Status
Conditions
About
Chronic myeloid leukemia (CML) is a stem cell (SC) neoplasm which originates from an incomplete process of differentiation of the hematopoietic stem cells (HSCs) to the adult cells which lead to accumulation of their immature form into the BM and the peripheral blood. It is characterized by the reciprocal translocation. The resulting oncoprotein, BCR/ABL1, is considered essential for the initiation and manifestation of the disease . In CML, leukemic stem cell (LSC) supposedly resides within the CD45+/ CD34+/CD38-/Lin- fraction of the leukemic clone (3). However, normal hematopoietic SC also exhibit this phenotype so that additional markers are required to discriminate CML LSC from normal SC. CD34+/CD38-/Lin- CML LSC specifically co-express dipeptidylpeptidase IV(DPPIV=CD26). This enzyme disrupts LSC-niche interactions by degrading stroma derived factor-1 (SDF-1). Moreover, CD26 is a robust biomarker for the quantification and isolation of CML LSC (4). It was reported that CD26+ LSCs were significantly correlated with BCR-ABL1 transcript level at diagnosis and after three months of treatment with tyrosine kinase inhibitor (TKI) .
Enrollment
Sex
Ages
Volunteers
Inclusion criteria
Exclusion criteria
Loading...
Central trial contact
DR. Shaaban Helal, professor; Rowida Eid, Clinical Pathology Specialist
Data sourced from clinicaltrials.gov
Clinical trials
Research sites
Resources
Legal