作者
Hideki Makishima, Anna M Jankowska, Michael A McDevitt, Christine O'Keefe, Simon Dujardin, Heather Cazzolli, Bartlomiej Przychodzen, Courtney Prince, John Nicoll, Harish Siddaiah, Mohammed Shaik, Hadrian Szpurka, Eric Hsi, Anjali Advani, Ronald Paquette, Jaroslaw P Maciejewski
发表日期
2011/5/26
期刊
Blood, The Journal of the American Society of Hematology
卷号
117
期号
21
页码范围
e198-e206
出版商
American Society of Hematology
简介
Progression of chronic myelogenous leukemia (CML) to accelerated (AP) and blast phase (BP) is because of secondary molecular events, as well as additional cytogenetic abnormalities. On the basis of the detection of JAK2, CBL, CBLB, TET2, ASXL1, and IDH1/2 mutations in myelodysplastic/myeloproliferative neoplasms, we hypothesized that they may also contribute to progression in CML. We screened these genes for mutations in 54 cases with CML (14 with chronic phase, 14 with AP, 20 with myeloid, and 6 with nonmyeloid BP). We identified 1 CBLB and 2 TET2 mutations in AP, and 1 CBL, 1 CBLB, 4 TET2, 2 ASXL1, and 2 IDH family mutations in myeloid BP. However, none of these mutations were found in chronic phase. No cases with JAK2V617F mutations were found. In 2 cases, TET2 mutations were found concomitant with CBLB mutations. By single nucleotide polymorphism arrays, uniparental …
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