Mutations Associated with Imatinib Mesylate Resistance - Review
Chronic myeloid leukemia (CML) arises from the fusion of the BCR and the ABL1 genes. The BCR gene (chromosome 22q11.2) and the ABL1 gene (chromosome 9q34) fuse together due to reciprocal chromosome translocation forming the Philadelphia chromosome (Ph). This fusion gene codes tyrosine kinase which a...
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| Format: | Article |
| Language: | English |
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Pensoft Publishers
2018-12-01
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| Series: | Folia Medica |
| Subjects: | |
| Online Access: | http://www.degruyter.com/view/j/folmed.2018.60.issue-4/folmed-2018-0030/folmed-2018-0030.xml?format=INT |
| _version_ | 1818753801112256512 |
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| author | Linev Alexandar J. Ivanov Hristo J. Zhelyazkov Ivan G. Ivanova Hristina Goranova-Marinova Veselina S. Stoyanova Vili K. |
| author_facet | Linev Alexandar J. Ivanov Hristo J. Zhelyazkov Ivan G. Ivanova Hristina Goranova-Marinova Veselina S. Stoyanova Vili K. |
| author_sort | Linev Alexandar J. |
| collection | DOAJ |
| description | Chronic myeloid leukemia (CML) arises from the fusion of the BCR and the ABL1 genes. The BCR gene (chromosome 22q11.2) and the ABL1 gene (chromosome 9q34) fuse together due to reciprocal chromosome translocation forming the Philadelphia chromosome (Ph). This fusion gene codes tyrosine kinase which accelerates the cell division and reduces DNA repair. Imatinib mesylate is a selective inhibitor of this tyrosine kinase. It is the first-line treatment for CML-patients. However, it became clear that Philadelphia-positive (Ph+) cells could evolve to elude inhibition due to point mutations within the BCR-ABL kinase domain. To date more than 40 mutations have been identified and their early detection is important for clinical treatment. With the development of the new tyrosine kinase inhibitors (TKIs), associated with these mutations, the resistance problem seems to diminish, as some of the new drugs are less prone to resistance. The aim of this review is to focus on the diff erent mutations leading to resistance. |
| first_indexed | 2024-12-18T05:13:07Z |
| format | Article |
| id | doaj.art-b0a482e743544a8d81485e915ee0ffc1 |
| institution | Directory Open Access Journal |
| issn | 1314-2143 |
| language | English |
| last_indexed | 2024-12-18T05:13:07Z |
| publishDate | 2018-12-01 |
| publisher | Pensoft Publishers |
| record_format | Article |
| series | Folia Medica |
| spelling | doaj.art-b0a482e743544a8d81485e915ee0ffc12022-12-21T21:19:50ZengPensoft PublishersFolia Medica1314-21432018-12-0160461762310.2478/folmed-2018-0030folmed-2018-0030Mutations Associated with Imatinib Mesylate Resistance - ReviewLinev Alexandar J.0Ivanov Hristo J.1Zhelyazkov Ivan G.2Ivanova Hristina3Goranova-Marinova Veselina S.4Stoyanova Vili K.5Department of Pediatrics and Medical Genetics, Medical University of Plovdiv, Plovdiv, BulgariaDepartment of Pediatrics and Medical Genetics, Medical University of Plovdiv, Plovdiv, BulgariaDepartment of Medical Genetics, St George University Hospital, Medical University of Plovdiv, Plovdiv, BulgariaFirst Department of Internal Diseases, Department of Hematology, Medical University of Plovdiv, Plovdiv, BulgariaFirst Department of Internal Diseases, Department of Hematology, Medical University of Plovdiv, Plovdiv, BulgariaDepartment of Pediatrics and Medical Genetics, Medical University of Plovdiv, Plovdiv, BulgariaChronic myeloid leukemia (CML) arises from the fusion of the BCR and the ABL1 genes. The BCR gene (chromosome 22q11.2) and the ABL1 gene (chromosome 9q34) fuse together due to reciprocal chromosome translocation forming the Philadelphia chromosome (Ph). This fusion gene codes tyrosine kinase which accelerates the cell division and reduces DNA repair. Imatinib mesylate is a selective inhibitor of this tyrosine kinase. It is the first-line treatment for CML-patients. However, it became clear that Philadelphia-positive (Ph+) cells could evolve to elude inhibition due to point mutations within the BCR-ABL kinase domain. To date more than 40 mutations have been identified and their early detection is important for clinical treatment. With the development of the new tyrosine kinase inhibitors (TKIs), associated with these mutations, the resistance problem seems to diminish, as some of the new drugs are less prone to resistance. The aim of this review is to focus on the diff erent mutations leading to resistance.http://www.degruyter.com/view/j/folmed.2018.60.issue-4/folmed-2018-0030/folmed-2018-0030.xml?format=INTchronic myeloid leukemiaBCR-ABLpoint mutationimatinib resistance |
| spellingShingle | Linev Alexandar J. Ivanov Hristo J. Zhelyazkov Ivan G. Ivanova Hristina Goranova-Marinova Veselina S. Stoyanova Vili K. Mutations Associated with Imatinib Mesylate Resistance - Review Folia Medica chronic myeloid leukemia BCR-ABL point mutation imatinib resistance |
| title | Mutations Associated with Imatinib Mesylate Resistance - Review |
| title_full | Mutations Associated with Imatinib Mesylate Resistance - Review |
| title_fullStr | Mutations Associated with Imatinib Mesylate Resistance - Review |
| title_full_unstemmed | Mutations Associated with Imatinib Mesylate Resistance - Review |
| title_short | Mutations Associated with Imatinib Mesylate Resistance - Review |
| title_sort | mutations associated with imatinib mesylate resistance review |
| topic | chronic myeloid leukemia BCR-ABL point mutation imatinib resistance |
| url | http://www.degruyter.com/view/j/folmed.2018.60.issue-4/folmed-2018-0030/folmed-2018-0030.xml?format=INT |
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