INT86370

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Context Info
Confidence 0.54
First Reported 1999
Last Reported 2010
Negated 0
Speculated 3
Reported most in Body
Documents 10
Total Number 14
Disease Relevance 13.89
Pain Relevance 0.70

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

endosome (CDH1) cell adhesion (CDH1) Golgi apparatus (CDH1)
plasma membrane (CDH1) cytoplasm (CDH1)
CDH1 (Homo sapiens)
Pain Link Frequency Relevance Heat
metalloproteinase 8 98.68 Very High Very High Very High
Inflammation 70 91.36 High High
Pain 5 81.36 Quite High
COX-2 inhibitor 4 78.48 Quite High
cINOD 2 77.08 Quite High
palliative 3 72.84 Quite High
nud 3 53.00 Quite High
abdominal pain 3 52.48 Quite High
fibrosis 1 47.44 Quite Low
COX2 6 45.44 Quite Low
Disease Link Frequency Relevance Heat
Microsatellite Instability 48 99.86 Very High Very High Very High
Breast Cancer 56 99.64 Very High Very High Very High
Stomach Cancer 143 99.48 Very High Very High Very High
Cancer 447 99.46 Very High Very High Very High
Carcinoma 121 99.28 Very High Very High Very High
Chronic Periodontitis 30 99.28 Very High Very High Very High
Repression 4 99.20 Very High Very High Very High
Adhesions 11 98.16 Very High Very High Very High
Carcinoma In Situ 11 97.76 Very High Very High Very High
Periodontitis 50 97.72 Very High Very High Very High

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.
Spec (possibly) Regulation (regulating) of E-cadherin associated with reprotox - general 1 and adhesions
1) Confidence 0.54 Published 2010 Journal J Ethnopharmacol Section Abstract Doc Link 19897022 Disease Relevance 0.85 Pain Relevance 0.08
Moreover, experiments were performed in order to evaluate whether COX-2 pharmacological inhibition may affect beta-catenin/E-cadherin signalling pathway.
Spec (may) Regulation (affect) of E-cadherin
2) Confidence 0.44 Published 2009 Journal Chem. Biol. Interact. Section Abstract Doc Link 19682443 Disease Relevance 0.58 Pain Relevance 0.12
Expression of several transcriptional repressors has been shown to down-regulate CDH1 transcription [3].
Regulation (regulate) of CDH1
3) Confidence 0.34 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2680015 Disease Relevance 0.81 Pain Relevance 0
The alterations of E-cadherin, p16, and HER2/neu seem to affect the progression from EIC to serous carcinoma [10].
Regulation (alterations) of E-cadherin associated with carcinoma in situ and carcinoma
4) Confidence 0.24 Published 2010 Journal Obstetrics and Gynecology International Section Body Doc Link PMC2846683 Disease Relevance 2.09 Pain Relevance 0
E-cadherin immunoreactivity was weakly present in their cytoplasm and beta-catenin was negative.
Regulation (immunoreactivity) of E-cadherin
5) Confidence 0.18 Published 2006 Journal Virchows Arch. Section Abstract Doc Link 17033799 Disease Relevance 0.83 Pain Relevance 0.07
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.
Regulation (regulation) of E-cadherin associated with repression
6) Confidence 0.16 Published 2010 Journal BMC Clin Pathol Section Body Doc Link PMC2829523 Disease Relevance 0.59 Pain Relevance 0
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.


Regulation (hypermethylation) of E-Cadherin associated with chronic periodontitis, periodontitis, cancer and breast cancer
7) Confidence 0.11 Published 2010 Journal J Transl Med Section Body Doc Link PMC2998472 Disease Relevance 1.43 Pain Relevance 0.16
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.
Regulation (regulation) of E-cadherin associated with cancer, congenital anomalies and microsatellite instability
8) Confidence 0.07 Published 1999 Journal Ann. Acad. Med. Singap. Section Abstract Doc Link 10672411 Disease Relevance 1.87 Pain Relevance 0.12
This set of data shows that the epigenetic change in E-Cadherin and Cyclooxygenase-2 is associated with chronic periodontitis.
Regulation (change) of E-Cadherin associated with chronic periodontitis
9) Confidence 0.07 Published 2010 Journal J Transl Med Section Abstract Doc Link PMC2998472 Disease Relevance 1.17 Pain Relevance 0.05
This was associated with a more prominent down-regulation of E-cadherin and a stronger up-regulation of MMPs and urokinase receptor.
Regulation (regulation) of E-cadherin associated with metalloproteinase
10) Confidence 0.05 Published 2008 Journal BMC Cancer Section Body Doc Link PMC2596176 Disease Relevance 0.65 Pain Relevance 0.05
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.18–20 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.
Spec (analyses) Regulation (alterations) of E-cadherin associated with stomach cancer
11) Confidence 0.03 Published 2010 Journal Journal of Medical Genetics Section Body Doc Link PMC2991043 Disease Relevance 0.45 Pain Relevance 0
The diminished or absent E-cadherin immunoreactivity observed in HDGC and its precursor lesions is consistent with bi-allelic dysfunction of the CDH1 gene.
Regulation (immunoreactivity) of E-cadherin associated with stomach cancer
12) Confidence 0.02 Published 2010 Journal Journal of Medical Genetics Section Body Doc Link PMC2991043 Disease Relevance 0.46 Pain Relevance 0
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].
Regulation (regulation) of E-cadherin associated with cancer
13) Confidence 0.01 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2958829 Disease Relevance 0.92 Pain Relevance 0
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.
Regulation (levels) of E cadherin
14) Confidence 0.01 Published 2003 Journal Breast Cancer Res Section Body Doc Link PMC314417 Disease Relevance 1.17 Pain Relevance 0.06

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