ALK activation by the CLTC-ALK fusion is a recurrent event in large B-cell lymphoma
ALK activation by the CLTC-ALK fusion is a recurrent event in large B-cell lymphoma
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DOI：
10.1182/blood-2003-04-1050
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发表时间：
2003-10-01
期刊：
影响因子：
20.3
通讯作者：
Wlodarska, I
中科院分区：
文献类型：
--
作者：
De Paepe, P;Baens, M;Wlodarska, I
我们报告了3例大B细胞淋巴瘤（LBCL）伴间变性淋巴瘤激酶（ALK）颗粒状胞浆染色。所有病例在形态学和免疫组化上表现出惊人的相似之处，其特征在于大量的CD 20（-）/CD 138（+）浆母细胞样细胞的单态性增殖。其中1例最初诊断为空型间变性大细胞淋巴瘤（ALCL），B细胞表型仅在复发时才变得明显。荧光原位杂交（FISH）和分子研究导致在所有3例病例中检测到CLTC-ALK重排，没有任何全长ALK受体表达的证据。2例染色体核型为t（2;17）（p23;q23）。尽管之前在ALK阳性T-/null细胞ALCL和炎性肌纤维母细胞瘤中发现了类似的CLTC-ALK畸变，但其与ALK阳性LBCL的相关性似乎具有特异性且令人感兴趣。(C)2003年，美国血液学会。
We present 3 cases of large B-cell lymphoma (LBCL) with a granular cytoplasmic staining for anaplastic lymphoma kinase (ALK). All of the cases showed striking similarities in morphology and immunohistochemical profile characterized by a massive monomorphic proliferation of CD20(-)/CD138(+) plasmablast-like cells. In one of the cases, initially diagnosed as a null-type anaplastic large cell lymphoma (ALCL), the B-cell phenotype became evident only at recurrence. Fluorescent in situ hybridization (FISH) and molecular studies led to the detection of a CLTC-ALK rearrangement in all 3 cases, without any evidence of full-length ALK receptor expression. The associated t(2;17)(p23;q23) was demonstrated in the karyotype of 2 cases. Although a similar CLTC-ALK aberration was previously identified in ALK-positive T-/null cell ALCL and inflammatory myofibroblastic tumor, its association with ALK-positive LBCL seems to be specific and intriguing. (C) 2003 by The American Society of Hematology.