The Role of JAK2 Gene in Imatinib-Resistant Chronic Myeloid Leukemia: A Review
Indra Wijaya, Kevin Yonatan Budiman, Muhammad Hasan Bashari, Lelani Reniarti, Rully Marsis Amirullah Roesli
Chronic myeloid leukemia (CML) is still an incurable disease. Despite the effective treatment with commercially available tyrosine kinase inhibitors (TKIs), CML is still of interest to many researchers worldwide. Imatinib was the first available TKI and is still the gold standard for CML therapy worldwide. Recently, there is growing evidence of imatinib-resistant CML. Researchers have hypothesized various extrinsic factors that could contribute to imatinib-resistant CML. Among such suspected factors, the dysregulation of the Janus-kinase-2 (JAK2) gene has been the subject of research by several groups to reveal its role in CML. Trials of treatment with JAK2 inhibitors in patients with CML, who have JAK2 gene mutations, show a relatively good therapeutic response, but to date, the role of the JAK2 gene in CML is still being debated due to different studies results. In this review, controversies about the JAK2 gene in the imatinib-resistant CML and the recent clinical trials with JAK2 inhibitor are discussed.