尼罗替尼
博舒替尼
达沙替尼
酪氨酸激酶
伊马替尼
帕纳替尼
医学
原癌基因酪氨酸蛋白激酶Src
酪氨酸激酶抑制剂
髓系白血病
癌症研究
甲磺酸伊马替尼
药理学
血小板源性生长因子受体
内科学
生物信息学
生物
受体
癌症
生长因子
作者
Massimo Breccia,Matteo Molica,Giuliana Alimena
标识
DOI:10.1016/j.leukres.2014.09.016
摘要
Tyrosine kinase inhibitors (TKIs) advent has deeply changed the outcome of chronic myeloid leukemia (CML) patients, with improved rates of response and overall survival. However, for this success some patients paid the price of a number of peculiar side effects, the so-called off-target side effects, specific for each one TKI. These effects are due to non-selective inhibition of other tyrosine kinase receptors, such as PDGFR, c-KIT, Src, VEGF. Consequences of this inhibition, some metabolic changes during the treatment with TKIs are reported. Aim of present review is to report metabolic changes and potential mechanisms involved in the pathogenesis related to imatinib, second (nilotinib and dasatinib) and third generation (bosutinib and ponatinib) TKIs.
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