INT193674

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Context Info
Confidence 0.47
First Reported 2006
Last Reported 2009
Negated 2
Speculated 0
Reported most in Body
Documents 10
Total Number 11
Disease Relevance 4.30
Pain Relevance 0.36

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

cytosol (Bcr) signal transduction (Bcr) plasma membrane (Bcr)
intracellular (Bcr) enzyme binding (Bcr) kinase activity (Bcr)
Anatomy Link Frequency
B cell 1
arm 1
Bcr (Mus musculus)
Pain Link Frequency Relevance Heat
Potency 35 99.12 Very High Very High Very High
cytokine 59 88.72 High High
tolerance 62 80.24 Quite High
abdominal pain 6 47.20 Quite Low
headache 7 44.88 Quite Low
Piles 3 31.68 Quite Low
Inflammation 42 5.00 Very Low Very Low Very Low
Central nervous system 15 5.00 Very Low Very Low Very Low
cva 6 5.00 Very Low Very Low Very Low
halothane 6 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Myeloid Leukemia 418 100.00 Very High Very High Very High
Apoptosis 135 100.00 Very High Very High Very High
Leukemia 75 100.00 Very High Very High Very High
Disease 65 89.72 High High
Blast Crisis 56 88.04 High High
Renal Disease 9 82.16 Quite High
Recurrence 24 72.64 Quite High
Aspergillus Infection 3 70.36 Quite High
Hyperplasia 3 70.12 Quite High
Thrombocytopenia 30 65.04 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Like imatinib, nilotinib does not inhibit Src kinase and does not bind to the inactive conformation of Bcr-Abl.
Bcr-Abl Neg (not) Binding (bind) of
1) Confidence 0.47 Published 2008 Journal Drug design, development and therapy Section Body Doc Link PMC2761189 Disease Relevance 0 Pain Relevance 0
Dasatinib binds multiple conformations of BCR-ABL [30], unlike imatinib and nilotinib [31,32].
BCR Binding (binds) of
2) Confidence 0.42 Published 2008 Journal J Hematol Oncol Section Body Doc Link PMC2567340 Disease Relevance 0.53 Pain Relevance 0.03
Recently, dasatinib-induced BCR-ABL inhibition was shown to be sufficient to commit chronic myeloid leukemia cells irreversibly to apoptosis and suggested that in patients with CML receiving dasatinib once daily, response correlates with the magnitude of BCR-ABL kinase inhibition, demonstrating the potential clinical utility of intermittent potent kinase inhibitor therapy.31
BCR Binding (inhibition) of associated with leukemia, myeloid leukemia and apoptosis
3) Confidence 0.36 Published 2009 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2697539 Disease Relevance 1.02 Pain Relevance 0
Overall, 162 patients were followed with mutational analysis: 26% retained a BCR-ABL mutation, 26% lost a mutation, 27% developed a mutation, and the remaining belonged to > 1 mutational category.24
BCR Binding (mutation) of
4) Confidence 0.36 Published 2009 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2697539 Disease Relevance 0.24 Pain Relevance 0
Clinically relevant mutations disrupt critical contact points between imatinib and Bcr-Abl or may favor the active conformation of Bcr-Abl, to which imatinib is unable to bind (Deininger et al 2005; Shah 2005).
Bcr-Abl Neg (unable) Binding (bind) of
5) Confidence 0.36 Published 2008 Journal Drug design, development and therapy Section Body Doc Link PMC2761189 Disease Relevance 0.36 Pain Relevance 0
Imatinib mesylate (Gleevec®; Novartis Pharma, East Hanover, NJ, USA) is a very specific inhibitor of BCR-ABL tyrosine kinase activity of the 2-phenylamino pyrimidine class, and it is approved by the Food and Drug Administration as frontline therapy for patients with CML.6 Imatinib acts by binding and stabilizing the inactive form of BCR-ABL, thereby inhibiting its autophosphorylation and the phosphorylation of its substrate, abrogating proliferation and inducing apoptosis of BCR-ABL–positive cells.4,7 The superiority of imatinib for successful clinical outcomes of patients with CML was confirmed by the International Randomized Study of Interferon plus low-dose cytarabine, the previous standard of care, vs STI571, or the imatinib (IRIS) trial, in which 553 patients were randomized to each arm.8 Imatinib induced high rates of complete hematologic response (96% at 1 year, which increased to 98% at 5 years),8 a major cytogenetic response (86% at 1 year, which increased to 92% at 5 years), a complete cytogenetic response (69% at 1 year and 87% at 5 years), a progression-free survival rate without accelerated or blast crisis (93% at 6 years), overall progression-free survival (83% at 6 years) and overall survival (95% at 6 years, taking into consideration only CML-related deaths; and 88% at 6 years when deaths from any cause were included).8–10
BCR Binding (binding) of in arm associated with myeloid leukemia, blast crisis and apoptosis
6) Confidence 0.35 Published 2009 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2697539 Disease Relevance 0.85 Pain Relevance 0
Such mutations inhibit the ability of imatinib to bind to BCR-ABL by corrupting the binding sites or preventing the kinase domain from assuming the inactive conformation required for imatinib binding [11].
BCR Binding (bind) of
7) Confidence 0.31 Published 2008 Journal J Hematol Oncol Section Body Doc Link PMC2567340 Disease Relevance 0.32 Pain Relevance 0
The increased potency of dasatinib, combined with its ability to bind multiple conformation of BCR-ABL, produces significant efficacy in patients with CML and Ph+ ALL.
BCR Binding (bind) of associated with myeloid leukemia and potency
8) Confidence 0.31 Published 2008 Journal J Hematol Oncol Section Body Doc Link PMC2567340 Disease Relevance 0.42 Pain Relevance 0.05
Binding of such a complex to BCR triggers endocytosis, causing effective delivery of the denatured chromatin fragments to endosome-associated TLR-9.
BCR Binding (Binding) of
9) Confidence 0.08 Published 2006 Journal Theor Biol Med Model Section Body Doc Link PMC1508139 Disease Relevance 0.24 Pain Relevance 0.08
Binding of such a complex to BCR triggers endocytosis, causing effective delivery of the denatured chromatin fragments to endosome-associated TLR-9.
BCR Binding (Binding) of
10) Confidence 0.06 Published 2006 Journal Theor Biol Med Model Section Body Doc Link PMC1508139 Disease Relevance 0.24 Pain Relevance 0.08
Antigen (epitope-specific) recognition by B-cell receptors (BCR) induces signals that cause B cell proliferation and antibody production.
BCR Binding (recognition) of in B cell
11) Confidence 0.06 Published 2006 Journal Theor Biol Med Model Section Body Doc Link PMC1508139 Disease Relevance 0.07 Pain Relevance 0.12

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