Am J Blood Res 2013;3(3):191-200
Review Article
Changes in molecular biology of chronic myeloid leukemia in tyrosine kinase
inhibitor era
Melda Comert, Yusuf Baran, Guray Saydam
Department of Hematology, Medical School, Ege University, Izmir, Turkey; Department of Molecular Biology and Genetics, Izmir
Institute of Technology, Urla, Izmir, Turkey
Received July 11, 2013; Accepted August 7, 2013; Epub August 19, 2013; Published August 30, 2013
Abstract: Chronic myeloid leukemia (CML) is a clonal myeloproliferative disease characterized by a reciprocal translocation
between long arms of chromosomes 9 and 22 t(9;22) that generates the BCR-ABL fusion gene. If left untreated, newly
diagnosed chronic phase CML patients finally progress to accelerated and blastic phase. After the introduction of tyrosine
kinase inhibitors (TKIs), treatment strategies of CML changed dramatically. However, the development of resistance to TKIs
started to create problems over time. In this review, the current information about CML biology before and after imatinib
mesylate treatment is summarized. (AJBR1307001).
Keywords: Chronic myeloid leukemia, moleculer biology, imatinib mesylate
Address correspondence to: Dr. Yusuf Baran, Department of Molecular Biology and Genetics, Science Faculty, Izmir Institute
of Technology, Urla, 35430, Izmir, Turkey. Tel: +90 232 7507315; Fax: +90 232 7507302; E-mail: yusufbaran@iyte.edu.tr; Dr.
Guray Saydam, Department of Hematology, Medical School, Ege University, 35100, Bornova, Izmir, Turkey. Tel: +90 232
3903530; Fax: +90 232 3903530; E-mail: guray.saydam@ege.edu.tr
Review Article
Changes in molecular biology of chronic myeloid leukemia in tyrosine kinase
inhibitor era
Melda Comert, Yusuf Baran, Guray Saydam
Department of Hematology, Medical School, Ege University, Izmir, Turkey; Department of Molecular Biology and Genetics, Izmir
Institute of Technology, Urla, Izmir, Turkey
Received July 11, 2013; Accepted August 7, 2013; Epub August 19, 2013; Published August 30, 2013
Abstract: Chronic myeloid leukemia (CML) is a clonal myeloproliferative disease characterized by a reciprocal translocation
between long arms of chromosomes 9 and 22 t(9;22) that generates the BCR-ABL fusion gene. If left untreated, newly
diagnosed chronic phase CML patients finally progress to accelerated and blastic phase. After the introduction of tyrosine
kinase inhibitors (TKIs), treatment strategies of CML changed dramatically. However, the development of resistance to TKIs
started to create problems over time. In this review, the current information about CML biology before and after imatinib
mesylate treatment is summarized. (AJBR1307001).
Keywords: Chronic myeloid leukemia, moleculer biology, imatinib mesylate
Address correspondence to: Dr. Yusuf Baran, Department of Molecular Biology and Genetics, Science Faculty, Izmir Institute
of Technology, Urla, 35430, Izmir, Turkey. Tel: +90 232 7507315; Fax: +90 232 7507302; E-mail: yusufbaran@iyte.edu.tr; Dr.
Guray Saydam, Department of Hematology, Medical School, Ege University, 35100, Bornova, Izmir, Turkey. Tel: +90 232
3903530; Fax: +90 232 3903530; E-mail: guray.saydam@ege.edu.tr
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