INT133647

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Context Info
Confidence 0.57
First Reported 2001
Last Reported 2011
Negated 1
Speculated 2
Reported most in Body
Documents 149
Total Number 162
Disease Relevance 106.84
Pain Relevance 17.90

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

nucleus (HDAC9) transcription factor binding (HDAC9) cytoplasm (HDAC9)
Anatomy Link Frequency
alveolar macrophages 4
tails 3
blood 2
lung 2
liver 2
HDAC9 (Homo sapiens)
Pain Link Frequency Relevance Heat
agonist 211 99.90 Very High Very High Very High
rheumatoid arthritis 1005 99.84 Very High Very High Very High
Inflammation 869 99.70 Very High Very High Very High
Thermal hyperalgesia 42 99.70 Very High Very High Very High
carbamazepine 39 99.68 Very High Very High Very High
antidepressant 132 99.44 Very High Very High Very High
bDMF 94 99.08 Very High Very High Very High
depression 286 98.84 Very High Very High Very High
Spinal cord 125 98.74 Very High Very High Very High
Potency 89 98.72 Very High Very High Very High
Disease Link Frequency Relevance Heat
Fatigue 461 99.92 Very High Very High Very High
Anaemia 130 99.92 Very High Very High Very High
Affective Disorder 70 99.92 Very High Very High Very High
Myeloproliferative Disorder 152 99.90 Very High Very High Very High
Asthma 103 99.88 Very High Very High Very High
Stress 212 99.86 Very High Very High Very High
Apoptosis 1306 99.84 Very High Very High Very High
Rheumatoid Arthritis 1099 99.84 Very High Very High Very High
Cancer 4602 99.80 Very High Very High Very High
Sarcoma 92 99.76 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The difference between the gene expression profiles resulting from the inhibition of class I HDACs and those following the inhibition of class IIa HDACs is also of interest, in view of their different effect on thermal hyperalgesia.
Negative_regulation (inhibition) of HDAC associated with thermal hyperalgesia
1) Confidence 0.57 Published 2010 Journal Mol Pain Section Body Doc Link PMC2942827 Disease Relevance 0.81 Pain Relevance 0.81
The difference between the gene expression profiles resulting from the inhibition of class I HDACs and those following the inhibition of class IIa HDACs is also of interest, in view of their different effect on thermal hyperalgesia.
Negative_regulation (inhibition) of HDAC associated with thermal hyperalgesia
2) Confidence 0.57 Published 2010 Journal Mol Pain Section Body Doc Link PMC2942827 Disease Relevance 0.81 Pain Relevance 0.81
MS-275 is a synthetic benzamide derivative that has been shown to inhibit HDACs, and has anti-tumor activity in many preclinical models [25,85-88].
Negative_regulation (inhibit) of HDAC associated with cancer
3) Confidence 0.42 Published 2010 Journal J Hematol Oncol Section Body Doc Link PMC2827364 Disease Relevance 1.66 Pain Relevance 0.07
Recently, the role of gene repression through modulation such as acetylation in cancer patients has been clinically validated with several inhibitors of HDACs.
Negative_regulation (inhibitors) of HDAC associated with cancer and repression
4) Confidence 0.42 Published 2010 Journal J Hematol Oncol Section Abstract Doc Link PMC2827364 Disease Relevance 0.85 Pain Relevance 0
Therefore, our data suggest that CFA-upregulated class IIa HDACs in the spinal cord may facilitate CFA-induced thermal hyperalgesia, and that the inhibition of class IIa HDACs may be sufficient to attenuate the hyperalgesia.
Negative_regulation (inhibition) of HDAC in spinal cord associated with hyperalgesia, thermal hyperalgesia and spinal cord
5) Confidence 0.42 Published 2010 Journal Mol Pain Section Body Doc Link PMC2942827 Disease Relevance 0.57 Pain Relevance 0.76
We also demonstrate that this marker of functional HDAC inhibition occurs almost immediately (15 min) after exposure of F9 cells to VPA, whereas no influence on the HDAC protein levels (HDAC 2 and HDAC 3) could be detected even after 24 h of treatment.
Negative_regulation (inhibition) of HDAC
6) Confidence 0.41 Published 2006 Journal Chem. Res. Toxicol. Section Abstract Doc Link 16485903 Disease Relevance 0.29 Pain Relevance 0.06
The same has been observed regarding H3 and H4 histone hyperacetylation and/or inhibition of HDAC activity by a number of agents including valproic acid [48].
Negative_regulation (inhibition) of HDAC
7) Confidence 0.41 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762324 Disease Relevance 0.09 Pain Relevance 0
There was a statistically significant decrease in global 5mC content and HDAC activity.
Negative_regulation (decrease) of HDAC
