Detection of the STAT5B–RARA fusion transcript in acute promyelocytic leukemia with the normal chromosome 17 on G‐banding
Detection of the STAT5B–RARA fusion transcript in acute promyelocytic leukemia with the normal chromosome 17 on G‐banding
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DOI：
10.1111/j.1600-0609.2008.01042.x
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发表时间：
2008-05
影响因子：
3.1
通讯作者：
Manabu Kusakabe;K. Suzukawa;T. Nanmoku;N. Obara;Y. Okoshi;H. Mukai;Y. Hasegawa;H. Kojima;Y. Kawakami;H. Ninomiya;T. Nagasawa
中科院分区：
文献类型：
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作者：
Manabu Kusakabe;K. Suzukawa;T. Nanmoku;N. Obara;Y. Okoshi;H. Mukai;Y. Hasegawa;H. Kojima;Y. Kawakami;H. Ninomiya;T. Nagasawa
急性早幼粒细胞白血病（APL）以17q21染色体重排为特征，导致编码视黄酸受体α (RARA)的基因与许多替代伴侣基因融合。信号换能器和转录激活因子5 β (STAT5B)是可选的伙伴之一。我们报道了一例罕见的APL患者具有STAT5B-RARA融合转录物和正常的17号染色体G -带。所有反式维甲酸的施用改善了弥散性血管内凝血，但未减少外周血和骨髓中的白血病细胞。基于基因组数据库的数据，探讨了STAT5B与RARA通过染色体重排融合的分子机制。本文还讨论了伴有STAT5B-RARA的APL的临床特点。
Acute promyelocytic leukemia (APL) is characterized by chromosomal rearrangements of 17q21, leading to fusion of the gene‐encoding retinoic acid receptor alpha (RARA) with a number of alternative partner genes. Signal transducer and activator of transcription 5 beta (STAT5B) is one of the alternative partners. We report a rare case of APL with STAT5B–RARA fusion transcript and the normal chromosome 17 on G‐banding. Administration of all trans‐retinoic acid improved disseminated intravascular coagulation without decrease of the leukemia cells in his peripheral blood and bone marrow. The molecular mechanism of fusion between STAT5B and RARA by chromosomal rearrangement is discussed based on the data from genome database. Clinical characteristics of APL with STAT5B–RARA are also discussed.