INT18523

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Context Info
Confidence 0.59
First Reported 1990
Last Reported 2010
Negated 0
Speculated 1
Reported most in Abstract
Documents 15
Total Number 16
Disease Relevance 14.20
Pain Relevance 5.92

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

cytosol (ALOX15) oxidoreductase activity (ALOX15) nucleolus (ALOX15)
nucleus (ALOX15) lipid metabolic process (ALOX15) cytoplasm (ALOX15)
Anatomy Link Frequency
RKO 2
HT-29 1
follicle 1
ALOX15 (Homo sapiens)
Pain Link Frequency Relevance Heat
cINOD 88 99.76 Very High Very High Very High
cOX1 2 99.58 Very High Very High Very High
Inflammation 3 99.40 Very High Very High Very High
Antinociceptive 5 99.36 Very High Very High Very High
Analgesic 1 98.74 Very High Very High Very High
aspirin 2 85.84 High High
COX-2 inhibitor 5 81.28 Quite High
dopaminergic neurodegeneration 2 51.92 Quite High
COX2 3 25.00 Low Low
Disease Link Frequency Relevance Heat
Esophageal Cancer 49 99.68 Very High Very High Very High
INFLAMMATION 29 99.52 Very High Very High Very High
Cancer 28 99.40 Very High Very High Very High
Apoptosis 83 99.26 Very High Very High Very High
Rupture 5 99.12 Very High Very High Very High
Colon Cancer 43 98.12 Very High Very High Very High
Stomach Cancer 6 95.14 Very High Very High Very High
Disease 4 95.12 Very High Very High Very High
Nociception 3 92.52 High High
Breast Cancer 37 85.44 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We found that: (a) 15-LOX-1 was down-regulated in human esophageal carcinomas; (b) NSAIDs induced 15-LOX-1 expression during apoptosis in esophageal cancer cells; and (c) 15-LOX-1 inhibition suppressed NSAID-induced apoptosis, which was restored by 13-S-hydroxyoctadecadienoic acid but not by its parent compound, linoleic acid.
Negative_regulation (down) of 15-LOX-1 associated with cinod, apoptosis and esophageal cancer
1) Confidence 0.59 Published 2001 Journal Cancer Res. Section Abstract Doc Link 11406566 Disease Relevance 1.70 Pain Relevance 0.68
In the present study, we tested whether 15-LOX-1 is down-regulated in human esophageal cancers using paired normal and tumor human surgical samples and whether NSAIDs can up-regulate 15-LOX-1 to restore apoptosis in esophageal cancer cells.
Spec (whether) Negative_regulation (regulated) of 15-LOX-1 associated with cancer, cinod, apoptosis and esophageal cancer
2) Confidence 0.59 Published 2001 Journal Cancer Res. Section Abstract Doc Link 11406566 Disease Relevance 1.57 Pain Relevance 0.64
METHODS: We assessed 15-LOX-1 protein expression and enzymatic activity, 13-S-HODE levels, and 15-LOX-1 inhibition in association with cellular growth inhibition and apoptosis induced by NSAIDs (primarily sulindac and NS-398) in two colorectal cancer cell lines (RKO and HT-29).
Negative_regulation (inhibition) of 15-LOX-1 in RKO
3) Confidence 0.59 Published 2000 Journal J. Natl. Cancer Inst. Section Body Doc Link 10904086 Disease Relevance 0.18 Pain Relevance 0
We found that: (a) 15-LOX-1 was down-regulated in human esophageal carcinomas; (b) NSAIDs induced 15-LOX-1 expression during apoptosis in esophageal cancer cells; and (c) 15-LOX-1 inhibition suppressed NSAID-induced apoptosis, which was restored by 13-S-hydroxyoctadecadienoic acid but not by its parent compound, linoleic acid.
Negative_regulation (inhibition) of 15-LOX-1 associated with cinod, apoptosis and esophageal cancer
4) Confidence 0.51 Published 2001 Journal Cancer Res. Section Abstract Doc Link 11406566 Disease Relevance 1.69 Pain Relevance 0.67
We found that: (a) 15-LOX-1 was down-regulated in human esophageal carcinomas; (b) NSAIDs induced 15-LOX-1 expression during apoptosis in esophageal cancer cells; and (c) 15-LOX-1 inhibition suppressed NSAID-induced apoptosis, which was restored by 13-S-hydroxyoctadecadienoic acid but not by its parent compound, linoleic acid.
Negative_regulation (regulated) of 15-LOX-1 associated with cinod, apoptosis and esophageal cancer
5) Confidence 0.43 Published 2001 Journal Cancer Res. Section Abstract Doc Link 11406566 Disease Relevance 1.70 Pain Relevance 0.68
They also support the concept that the loss of the proapoptotic role of 15-LOX-1 in epithelial cancers is not limited to human colorectal cancers.
Negative_regulation (loss) of 15-LOX-1 associated with cancer and colon cancer
6) Confidence 0.43 Published 2001 Journal Cancer Res. Section Abstract Doc Link 11406566 Disease Relevance 1.72 Pain Relevance 0.60