8) Confidence 0.41 Published 2006 Journal PLoS ONE Section Abstract Doc Link PMC1762324 Disease Relevance 0.64 Pain Relevance 0
The results of this proof-of-principle study demonstrate that this therapy is safe, that it achieves the molecular changes expected from use of a demethylating and an HDAC inhibitor and appear to increase the efficacy of conventional cytotoxic agents.
Negative_regulation (inhibitor) of HDAC
9) Confidence 0.41 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762324 Disease Relevance 0.51 Pain Relevance 0
On the other hand, the ability of valproic acid to hyperacetylate H3 and H4 histones and to inhibit HDAC has been also demonstrated in the peripheral blood of patients with hematological neoplasms [10], [9].
Negative_regulation (inhibit) of HDAC in blood associated with hematologic neoplasms
10) Confidence 0.41 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762324 Disease Relevance 0.34 Pain Relevance 0
Moreover, it has been shown that p53 induction by HDAC inhibitors may completely deplete mutant p53, and such a sudden restoration is highly cytotoxic to cells harboring mutant p53 [59].
Negative_regulation (inhibitors) of HDAC
11) Confidence 0.40 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762324 Disease Relevance 0.27 Pain Relevance 0
The purpose of this study was to determine if teratogenic side effects of VPA could be linked to its HDAC inhibition ability by studying a large set of structurally diverse derivatives based on the VPA core structure.
Negative_regulation (inhibition) of HDAC
12) Confidence 0.36 Published 2006 Journal Chem. Res. Toxicol. Section Abstract Doc Link 16485903 Disease Relevance 0.32 Pain Relevance 0.07
Hydralazine and magnesium valproate produce DNA demethylation, HDAC inhibition, and gene reactivation in primary tumors.
Negative_regulation (inhibition) of HDAC associated with cancer
13) Confidence 0.35 Published 2006 Journal PLoS ONE Section Abstract Doc Link PMC1762324 Disease Relevance 0.54 Pain Relevance 0
To date, only a limited number of clinical trials has been reported using both a demethylating and an HDAC inhibitor for treatment of hematological [9] and solid tumors [10].
Negative_regulation (inhibitor) of HDAC associated with solid tumor
14) Confidence 0.35 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762324 Disease Relevance 0.47 Pain Relevance 0
These data, along with our findings of significant DNA hypomethylation and HDAC inhibition, strongly indicate that hydralazine and magnesium valproate up-regulate the expression of a significant number of genes in a clinical scenario.
Negative_regulation (inhibition) of HDAC
15) Confidence 0.35 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762324 Disease Relevance 0.22 Pain Relevance 0
In this proof-of-concept study, we demonstrate that treatment with hydralazine and magnesium valproate exerts its proposed molecular effects of DNA demethylation, HDAC inhibition, and gene reactivation in primary tumors of patients with breast cancer.
Negative_regulation (inhibition) of HDAC associated with cancer and breast cancer
16) Confidence 0.35 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762324 Disease Relevance 0.53 Pain Relevance 0
With respect to valproic acid levels, we found a mean concentration of 87.5 µg/mL, which is within ranges observed in our previous phase I study demonstrating histone hyperacetylation and HDAC inhibition, in which mean concentrations observed were 94.06 µg/mL, 123.46 µg/mL, and 90.93 µg/mL for dose levels of 20, 30, and 40 mg/kg, respectively.
Negative_regulation (inhibition) of HDAC
17) Confidence 0.35 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762324 Disease Relevance 0 Pain Relevance 0
HDAC inhibition was observed in PBMCs.
Negative_regulation (inhibition) of HDAC
18) Confidence 0.35 Published 2010 Journal J Hematol Oncol Section Body Doc Link PMC2827364 Disease Relevance 1.38 Pain Relevance 0
Inhibition of HDAC activity was observed in patients' PBMCs.
Negative_regulation (Inhibition) of HDAC
19) Confidence 0.35 Published 2010 Journal J Hematol Oncol Section Body Doc Link PMC2827364 Disease Relevance 1.59 Pain Relevance 0.10
HDAC inhibitors can block androgen receptor -mediated transcriptional activation of many genes and thus may result in possible benefit in treating Castration-resistant prostate cancer [110].
Negative_regulation (inhibitors) of HDAC associated with reprotox - general 1
20) Confidence 0.35 Published 2010 Journal J Hematol Oncol Section Body Doc Link PMC2827364 Disease Relevance 1.11 Pain Relevance 0.03

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