Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With the availability of molecular monitoring of BCR-ABL1 and the use of tyrosine kinase inhibitors, treatment in chronic myeloid leukemia (CML) is now molecularly focused. Eighty-three samples taken at different time points from 38 CML patients; were subjected to T315I mutation analysis and gene expression analysis of AHI1; a novel gene that is thought to have a role in both BCR-ABL1 mediated leukemic transformation and response to tyrosine kinase inhibitors. Only one patient (2.63%) harboured the T315I mutation. While no significant difference in AHI1 expression was observed between newly diagnosed CML samples and non-CML controls; CML samples under imatinib therapy had levels significantly higher than both newly diagnosed samples and controls. In the first 6 months of imatinib therapy, AHI1 expression was found to increase and then gradually decrease. There was no significant difference between imatinib responders and non-responders, while dasatinib caused significantly lower AHI1 levels. It is proposed that the change in AHI1 expression during CML therapy might be under the control of mechanisms independent from BCR-ABL1. AHI1 mediated signalling could be better understood by analyzing AHI1 gene expression levels in a greater number of patients and concurrently investigating JAK/STAT and Src family kinases pathways.
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PMID:AHI1 gene expression levels and BCR-ABL1 T315I mutations in chronic myeloid leukemia patients. 2218 70