Open AccessImatinib resistance was reversed by nilotinib in the acute transformation of chronic myeloid leukemia: A case report
Author(s) -
Xiao Meng,
Zhou Hongjing,
Li Shuguo,
Xin Chunlei,
Zhao Tongfeng,
Hao Yunliang,
Li Shumei,
Liang Yanyan
Publication year - 2017
Publication title -
precision radiation oncology
Language(s) - English
Resource type - Journals
ISSN - 2398-7324
DOI - 10.1002/pro6.31
Subject(s) - nilotinib , imatinib , myeloid leukemia , cancer research , tyrosine kinase inhibitor , philadelphia chromosome , tyrosine kinase , medicine , fusion gene , dasatinib , oncology , immunology , biology , chromosomal translocation , genetics , gene , cancer , receptor
Abstract Chronic myeloid leukemia (CML) is a clonal malignant hematopoietic disorder that arises in a hematopoietic stem cell. Its characteristic cytogenetic abnormality is an abnormal chromosome 22 called the Philadelphia (Ph) chromosome. The BCR ‐ ABL1 fusion gene in this chromosome can encode a tyrosine protein kinase and is the molecular basis of CML pathogenesis. The tyrosine kinase inhibitor (TKI) imatinib is the ‘gold standard’ therapy for the treatment of CML. However, around 30% of the patients develop imatinib resistance. In this report, we will illustrate a case of an adult female with acute transformation of CML whose imatinib resistance was reversed by nilotinib and has had a long‐term survival.