t(7;11)(p15;p15) 慢性髓性白血病进展为原始细胞转化，显示一种新的NUP98/HOXA11融合。

t(7;11)(p15;p15) Chronic myeloid leukaemia developed into blastic transformation showing a novel NUP98/HOXA11 fusion.

作者信息

Suzuki Akitaka, Ito Yoshikazu, Sashida Goro, Honda Seiko, Katagiri Tomoko, Fujino Takashi, Nakamura Takuro, Ohyashiki Kazuma

机构信息

First Department of Internal Medicine, Tokyo Medical University, Japan.

出版信息

Br J Haematol. 2002 Jan;116(1):170-2. doi: 10.1046/j.1365-2141.2002.03246.x.

DOI:10.1046/j.1365-2141.2002.03246.x

PMID:11841413

Abstract

We encountered a patient with Philadelphia-negative chronic myeloid leukaemia, with t(7;11)(p15;p15), in whom acute leukaemia phase (acute myeloid leukaemia-M2 morphology) developed within a short period. We detected a novel gene fusion between NUP98 and HOXA11 both in the chronic phase and in the acute leukaemia phase in this case. Although it is well known that a fusion of NUP98-HOXA9 in myeloid malignancies is created by the t(7;11)(p15;p15), this case suggests the possibility that HOXA11 might be another partner gene for NUP98 in t(7;11)(p15;p15) leukaemia.

摘要

我们遇到一名费城染色体阴性的慢性髓性白血病患者，其核型为t(7;11)(p15;p15)，该患者在短时间内进展为急性白血病期（急性髓性白血病-M2形态）。在该病例的慢性期和急性白血病期，我们均检测到一种新的NUP98与HOXA11基因融合。虽然已知在髓系恶性肿瘤中，t(7;11)(p15;p15)会导致NUP98-HOXA9融合，但该病例提示，在t(7;11)(p15;p15)白血病中，HOXA11可能是NUP98的另一个伙伴基因。