Chronic myeloid leukemia (CML) epitomises successful targeted therapy with 90% patients in chronic phase treated with tyrosine kinase inhibitors (TKIs) attaining remission. This success eludes 80% patients in advanced phase of blast crisis (BC) who are resistant to TKIs and have poor survival. Since continued administration of TKIs is necessary to sustain remission, patients are on TKIs for a longer period with higher probability of resistance, relapse and progression to BC.

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.