CD26/DPP-4 in Chronic Myeloid Leukemia

• Published in: Cancers Vol. 14; no. 4; p. 891
• Main Authors: Sicuranza, Anna, Raspadori, Donatella, Bocchia, Monica
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 11.02.2022; MDPI
• Subjects: Apoptosis; BCR-ABL protein; Bone marrow; CD34 antigen; CD38 antigen; Chronic myeloid leukemia; Cytometry; Diagnosis; Dipeptidyl-peptidase IV; Disease; Experiments; Flow cytometry; Fusion protein; Gene expression; Genotype & phenotype; Hematological diseases; Hematology; Leukemia; Lung cancer; Lymphocytes; Melanoma; Membrane proteins; Mesothelioma; Myeloid leukemia; Patients; Peptides; Peripheral blood; Protein-tyrosine kinase; Proteins; Review; Solid tumors; Stem cells; Transcription; Tumor necrosis factor-TNF; Tumors; TFR; CD26; CML; LSCs; TKIs; BCR-ABL
• ISSN: 2072-6694; 2072-6694
• DOI: 10.3390/cancers14040891

CD26 expression is altered in many solid tumors and hematological malignancies. Recently, it has been demonstrated that it is a specific marker expressed on LSCs of CML, both in BM and PB samples, and absent on CD34+/CD38− stem cells in normal subjects or on LSCs of other myeloid neoplasms. CD26+ LSCs have been detected by flow-cytometry assays in all PB samples of Chronic-Phase CML patients evaluated at diagnosis. Additionally, it has been demonstrated that most CML patients undergoing Tyrosine Kinase Inhibitors (TKIs) treatment still harbored circulating measurable residual CD26+ LSCs, even when displaying a consistent deep molecular response without any significant association among the amounts of BCR-ABL transcript and CD26+ LSCs. Preliminary data of our Italian prospective multicenter study showed that CML patients with a poorer response presented with a higher number of CD26+ LSCs at diagnosis. These data confirmed that CD26 is a specific marker of CML and suggest that it could be considered for the monitoring of therapeutic responses.