INT199561

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Context Info
Confidence 0.36
First Reported 2006
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 8
Total Number 8
Disease Relevance 4.77
Pain Relevance 0.16

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)
Abl1 (Mus musculus)
Pain Link Frequency Relevance Heat
Potency 21 95.44 Very High Very High Very High
Kinase C 1 83.88 Quite High
adenocard 1 49.52 Quite Low
rheumatoid arthritis 3 38.52 Quite Low
Paracetamol 12 24.20 Low Low
cytokine 5 23.64 Low Low
anticonvulsant 3 7.52 Low Low
Central nervous system 25 5.00 Very Low Very Low Very Low
headache 11 5.00 Very Low Very Low Very Low
corticosteroid 9 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Genetic Translocation 1 99.72 Very High Very High Very High
Myeloid Leukemia 554 97.08 Very High Very High Very High
Chronic Myeloid Leukemia 7 96.88 Very High Very High Very High
Philadelphia Chromosome 18 94.56 High High
Cancer 75 92.88 High High
Fever 11 91.36 High High
Colitis 3 90.56 High High
Cytomegalovirus Infection 3 89.68 High High
Pneumonia 4 89.48 High High
Pleural Effusion 61 88.96 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
First, amplification of the bcr-abl gene and consequently the production of a higher amount of Bcr-Abl protein has been observed in cell line models selected for imatinib resistance (le Coutre et al 2000; Mahon et al 2000; Weisberg and Griffin 2001).
Positive_regulation (amount) of Gene_expression (production) of Abl
1) Confidence 0.36 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2503652 Disease Relevance 0.28 Pain Relevance 0
Decreasing the protein expression of a target kinase is also capable of restoring sensitivity to imatinib in cells overexpressing bcr-abl as well as in cells expressing a mutant bcr-abl variant conferring partially resistance to imatinib.
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of abl
2) Confidence 0.36 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2503652 Disease Relevance 0.14 Pain Relevance 0
Decreasing the protein expression of a target kinase is also capable of restoring sensitivity to imatinib in cells overexpressing bcr-abl as well as in cells expressing a mutant bcr-abl variant conferring partially resistance to imatinib.
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of abl
3) Confidence 0.33 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2503652 Disease Relevance 0.13 Pain Relevance 0
This translocation fuses the genes encoding BCR and ABL, resulting in expression of the constitutively active protein tyrosine kinase, BCR-ABL.
Positive_regulation (resulting) of Gene_expression (expression) of ABL
4) Confidence 0.23 Published 2008 Journal OncoTargets and therapy Section Body Doc Link PMC2994207 Disease Relevance 1.46 Pain Relevance 0
These include upregulation of the ABCB1 or ABCG2 drug efflux pumps,58,63,64 downregulation of human organic cation transporter 1 (hOCT1) drug influx transporters,65,66 overexpression of Lyn, a Src-family kinase,67 and other Bcr-Abl-independent mechanisms.
Positive_regulation (overexpression) of Gene_expression (overexpression) of Abl
5) Confidence 0.20 Published 2009 Journal OncoTargets and therapy Section Body Doc Link PMC2886328 Disease Relevance 0.52 Pain Relevance 0.05
Dasatinib resistance, due to Bcr-Abl kinase mutation and potentially overexpression of drug efflux transporters, will represent the next therapeutic challenge in CML.
Positive_regulation (overexpression) of Gene_expression (overexpression) of Bcr-Abl kinase associated with myeloid leukemia
6) Confidence 0.19 Published 2009 Journal OncoTargets and therapy Section Body Doc Link PMC2886328 Disease Relevance 0.61 Pain Relevance 0.04
The two most common affect the BCR-ABL gene itself, namely mutations in its tyrosine kinase domain and overexpression of the Bcr-Abl protein due to amplification of the BCR-ABL gene.58–62 The third mechanism is represented by phenomena which lead to Bcr-Abl-independent resistance.
Positive_regulation (overexpression) of Gene_expression (overexpression) of Abl
7) Confidence 0.19 Published 2009 Journal OncoTargets and therapy Section Body Doc Link PMC2886328 Disease Relevance 0.90 Pain Relevance 0.03
This causes the production of the nonreceptor TK BCR–ABL fusion protein.
Positive_regulation (causes) of Gene_expression (production) of ABL
8) Confidence 0.17 Published 2006 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC1661649 Disease Relevance 0.73 Pain Relevance 0.04

General Comments

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