Apoptotic profiling of chronic myeloid leukaemia patients' platelets ex vivo before and after treatment with Imatinib.
Adolescent
Adult
Antineoplastic Agents
/ blood
Apoptosis
/ drug effects
Female
Humans
Imatinib Mesylate
/ blood
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
/ blood
Male
Middle Aged
Platelet Activation
/ drug effects
Platelet-Derived Growth Factor
/ antagonists & inhibitors
Protein Kinase Inhibitors
/ blood
Protein-Tyrosine Kinases
/ antagonists & inhibitors
Young Adult
Imatinib
apoptosis
chronic myeloid leukaemia
ex vivo
platelets
Journal
Cell biochemistry and function
ISSN: 1099-0844
Titre abrégé: Cell Biochem Funct
Pays: England
ID NLM: 8305874
Informations de publication
Date de publication:
Jun 2021
Jun 2021
Historique:
revised:
18
01
2021
received:
24
11
2020
accepted:
26
01
2021
pubmed:
12
2
2021
medline:
9
7
2021
entrez:
11
2
2021
Statut:
ppublish
Résumé
Chronic myeloid leukaemia (CML) is a malignancy of the haematopoietic stem cells. The first line of treatment for CML, especially in developing countries, remains the first-generation tyrosine kinase inhibitor, Imatinib. Patients with CML are frequently diagnosed with platelet abnormalities. However, the specific mechanism of platelet abnormalities in CML remains unclear and poorly understood. The aim of this study was therefore to determine the apoptotic profiles of CML patients ex vivo on platelets before and after treatment with Imatinib. Blood samples of healthy volunteers and CML patients at diagnosis and after 6 months treatment with Imatinib were collected. Platelet counts, viability and activation were determined. Results showed that CML patients' platelet counts were elevated upon diagnosis and these levels statistically significantly decreased after 6 months of treatment. Platelet activation was significantly increased after 6 months of treatment compared to levels at diagnosis (P-value < .05). Similarly, platelet apoptosis was also increased after 6 months of treatment. Abnormalities in platelet functioning found in this study may partly be due to clonal proliferation of haematopoietic cells in CML patients, specifically of megakaryocyte precursors as well as the inhibition of platelet tyrosine kinase's and the inhibition of platelet-derived growth factor.
Substances chimiques
Antineoplastic Agents
0
Platelet-Derived Growth Factor
0
Protein Kinase Inhibitors
0
Imatinib Mesylate
8A1O1M485B
Protein-Tyrosine Kinases
EC 2.7.10.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
562-570Subventions
Organisme : Cancer Association of South Africa
ID : AOV741
Organisme : Cancer Association of South Africa
ID : AOW228
Organisme : Medical Research Council of South Africa
ID : AOW110
Organisme : National Research Foundation
ID : N00375
Organisme : National Research Foundation
ID : N00591
Organisme : School of Medicine Research Committee of the Faculty of Health Sciences, University of Pretoria
ID : AOR984
Organisme : Struwig-Germeshuysen Research Trust
ID : AON074
Informations de copyright
© 2021 John Wiley & Sons Ltd.
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