||
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EMT can be induced by a variety of molecules characterized by one common activity which is the down-regulation of E-cadherin by transcriptional repression. | |||||||||||||||
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This study is to determine the relationship between hypermethylation in chronic periodontitis and breast cancer by comparing the hypermethylation of the E-Cadherin and COX-2 genes in the infected gingival tissues of the periodontitis patients and the neoplastic tissues of cancer patients.
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It is believed that as a result of the accumulation of molecular genetic abnormalities, a cancer eventually develops and metastasizes. p53 mutation, cyclin overexpression (especially in intestinal type), microsatellite instability, down regulation of E-cadherin (especially in diffuse type), and telomerase reactivation are some prominent examples. | |||||||||||||||
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This set of data shows that the epigenetic change in E-Cadherin and Cyclooxygenase-2 is associated with chronic periodontitis. | |||||||||||||||
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This was associated with a more prominent down-regulation of E-cadherin and a stronger up-regulation of MMPs and urokinase receptor. | |||||||||||||||
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Whenever possible, it is important to define the pathogenicity of CDH1 variants including missense alterations, and the following terminology should be used to classify these variants: silent polymorphism, variant of uncertain significance, likely deleterious variant.17 Assessment of pathogenicity of such missense mutations relies on in vitro assays of E-cadherin dependent cellular aggregation and invasion or in silico analyses that predict alterations in E-cadherin protein function based upon conserved evolutionary motifs.1820 Furthermore, it is likely that there are additional genetic loci independent of CDH1 that confer an increased risk of diffuse gastric cancer, and careful identification and characterisation of such diffuse gastric cancer families without known pathogenic CDH1 mutations is a prerequisite to defining these loci. | |||||||||||||||
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The diminished or absent E-cadherin immunoreactivity observed in HDGC and its precursor lesions is consistent with bi-allelic dysfunction of the CDH1 gene. | |||||||||||||||
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TFAP2A plays crucial role in tumor growth and progression by regulation of E-cadherin, MMP-2, c-kit, p21WAF-1, HER-2, BCL-2, insulin like growth factor receptor-1 and Smad signaling [25]. | |||||||||||||||
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Material obtained by aspiration techniques can be used to evaluate the expression of receptors such as oestrogen receptor and progesterone receptor, as well as the levels of expression of other markers such as E cadherin and p53. | |||||||||||||||
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