INT241515

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.30
First Reported 2008
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 5
Disease Relevance 1.36
Pain Relevance 0.09

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

mitochondrion (Abl1) DNA binding (Abl1) cytoplasm (Abl1)
cytosol (Abl1) nucleolus (Abl1) cell adhesion (Abl1)
Anatomy Link Frequency
platelet 2
Abl1 (Mus musculus)
Pain Link Frequency Relevance Heat
Potency 21 99.08 Very High Very High Very High
cva 3 29.28 Quite Low
headache 9 21.36 Low Low
Central nervous system 21 5.00 Very Low Very Low Very Low
corticosteroid 7 5.00 Very Low Very Low Very Low
cytokine 4 5.00 Very Low Very Low Very Low
Paracetamol 4 5.00 Very Low Very Low Very Low
Bioavailability 3 5.00 Very Low Very Low Very Low
rheumatoid arthritis 3 5.00 Very Low Very Low Very Low
imagery 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Hyperplasia 13 100.00 Very High Very High Very High
Myeloid Leukemia 397 92.56 High High
Leukemia 71 77.64 Quite High
Philadelphia Chromosome 14 76.88 Quite High
Apoptosis 11 63.36 Quite High
Solid Tumor 3 54.88 Quite High
Blast Crisis 35 46.88 Quite Low
Pleural Effusion 57 34.32 Quite Low
Diarrhoea 15 32.88 Quite Low
Cancer 32 32.20 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Imatinib is a 2-phenylaminopyrimidin derivate (Figure 1) and was initially developed as a specific platelet-derived growth factor receptor (PDGFR) inhibitor, but was later found to inhibit autophosphorylation of Abl and c-Kit.
Negative_regulation (inhibit) of Phosphorylation (autophosphorylation) of Abl in platelet
1) Confidence 0.30 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2503652 Disease Relevance 0.46 Pain Relevance 0
Nilotinib inhibits Abl-catalyzed peptide substrate phosphorylation with a 20-fold higher potency than imatinib (IC50 [concentration of inhibitor resulting in a 50% reduction in cell viability]: 15 versus 280 nmol/L).
Negative_regulation (inhibits) of Phosphorylation (phosphorylation) of Abl-catalyzed associated with potency
2) Confidence 0.27 Published 2008 Journal Drug design, development and therapy Section Body Doc Link PMC2761189 Disease Relevance 0 Pain Relevance 0.09
Biochemical assays using purified GST-Abl kinase and cellular proliferation and Bcr-Abl tyrosine phosphorylation assays revealed that dasatinib was approximately 325 times more potent than imatinib.13 Dasatinib was also able to inhibit the cellular proliferation, peptide substrate and Bcr-Abl tyrosine phosphorylation of all Bcr-Abl mutants at nanomolar concentrations with the exception of the T315I mutant.13 In addition, in vivo studies in murine models demonstrated the activity of dasatinib in inhibiting the leukemic cell growth and prolonging the survival of mice harboring wild type Bcr-Abl and the M351T, but not the T315I mutant.9

Clinical efficacy of dasatinib

Negative_regulation (inhibit) of Phosphorylation (phosphorylation) of Abl associated with hyperplasia
3) Confidence 0.17 Published 2009 Journal OncoTargets and therapy Section Body Doc Link PMC2886328 Disease Relevance 0.25 Pain Relevance 0
Biochemical assays using purified GST-Abl kinase and cellular proliferation and Bcr-Abl tyrosine phosphorylation assays revealed that dasatinib was approximately 325 times more potent than imatinib.13 Dasatinib was also able to inhibit the cellular proliferation, peptide substrate and Bcr-Abl tyrosine phosphorylation of all Bcr-Abl mutants at nanomolar concentrations with the exception of the T315I mutant.13 In addition, in vivo studies in murine models demonstrated the activity of dasatinib in inhibiting the leukemic cell growth and prolonging the survival of mice harboring wild type Bcr-Abl and the M351T, but not the T315I mutant.9

Clinical efficacy of dasatinib

Negative_regulation (inhibit) of Phosphorylation (phosphorylation) of Abl associated with hyperplasia
4) Confidence 0.17 Published 2009 Journal OncoTargets and therapy Section Body Doc Link PMC2886328 Disease Relevance 0.25 Pain Relevance 0
Biochemical assays using purified GST-Abl kinase and cellular proliferation and Bcr-Abl tyrosine phosphorylation assays revealed that dasatinib was approximately 325 times more potent than imatinib.13 Dasatinib was also able to inhibit the cellular proliferation, peptide substrate and Bcr-Abl tyrosine phosphorylation of all Bcr-Abl mutants at nanomolar concentrations with the exception of the T315I mutant.13 In addition, in vivo studies in murine models demonstrated the activity of dasatinib in inhibiting the leukemic cell growth and prolonging the survival of mice harboring wild type Bcr-Abl and the M351T, but not the T315I mutant.9

Clinical efficacy of dasatinib

Negative_regulation (inhibit) of Phosphorylation (phosphorylation) of Abl associated with hyperplasia
5) Confidence 0.17 Published 2009 Journal OncoTargets and therapy Section Body Doc Link PMC2886328 Disease Relevance 0.39 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox