INT108086

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Context Info
Confidence 0.58
First Reported 2003
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 17
Total Number 17
Disease Relevance 7.70
Pain Relevance 3.99

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

nucleus (AKR1C3) intracellular (AKR1C3) cytoplasm (AKR1C3)
Anatomy Link Frequency
HL-60 2
AKR1C3 (Homo sapiens)
Pain Link Frequency Relevance Heat
cINOD 39 99.76 Very High Very High Very High
diclofenac 3 99.60 Very High Very High Very High
Potency 3 98.28 Very High Very High Very High
Pain 2 96.96 Very High Very High Very High
Inflammation 7 96.60 Very High Very High Very High
withdrawal 1 95.68 Very High Very High Very High
COX-2 inhibitor 1 94.80 High High
antagonist 1 87.60 High High
corticosteroid 4 30.04 Quite Low
cytokine 2 25.00 Low Low
Disease Link Frequency Relevance Heat
Cancer 144 99.84 Very High Very High Very High
Breast Cancer 55 99.84 Very High Very High Very High
INFLAMMATION 26 99.40 Very High Very High Very High
Reprotox - General 1 20 99.16 Very High Very High Very High
Glioma 5 98.24 Very High Very High Very High
Hypoxia 7 98.08 Very High Very High Very High
Pain 2 96.96 Very High Very High Very High
Apoptosis 2 95.76 Very High Very High Very High
Endometriosis (extended) 3 95.72 Very High Very High Very High
Leukemia 4 93.84 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
AKR1C3 is potently inhibited by non-steroidal anti-inflammatory drugs suggesting that the cancer chemopreventive properties of these agents may be mediated either by inhibition of AKR1C3 or COX.
Negative_regulation (inhibition) of AKR1C3 associated with inflammation, cancer and cinod
1) Confidence 0.58 Published 2006 Journal Mol. Cell. Endocrinol. Section Abstract Doc Link 16417966 Disease Relevance 0.54 Pain Relevance 0.10
AKR1C3 is potently inhibited by non-steroidal anti-inflammatory drugs suggesting that the cancer chemopreventive properties of these agents may be mediated either by inhibition of AKR1C3 or COX.
Negative_regulation (inhibited) of AKR1C3 associated with inflammation, cancer and cinod
2) Confidence 0.58 Published 2006 Journal Mol. Cell. Endocrinol. Section Abstract Doc Link 16417966 Disease Relevance 0.57 Pain Relevance 0.10
Nonsteroidal anti-inflammatory drugs (NSAIDs) like indomethacin, flufenamic acid, and related compounds have been recently identified as potent inhibitors of AKR1C3.
Negative_regulation (inhibitors) of AKR1C3 associated with inflammation and cinod
3) Confidence 0.57 Published 2005 Journal Bioorg. Med. Chem. Lett. Section Abstract Doc Link 16183274 Disease Relevance 0.17 Pain Relevance 0.49
We report that some other NSAIDs (diclofenac and naproxen) also inhibit AKR1C3, with the IC(50) values in the low micromolar range.
Negative_regulation (inhibit) of AKR1C3 associated with cinod and diclofenac
4) Confidence 0.57 Published 2005 Journal Bioorg. Med. Chem. Lett. Section Abstract Doc Link 16183274 Disease Relevance 0.17 Pain Relevance 0.49
Very potent inhibitors of AKR1C3 are the non-steroidal anti-inflammatory drugs, e.g. indomethacin or flufenamic acid.
Negative_regulation (inhibitors) of AKR1C3 associated with inflammation and cinod
5) Confidence 0.43 Published 2009 Journal Chem. Biol. Interact. Section Abstract Doc Link 19007764 Disease Relevance 0.48 Pain Relevance 0.13
Our results reveal that AKR1C3 could be potentially un-competitively inhibited by 2'-hydroxyflavanone, whose IC(50) value of 300nM is clinically promising.
Negative_regulation (inhibited) of AKR1C3
6) Confidence 0.43 Published 2009 Journal Chem. Biol. Interact. Section Abstract Doc Link 19007764 Disease Relevance 0.35 Pain Relevance 0.13
In this study, some dietary flavonoids and other phenolic compounds were tested for their ability to specifically inhibit AKR1C3.
Negative_regulation (inhibit) of AKR1C3
7) Confidence 0.43 Published 2009 Journal Chem. Biol. Interact. Section Abstract Doc Link 19007764 Disease Relevance 0.41 Pain Relevance 0.13
