Value of CD26 Positive Stem Cell Marker in Patients With Classical Myeloproliferative Neoplasms

Classic Myeloproliferative neoplasms (MPNs) are a heterogeneous group of diseases including Chronic myeloid leukemia (CML), polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) (Levine et al., 2007).

According to WHO 2016 classification which also included chronic neutrophilic leukemia (CNL), chronic eosinophilic leukemia (CEL), and MPN, unclassifiable, Out of the four classic types of MPNs, CML is positive for BCR-ABL1gene , while PV, ET, and PMF are negative for BCR-ABL1 gene (Thapa and Rogers, 2019).

CML is characterized by a balanced genetic translocation, t(9;22)(q34;q11.2), involving a fusion of the Abelson gene (ABL1) from chromosome 9q34 with the breakpoint cluster region (BCR) gene on chromosome 22q11.2. This rearrangement is known as the Philadelphia chromosome, The molecular consequence of this translocation is the generation of a BCR-ABL1 fusion oncogene, which in turn translates into a BCR-ABL oncoprotein (Jabbour and Kantarjian, 2016).

The frontline therapy for patients with CML in chronic phase is tyrosine kinase inhibitors (TKIs) which directed against tyrosine kinase protein of BCR-ABL1 gene. It showed remarkable efficacy and high rates of cytogenetic response in the treatment of chronic phase CML (Yurttaş and Eşkazan, 2020).

However, drug resistance towards tyrosine kinase inhibitors soon emerged and hence limited the complete eradication of CML in patients receiving TKIs. This is primarily due to the mutations within the ABL kinase domain, and to a lesser degree, due to residual disease after treatment (Patel et al., 2018).