Genetics and tyrosine kinase inhibitors of chronic myeloid leukemia

被引:1
作者
Ganguly, Bani Bandana [1 ,2 ]
Kadam, Nitin N. [2 ]
机构
[1] MGM New Bombay Hosp, MGM Ctr Genet Res & Diag, Vashi Sect 3, Navi Mumbai 400703, India
[2] MGM Inst Hlth Sci, Navi Mumbai, India
来源
NUCLEUS-INDIA | 2019年 / 62卷 / 02期
关键词
Chronic myeloid leukemia; BCR-ABL domain mutations; Complex karyotype; Tyrosine kinase inhibitors; BCR-ABL; IMATINIB RESISTANCE; CYTOGENETIC RESPONSES; STRUCTURAL MECHANISM; CLINICAL RESISTANCE; SYNTHETIC LETHALITY; ANTITUMOR-ACTIVITY; TARGETED THERAPY; OCT-1; ACTIVITY; FOLLOW-UP;
D O I
10.1007/s13237-019-00271-6
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Chronic myeloid leukemia (CML) is caused by a reciprocal translocation between 9q34 and 22q11, which produces a chimeric BCR-ABL oncogene located on the Philadelphia chromosome i.e. rearranged 22. The fusion gene implicates in the overexpression of tyrosine kinase through binding with ATP in signal transduction. Therefore, targeted drug development aimed at inhibitors of tyrosine kinase (TKI) and formulated imatinib, which resulted in miraculous disease free survival in majority of the CML patients. However, drug-resistance remained a problem due mainly to emergence of missense point mutations in and around the BCR-ABL kinase domain. Loss of its sensitivity to leukemic stem cells guided development of altered TKIs such as dasatinib, nilotinib, bosutinib and ponatinib-each having specific sensitivity to different amino acid residues (T315I, Y253F/H, E255K/V, M351T, G250E, F359C/V, H396R/P, M244V, E355G, F317L, M237I, Q252H/R, D276G, L248V, F486S), have been implicated in similar to 85% of CML. At chromosomal level, trisomy 8, isochromosome 17q, amplification of the Philadelphia chromosome, additional translocations and complex karyotype are described in TKI-resistant CML. Therefore, mutational events at kinase domain and additional chromosome abnormalities could be considered for development and initiation of TKI-therapy, and cross-talk of complex mutations could lead to formulation of personalized TKI.
引用
收藏
页码:155 / 164
页数:10
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