Schuh A C, Sutherland D R, Horsfall W, Mills G B, Dube I, Baker M A, Siminovitch K, Bailey D, Keating A
Oncology Research, Toronto Hospital, Ontario.
Leukemia. 1990 Sep;4(9):631-6.
Until recently, T cells were believed not to be involved in chronic myeloid leukemia. We describe an example of CML in T lymphoblastic crisis with massive generalized lymphadenopathy in which the blasts were CD2(+), CD5(+), and CD7(+), variably CD1(+) and CD3(+), and both responded to and could be induced to produce the T cell growth factor, interleukin-2. Additionally, the blasts were shown to contain the CML-related tyrosine kinase P210bcr-abl rather than the smaller kinase associated with Ph1(+) ALL. Finally, the participation of the T lymphoid lineage in the CML clone was proven by the presence of the same BCR rearrangement in blasts as in granulocytes, suggesting the existence of a bone marrow progenitor common to the T cell and myeloid lineages.
直到最近,人们一直认为T细胞不参与慢性髓性白血病。我们描述了一例慢性髓性白血病处于T淋巴细胞母细胞危象并伴有广泛淋巴结肿大的病例,其中母细胞为CD2(+)、CD5(+)和CD7(+),CD1(+)和CD3(+)表达可变,且既对T细胞生长因子白细胞介素-2有反应又能被诱导产生该因子。此外,母细胞被证明含有与慢性髓性白血病相关的酪氨酸激酶P210bcr-abl,而非与Ph1(+)急性淋巴细胞白血病相关的较小激酶。最后,通过母细胞与粒细胞中存在相同的BCR重排,证实了T淋巴细胞系参与了慢性髓性白血病克隆,这表明存在一个T细胞系和髓细胞系共有的骨髓祖细胞。