Nonsteroidal anti-inflammatory drugs and their analogues as inhibitors of aldo-keto reductase AKR1C3: new lead compounds for the development of anticancer agents.
Negative_regulation (inhibitors) of AKR1C3 associated with inflammation and cinod
8) Confidence 0.42 Published 2005 Journal Bioorg. Med. Chem. Lett. Section Title Doc Link 16183274 Disease Relevance 0.20 Pain Relevance 0.51
R mRNA is significantly elevated whereas expression of AKR1C1-AKR1C3 mRNA is significantly decreased in tumor compared to normal breast tissue.
Negative_regulation (decreased) of AKR1C3 associated with cancer
9) Confidence 0.41 Published 2004 Journal BMC Cancer Section Body Doc Link PMC459223 Disease Relevance 0.60 Pain Relevance 0
The results provide the first evidence that expression levels of SRD5A1/2 are elevated whereas those of AKR1-3 are markedly decreased in breast carcinoma.
Negative_regulation (decreased) of AKR1-3 associated with breast cancer
10) Confidence 0.41 Published 2004 Journal BMC Cancer Section Body Doc Link PMC459223 Disease Relevance 0.66 Pain Relevance 0
Inhibition of AKR1C3 by indomethacin, a nonsteroidal anti-inflammatory drug (NSAID), caused PPARgamma-mediated terminal differentiation of the HL-60 cells.
Negative_regulation (Inhibition) of AKR1C3 in HL-60 associated with inflammation and cinod
11) Confidence 0.39 Published 2005 Journal Mol. Pharmacol. Section Abstract Doc Link 15475569 Disease Relevance 0.27 Pain Relevance 0.41
The second strategy exploits the selective inhibition of AKR1C3 by indomethacin, which did not inhibit highly related AKR1C1 or AKR1C2.
Negative_regulation (inhibition) of AKR1C3
12) Confidence 0.35 Published 2009 Journal Chem. Biol. Interact. Section Abstract Doc Link 19010312 Disease Relevance 0.44 Pain Relevance 0.26
The identification of NSAID analogs as specific inhibitors of AKR1C3 will help validate its role in the proliferation of breast cancer cells.
Negative_regulation (inhibitors) of AKR1C3 associated with cinod and reprotox - general 1
13) Confidence 0.35 Published 2009 Journal Chem. Biol. Interact. Section Abstract Doc Link 19010312 Disease Relevance 0.39 Pain Relevance 0.31
In addition, PGJ2 but not PGF2alpha recapitulated the potentiation of HL-60 differentiation by PGD2 and AKR1C3 inhibitors.
Negative_regulation (inhibitors) of AKR1C3 in HL-60
14) Confidence 0.35 Published 2003 Journal Cancer Res. Section Abstract Doc Link 12543809 Disease Relevance 0.19 Pain Relevance 0.29
Possible future targeting for "hypoxic" glioma cells includes the targets for the AP-1 transcription factor complex (FOS), as well as blockade of the enzyme AKR1C3 with nonsteroidal anti-inflammatory drugs.
Negative_regulation (blockade) of AKR1C3 associated with inflammation, hypoxia, cinod and glioma
15) Confidence 0.28 Published 2007 Journal Neurosurg Rev Section Abstract Doc Link 17486380 Disease Relevance 1.09 Pain Relevance 0.10
Two strategies for AKR1C3 inhibition based on non-steroidal anti-inflammatory drugs were developed.
Negative_regulation (inhibition) of AKR1C3 associated with inflammation and cinod
16) Confidence 0.26 Published 2009 Journal Chem. Biol. Interact. Section Abstract Doc Link 19010312 Disease Relevance 0.49 Pain Relevance 0.14
Since these five synthases, are involved in various important biological processes, they are potential drug targets and drugs are already in the market for the inhibition of PGDS, PGFS, PGIS and TXAS. mPGES-1 is being sought after as a novel target to relieve pain and inflammation after the withdrawal of popular COX-2 inhibitors from the market [8].
Negative_regulation (inhibition) of PGFS associated with pain, inflammation, cox-2 inhibitor and withdrawal
17) Confidence 0.09 Published 2010 Journal BMC Bioinformatics Section Body Doc Link PMC3009524 Disease Relevance 0.70 Pain Relevance 0.41

General Comments

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