Goda H, Abe Y, Yufu Y, Muta K, Katsuno M, Goto T, Sadamura S, Nishimura J, Nawata H, Hirata J
Third Department of Internal Medicine, Faculty of Medicine, Kyushu University.
Rinsho Ketsueki. 1992 Aug;33(8):1046-51.
A 27-year-old male with systemic lymphadenopathy was diagnosed as lymphoblastic-type lymphoma by inguinal lymph node biopsy in September, 1990. Bone marrow at the initial diagnosis contained 55.4% lymphoblasts with a phenotype of peroxidase (-), CD7 (+), CD4 (-), CD8 (-). Lymphadenopathy and lymphoblasts in bone marrow disappeared after MACOP-B therapy. In December, 1990, however, the patient again noticed swelling of cervical lymph nodes. At this time, the bone marrow contained 36.4% myeloblasts with a peroxidase (+), CD7 (+), CD13 (+), CD33 (+) phenotype. Cytogenetic and genetic study revealed that the lymphoblasts at the initial diagnosis and the myeloblasts at relapse shared an common abnormal karyotype, 11p-, and the same rearranged band of T-cell receptor delta, gamma, beta genes, suggesting that these two blasts originated from the same clone. The blasts obtained from the cervical lymph node at relapse were still negative for peroxidase, in contrast to the blasts from bone marrow. These findings suggest that this leukemia originated from a stem cell and differentiated along multilineage pathways.
一名27岁男性，有全身淋巴结肿大，1990年9月经腹股沟淋巴结活检诊断为淋巴母细胞型淋巴瘤。初诊时骨髓中淋巴母细胞占55.4%，其表型为过氧化物酶（-）、CD7（+）、CD4（-）、CD8（-）。经MACOP - B方案治疗后，淋巴结肿大及骨髓中的淋巴母细胞消失。然而，1990年12月，患者再次发现颈部淋巴结肿大。此时，骨髓中原始粒细胞占36.4%，其表型为过氧化物酶（+）、CD7（+）、CD13（+）、CD33（+）。细胞遗传学和基因研究显示，初诊时的淋巴母细胞与复发时的原始粒细胞具有相同的异常核型11p-，以及相同的T细胞受体δ、γ、β基因重排带，提示这两种母细胞起源于同一克隆。与骨髓中的母细胞不同，复发时从颈部淋巴结获取的母细胞过氧化物酶仍为阴性。这些发现提示，这种白血病起源于干细胞，并沿多系途径分化。
