Dastugue N, Kuhlein E, Duchayne E, Roubinet F, Bourrouillou G, Attal M, Pris J, Colombies P
Blood. 1986 Oct;68(4):949-53.
A blastic crisis of chronic myeloid leukemia without a detectable chronic phase is reported. At diagnosis, blast cells present t(9;22)(q34;q11),t(14;14)(q11;q32) translocations and early B cell phenotype (DR +, TdT +, B4 +, BA1 +, J5 +). At relapse, the malignant clone evolves to a biphenotypic expression, the initial markers remain unchanged, and two myeloid antigens (My 7, My 9) appear. The wide overlap in percentages of blast cells displaying lymphoid and myeloid markers shows that a single clone bears antigens of both lineages. Simultaneous occurrence of a t(14;14)(q11;q32) translocation, usually found in T cell malignancies, and of a B cell phenotype raises the question of the relationship between chromosomal changes and surface marker expression. The malignant cell is assumed to be a progenitor cell, already committed to lymphoid lineage and retaining the potential to switch to myeloid lineage.
报道了1例无明显慢性期的慢性髓性白血病急变期病例。诊断时，原始细胞存在t(9;22)(q34;q11)、t(14;14)(q11;q32)易位及早期B细胞表型（DR +、TdT +、B4 +、BA1 +、J5 +）。复发时，恶性克隆演变为双表型表达，初始标志物保持不变，并出现两种髓系抗原（My 7、My 9）。显示淋巴系和髓系标志物的原始细胞百分比有广泛重叠，表明单个克隆携带两个谱系的抗原。通常见于T细胞恶性肿瘤的t(14;14)(q11;q32)易位与B细胞表型同时出现，这就引发了染色体变化与表面标志物表达之间关系的问题。恶性细胞被认为是一种祖细胞，已定向于淋巴系，但仍保留向髓系转换的潜能。
