Shimamoto T, Ohyashiki J H, Ohyashiki K, Kawakubo K, Inatomi Y, Fujieda H, Nakazawa S, Kimura N, Miyauchi J, Toyama K
First Department of Internal Medicine, Tokyo Medical College, Japan.
Cancer Genet Cytogenet. 1994 Mar;73(1):69-74. doi: 10.1016/0165-4608(94)90185-6.
Six patients with acute myeloid leukemia (AML) expressing CD7 antigen (CD7+ AML) were studied. They consisted of five patients with M1 and one with an M2 morphology. Two cases expressed other lymphoid-associated antigens, in addition to CD7. The complete remission rate was 50%. One patient had central nervous system recurrence. Cytogenetic analysis demonstrated normal karyotypes in all the cases. All but one had germline configurations of the T-cell receptor (TCR) genes and immunoglobulin heavy chain gene. However, all did not have detectable recombinase activating gene-1 activity by the RT-PCR technique. We performed colony formation assay in two patients, and no enhancement of colony formation by granulocyte colony-stimulating factor was noted. The results presented here, together with those reported previously, suggest that CD7+ AML may demonstrate lineage infidelity.
对6例表达CD7抗原的急性髓系白血病（AML）患者（CD7+ AML）进行了研究。其中包括5例M1型和1例M2型形态的患者。2例除CD7外还表达其他淋巴相关抗原。完全缓解率为50%。1例患者出现中枢神经系统复发。细胞遗传学分析显示所有病例核型均正常。除1例外，所有患者的T细胞受体（TCR）基因和免疫球蛋白重链基因均为种系构型。然而，通过逆转录聚合酶链反应（RT-PCR）技术，所有患者均未检测到重组激活基因-1活性。我们对2例患者进行了集落形成试验，未发现粒细胞集落刺激因子增强集落形成。本文呈现的结果以及先前报道的结果表明，CD7+ AML可能表现出谱系不忠实。
