INT350521

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Context Info
Confidence 0.23
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.55
Pain Relevance 0

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

cytosol (ABL1) protein modification process (ABL1) mitochondrion (ABL1)
nucleolus (ABL1) nucleus (ABL1) DNA binding (ABL1)
ABL1 (Homo sapiens)
Pain Link Frequency Relevance Heat
cytokine 3 5.00 Very Low Very Low Very Low
palliative 1 5.00 Very Low Very Low Very Low
chemokine 1 5.00 Very Low Very Low Very Low
Nicotine 1 5.00 Very Low Very Low Very Low
Inflammation 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Myeloid Leukemia 25 99.54 Very High Very High Very High
Apoptosis 21 99.40 Very High Very High Very High
Cancer 9 66.16 Quite High
Blast Crisis 1 34.00 Quite Low
Philadelphia Chromosome 1 16.92 Low Low
Myeloproliferative Disorder 45 9.28 Low Low
Chronic Myeloid Leukemia 4 8.68 Low Low
Myelodysplastic Syndromes 38 5.00 Very Low Very Low Very Low
Myelofibrosis 30 5.00 Very Low Very Low Very Low
Chronic Neutrophilic Leukemia 7 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In most of the studies performed the primary mechanism by which HDACi appeared to induce apoptosis in CML cells was through the reduction of BCR-ABL levels and therefore downregulation of the multiple signalling pathways controlling survival of the neoplastic cells.
Negative_regulation (downregulation) of Negative_regulation (reduction) of BCR-ABL associated with myeloid leukemia and apoptosis
1) Confidence 0.23 Published 2010 Journal Invest New Drugs Section Body Doc Link PMC3003795 Disease Relevance 0.55 Pain Relevance 0

General Comments

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