Imatinib resistance in a novel translocation der(17)t(1;17)(q25;p13) with loss of TP53 but without BCR/ABL kinase domain mutation in chronic myelogenous leukemia
- 作者：Katsuya Yamamoto ; Kimikazu Yakushijin ; Shinichiro Nishikawa ; Kentaro Minagawa ; Yoshio Katayama ; Manabu Shimoyama ; Toshimitsu Matsui
- 关键词：Hydrodynamic instabilities ; Evans function ; Singular differential equations ; Weakly nonlinear solutions ; Semiclassical analysis ; Fluid mechanics
- 刊名：Cancer Genetics and Cytogenetics
- 出版年：2008
- 期刊代码：43_01654608
- 类别：med
- 出版时间：May 2008
- 卷：183
- 期：1
- 页码：77-81
- 文件大小：732 K
摘要
We describe here two novel translocations, t(7;14)(p22;q13) and der(17)t(1;17)(q25;p13), in a 41-year-old man with an accelerated phase (AP) of chronic myelogenous leukemia (CML). Chromosome analysis initially showed 46,XY,t(7;14)(p13;q22),t(9;22)(q34;q11.2)[20]. In 3 years, the karyotype evolved to 45,X,−Y,der(7)t(7;14)(p13;q22),t(9;22)(q34;q11.2),−14,der(17)t(1;17)(q25;p13),+der(22)t(9;22)[20], accompanied with a resistance to imatinib mesylate. The TP53 was deleted from the der(17)t(1;17)(q25;p13), but there was no mutation of TP53 in the remaining allele. Mutations in the BCR/ABL kinase domain could not be detected as well. Morphologically, dysplastic changes including pseudo-Pelger–Huët anomaly appeared in the bone marrow cells. These findings suggest that the t(7;14)(p22;q13) translocation had a crucial role in the progression to CML-AP, and that the resistance to imatinib may be due to the additional cytogenetic abnormalities, including der(17)t(1;17)(q25;p13), but not to BCR/ABL mutations.