Chronic myeloid leukemia (CML) epitomises successful targeted therapy with 90% patients in chronic phase treated with tyrosine kinase inhibitor (TKI) attaining remission. This success eludes 80% patients in advanced blast crisis (BC) resistant to TKIs due to either kinase domain mutations in the transforming protein Bcr/Abl preventing TKI binding or progression of leukemic cells to Bcr/Abl independent phenotype wherein alternate signalling pathways drive the disease. This brings in a need to identify alternate therapeutic targets for TKI resistant CML-BC.

The molecular mechanism mediating expression of senescent cell antigen-aggregated or cleaved band 3 and externalized phosphatidylserine (PS) on the surface of aged erythrocytes and their premature expression in certain anemias is not completely elucidated. The erythrocytes with these surface modifications undergo macrophage-mediated phagocytosis. In this study, the role of protein kinase C (PKC) isoforms in the expression of these surface modifications was investigated.