Genotoxicity associated with the use of tyrosine kinase inhibitors in patients with chronic myeloid leukemia

Genotoxicity associated with the use of tyrosine kinase inhibitors in patients with chronic... Dear Editor,Chronic myeloid leukemia (CML) is a clonal myeloproliferative disease in which proliferation of massive cells from the myeloid lineage occurs. The Philadelphia (Ph) chromosome is a CML genetic abnormality characteristic, and results from a reciprocal translocation between the long arms of chromosomes 9 and 22, generating a BCR‐ABL oncoprotein with constitutively activated tyrosine kinase activity [Druker et al., ].The development of tyrosine kinase inhibitors (TKIs) has revolutionized CML treatment because they are able to block cell proliferation of malignant clones by interfering with the interaction between a BCR‐ABL1 oncoprotein and adenosine triphosphate (ATP) [Jabbour and Kantarjian, ].Despite the success of TKIs for CML treatment, these drugs need to be monitored because of the occurrence of adverse events. Reports in the literature have described special situations with regard to TKI treatment safety. Some authors have reported the occurrence of cytogenetic changes in Ph– cells during treatment with imatinib and the presence of secondary disease that resembled myelodysplastic syndrome or acute myeloid leukemia has been observed in some patients [Medina et al., ; Loriaux and Deininger, ; Jabbour et al., ]. In another study, it was observed that stem cells from normal donors acquired post‐transplant cytogenetic changes during therapy with http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Environmental and Molecular Mutagenesis Wiley
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Publisher
Wiley Subscription Services, Inc., A Wiley Company
Copyright
© 2018 Wiley Periodicals, Inc.
ISSN
0893-6692
eISSN
1098-2280
D.O.I.
10.1002/em.22164
Publisher site
See Article on Publisher Site

Abstract

Dear Editor,Chronic myeloid leukemia (CML) is a clonal myeloproliferative disease in which proliferation of massive cells from the myeloid lineage occurs. The Philadelphia (Ph) chromosome is a CML genetic abnormality characteristic, and results from a reciprocal translocation between the long arms of chromosomes 9 and 22, generating a BCR‐ABL oncoprotein with constitutively activated tyrosine kinase activity [Druker et al., ].The development of tyrosine kinase inhibitors (TKIs) has revolutionized CML treatment because they are able to block cell proliferation of malignant clones by interfering with the interaction between a BCR‐ABL1 oncoprotein and adenosine triphosphate (ATP) [Jabbour and Kantarjian, ].Despite the success of TKIs for CML treatment, these drugs need to be monitored because of the occurrence of adverse events. Reports in the literature have described special situations with regard to TKI treatment safety. Some authors have reported the occurrence of cytogenetic changes in Ph– cells during treatment with imatinib and the presence of secondary disease that resembled myelodysplastic syndrome or acute myeloid leukemia has been observed in some patients [Medina et al., ; Loriaux and Deininger, ; Jabbour et al., ]. In another study, it was observed that stem cells from normal donors acquired post‐transplant cytogenetic changes during therapy with

Journal

Environmental and Molecular MutagenesisWiley

Published: Jan 1, 2018

References

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