Abstract
The characterisation of the molecular mechanism of disease allows classification of patients into subtypes and potentially identifies specific targets for therapeutic intervention. Tyrosine kinase mutations are central to specific targeted therapy. Investigation of kinase deregulation within particular patient groups, has led to identification of mutant tyrosine kinases associated with disease progression and therapy modulation. Biomarker-specific therapies emerged, taking a leading role in guided-therapy. The extensive use of the specific kinase inhibitors and the longevity of the treatment protocols due to the uncertainty of residual disease, gave rise to new challenges, namely secondary resistance to therapy. Although there are various mechanisms of acquired resistance, mutations in the drug target itself play a dominant role.
Highlights
The characterisation of the molecular mechanism of disease allows classification of patients into subtypes and potentially identifies specific targets for therapeutic intervention
Tyrosine kinase mutations are central to specific targeted therapy
Following extensive molecular classification of patients, the aim of this study was to identify variants and transcript isoforms of PPP2CA and its inhibiting subunits ALPHA4 and SET, using (1) cell lines derived from haematopoietic disease, and (2) Chronic Myeloid Leukemia (CML) and Acute Myeloid Leukemia (AML) patient material
Summary
Introduction The characterisation of the molecular mechanism of disease allows classification of patients into subtypes and potentially identifies specific targets for therapeutic intervention. Tyrosine kinase mutations are central to specific targeted therapy. Investigation of kinase deregulation within particular patient groups, has led to identification of mutant tyrosine kinases associated with disease progression and therapy modulation.
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