These findings demonstrate that 15-LOX-1 is down-regulated in human esophageal carcinomas and that NSAIDs induce apoptosis in esophageal cancer cells via up-regulation of 15-LOX-1.
Negative_regulation (down-regulated) of 15-LOX-1 associated with cinod, apoptosis and esophageal cancer
7) Confidence 0.43 Published 2001 Journal Cancer Res. Section Abstract Doc Link 11406566 Disease Relevance 1.63 Pain Relevance 0.64
Cancer Inst., 92: 1136-1142, 2000) that (a) 15-lipoxygenase-1 (15-LOX-1) protein and its product 13-S-hydroxyoctadecadienoic acid (13-S-HODE) are decreased; and (b) nonsteroidal anti-inflammatory drug (NSAID)-induced 15-LOX-1 expression is critical to NSAID-induced apoptosis in colorectal cancer cells expressing cyclooxygenase-2 (COX-2).
Negative_regulation (decreased) of 15-LOX-1 associated with inflammation, cancer, colon cancer, cinod and apoptosis
8) Confidence 0.42 Published 2000 Journal Cancer Res. Section Abstract Doc Link 11156377 Disease Relevance 0.87 Pain Relevance 0.76
Potentiation of antinociceptive effect of NSAIDs by a specific lipooxygenase inhibitor, acetyl 11-keto-beta boswellic acid.
Negative_regulation (inhibitor) of lipooxygenase associated with analgesic, cinod and antinociceptive
9) Confidence 0.39 Published 2006 Journal Indian J. Exp. Biol. Section Title Doc Link 16480179 Disease Relevance 0.24 Pain Relevance 0.51
Inhibition of 15-LOX-1 in RKO cells by treatment with caffeic acid blocked NS-398-induced 13-S-HODE production, cellular growth inhibition, and apoptosis (P =. 007, P<.0001, and P<.0001, respectively); growth inhibition and apoptosis were restored by adding exogenous 13-S-HODE (P<.0001 for each) but not its parent compound, linoleic acid (P = 1.0 for each).
Negative_regulation (Inhibition) of 15-LOX-1 in RKO
10) Confidence 0.38 Published 2000 Journal J. Natl. Cancer Inst. Section Body Doc Link 10904086 Disease Relevance 0.14 Pain Relevance 0
We found that: (i) SC-236 inhibited growth of gastric cancer cells mainly by inducing apoptosis; (ii) SC-236 induced 15-LOX-1 expression and increased endogenous 13-S-HODE product, instead of 15-S-HETE during apoptosis; (iii) SC-236 did not affect expression of COX-1, COX-2, 5-LOX and 12-LOX; and (iv) 15-LOX-1 inhibition suppressed SC-236 induced apoptosis.
Negative_regulation (inhibition) of 15-LOX-1 associated with apoptosis and stomach cancer
11) Confidence 0.28 Published 2003 Journal Carcinogenesis Section Abstract Doc Link 12584173 Disease Relevance 1.36 Pain Relevance 0.15
METHODS: We assessed 15-LOX-1 protein expression and enzymatic activity, 13-S-HODE levels, and 15-LOX-1 inhibition in association with cellular growth inhibition and apoptosis induced by NSAIDs (primarily sulindac and NS-398) in two colorectal cancer cell lines (RKO and HT-29).
Negative_regulation (inhibition) of 15-LOX-1 in HT-29
12) Confidence 0.20 Published 2000 Journal J. Natl. Cancer Inst. Section Body Doc Link 10904086 Disease Relevance 0.18 Pain Relevance 0
Meclomen (sodium meclofenamate) is a nonsteroidal anti-inflammatory drug (NSAID) with dual inhibition of both cyclooxygenase and lipooxygenase enzymes involved in arachidonic acid metabolism.
Negative_regulation (inhibition) of lipooxygenase associated with inflammation and cinod
13) Confidence 0.15 Published 1990 Journal Acta Virol. Section Abstract Doc Link 1975722 Disease Relevance 0.16 Pain Relevance 0.20
In this work, we state that COX-2 expression in the more aggressive cells is controlled by ACSL4 through the generation of lipooxygenase metabolites since inhibition of lipooxygenase activity blunted ACSL4-dependent increase in COX-2 expression.
Negative_regulation (inhibition) of lipooxygenase
14) Confidence 0.01 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2978721 Disease Relevance 0.14 Pain Relevance 0
Effects of selective inhibition of cyclooxygenase and lipooxygenase pathways in follicle rupture and ovulation in the rat.
Negative_regulation (inhibition) of lipooxygenase in follicle associated with rupture and cox1
15) Confidence 0.01 Published 2006 Journal Reproduction Section Title Doc Link 17008468 Disease Relevance 0.27 Pain Relevance 0.15
A new strategy for anti-inflammatory drug therapy is using a dual inhibitor of COX and lipooxygenase (LOX).
Negative_regulation (inhibitor) of lipooxygenase associated with inflammation
16) Confidence 0.00 Published 2008 Journal Neurosci. Lett. Section Abstract Doc Link 18760329 Disease Relevance 0.65 Pain Relevance 0.25

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