Value of CD26 Positive Leukemic Stem Cell in Myeloproliferative Neoplasm
NCT ID: NCT04312607
Last Updated: 2020-03-18
Study Results
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
Get a concise snapshot of the trial, including recruitment status, study phase, enrollment targets, and key timeline milestones.
UNKNOWN
80 participants
OBSERVATIONAL
2020-08-01
2022-03-01
Brief Summary
Review the sponsor-provided synopsis that highlights what the study is about and why it is being conducted.
To study CD26 expression on different phases of CML (chronic phase, accelerated phase, blastic phase).
To investigate whether CD26 positive stem cell are expressed only in Philadelphia chromosome positive MPN (CML) and/or in Philadelphia chromosome negative MPN (PV, ET, PMF).
Related Clinical Trials
Explore similar clinical trials based on study characteristics and research focus.
"Peripheral Blood Dipeptidylpeptidase IV (CD26) Positive Leukemic Stem Cells in Chronic Myeloid Leukemia as a Diagnostic Marker"
NCT05543161
Study of Bone Marrow Samples From Patients With Acute Leukemia
NCT00897559
Biomarker Study in Bone Marrow Samples From Patients With T-Cell Acute Lymphoblastic Leukemia
NCT01295476
Studying Biomarkers in Cell Samples From Young Patients With Acute Myeloid Leukemia
NCT01057290
Prospective Collection of Biological Data of Prognostic Relevance in Patients With B-Cell Chronic Lymphocytic Leukemia
NCT00917540
Detailed Description
Dive into the extended narrative that explains the scientific background, objectives, and procedures in greater depth.
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).
Dipeptidyl peptidase IV (DPPIV/CD26) is a transmembrane glycoprotein which has been proposed as an important tumor biomarker in different types of cancer, like melanoma, lung cancer, prostate cancer, gastric and colorectal cancer (Liang et al., 2017) .
CD26 expression in hematological malignancies has been widely studied. It was described as a marker of aggressiveness in T cell malignancies, such as T-acute lymphoblastic leukemias (T-ALL),and associated with poor prognosis and survival ,also found variable expression of CD26 in B cell chronic lymphocytic leukemia (B-CLL) (Enz et al., 2019).
Identification and characterization of leukemic stem cells (LSCs) in CML are one of the recently used investigations. These cells reside within the CD34 positive /CD38 negative and score positive for CD26 which is a marker, expressed in both bone marrow (BM) and peripheral blood (PB) samples, that discriminates CML cells from normal hematopoietic stem cells (HSCs) or from LSCs of other myeloid neoplasms (Raspadori et al., 2017).
the percentage of CD26 LSCs is significantly reduced to low or undetectable levels in CML patients who respond to TKI therapy; however, the percentage of CD26 LSCs remains at high levels in TKI-non responder patients and in patients who have relapsed after TKI therapy, indicating that CD26 could be a useful predictive biomarker for monitoring TKI treatment in CML patients (Raspadori et al., 2019).
Conditions
See the medical conditions and disease areas that this research is targeting or investigating.
Study Design
Understand how the trial is structured, including allocation methods, masking strategies, primary purpose, and other design elements.
COHORT
PROSPECTIVE
Study Groups
Review each arm or cohort in the study, along with the interventions and objectives associated with them.
Philadelphia chromosome positive
according to PCR detection of BCR-ABL gene CD26 expression on stem cells
BCR-ABL gene PCR
peripheral blood sampling for detection of Philadelphia chromosome and flowcytometry for detection of CD26 positive stem cells
Philadelphia chromosome negative
according to PCR detection of BCR-ABL gene CD26 expression on stem cells
BCR-ABL gene PCR
peripheral blood sampling for detection of Philadelphia chromosome and flowcytometry for detection of CD26 positive stem cells
Interventions
Learn about the drugs, procedures, or behavioral strategies being tested and how they are applied within this trial.
BCR-ABL gene PCR
peripheral blood sampling for detection of Philadelphia chromosome and flowcytometry for detection of CD26 positive stem cells
Other Intervention Names
Discover alternative or legacy names that may be used to describe the listed interventions across different sources.
Eligibility Criteria
Check the participation requirements, including inclusion and exclusion rules, age limits, and whether healthy volunteers are accepted.
Inclusion Criteria
Exclusion Criteria
* Pregnancy.
* Any associated Solid or hematopoietic neoplasm.
18 Years
ALL
No
Sponsors
Meet the organizations funding or collaborating on the study and learn about their roles.
Safaa AA Khaled
OTHER
Responsible Party
Identify the individual or organization who holds primary responsibility for the study information submitted to regulators.
Safaa AA Khaled
Value of CD26 positive stem cell marker in patients with classical myeloproliferative neoplasms
Principal Investigators
Learn about the lead researchers overseeing the trial and their institutional affiliations.
doha M ali, MD
Role: PRINCIPAL_INVESTIGATOR
Assiut University
Central Contacts
Reach out to these primary contacts for questions about participation or study logistics.
References
Explore related publications, articles, or registry entries linked to this study.
Levine RL, Pardanani A, Tefferi A, Gilliland DG. Role of JAK2 in the pathogenesis and therapy of myeloproliferative disorders. Nat Rev Cancer. 2007 Sep;7(9):673-83. doi: 10.1038/nrc2210.
Thapa B, Fazal S, Parsi M, Rogers HJ. Myeloproliferative Neoplasms. 2023 Aug 8. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from http://www.ncbi.nlm.nih.gov/books/NBK531464/
Jabbour E, Kantarjian H. Chronic myeloid leukemia: 2016 update on diagnosis, therapy, and monitoring. Am J Hematol. 2016 Feb;91(2):252-65. doi: 10.1002/ajh.24275.
Raspadori D, Pacelli P, Sicuranza A, Abruzzese E, Iurlo A, Cattaneo D, Gozzini A, Galimberti S, Barate C, Pregno P, Nicolosi M, Sora F, Annunziata M, Luciano L, Caocci G, Moretti S, Sgherza N, Fozza C, Russo S, Usala E, Liberati MA, Ciofini S, Trawinska MM, Gozzetti A, Bocchia M. Flow Cytometry Assessment of CD26+ Leukemic Stem Cells in Peripheral Blood: A Simple and Rapid New Diagnostic Tool for Chronic Myeloid Leukemia. Cytometry B Clin Cytom. 2019 Jul;96(4):294-299. doi: 10.1002/cyto.b.21764. Epub 2019 Feb 3.
Other Identifiers
Review additional registry numbers or institutional identifiers associated with this trial.
CD26 in MPN
Identifier Type: -
Identifier Source: org_study_id
More Related Trials
Additional clinical trials that may be relevant based on similarity analysis.