Nair C, Chopra H, Shinde S, Barbhaya S, Kumar A, Dhond S, Yejamanam B, Sapre R, Chougule A, Advani S
Department of Medical Oncology, Tata Memorial Hospital, Parel, Bombay, India.
Leuk Lymphoma. 1995 Oct;19(3-4):309-13. doi: 10.3109/10428199509107903.
Thirty-four patients with chronic myeloid leukemia in blast crisis (CML-BC) were evaluated for lineage differentiation with immunological markers and the presence of ultrastructural peroxidase. Eighteen (52.9%) were found to have myeloid blast crisis. Cytochemically, myeloperoxidase (MPO) could be detected only in six patients on light microscopy while in the remaining 12 patients, myeloid differentiation was confirmed only by demonstration of MPO either at ultrastructural level or by the reactivity with anti myeloperoxidase (anti MPO) antibody. Six (17.6%) had lymphoid blast crisis as identified by lymphoid specific markers (CD19; CD10; CD7; CD4) along with the absence of myeloid markers. Heterogenous blast cell populations with mixed lineage differentiation were seen in 4 (11.7%) patients. These cases showed both lymphoid (CD19, CD10) and myeloid (anti MPO and ultrastructural MPO) characteristics. A single case of megakaryoblastic blast crisis was identified with positivity for CD41 and CD42 along with the presence of platelet peroxidase at the ultrastructural level. Five cases (14%) of CML blast crisis remained unclassifiable. These results suggest that blast crisis in CML show an arrest of differentiation at an early stage when compared to de novo acute leukemias. This is particularly evident from the fact that MPO could only be demonstrated ultrastructurally or with anti MPO antibody in the majority of patients with myeloid differentiation. It is expected that utilisation of molecular studies including immunoglobulin and T-cell receptor gene rearrangement and m-RNA expression for myeloperoxidase will provide a better insight into the level of differentiation for the presently unclassifiable cases of CML-blast crisis.
对34例急变期慢性髓性白血病(CML-BC)患者进行了免疫标记谱系分化及超微结构过氧化物酶检测评估。发现18例(52.9%)为髓系急变期。细胞化学方面,光镜下仅在6例患者中检测到髓过氧化物酶(MPO),而在其余12例患者中,仅通过超微结构水平显示MPO或与抗髓过氧化物酶(抗MPO)抗体反应来确认髓系分化。6例(17.6%)通过淋巴系特异性标记物(CD19、CD10、CD7、CD4)以及髓系标记物缺失确定为淋巴系急变期。4例(11.7%)患者可见具有混合谱系分化的异质性原始细胞群体。这些病例同时显示淋巴系(CD19、CD10)和髓系(抗MPO和超微结构MPO)特征。通过CD41和CD42阳性以及超微结构水平存在血小板过氧化物酶确定1例巨核细胞系急变期。5例(14%)CML急变期患者仍无法分类。这些结果表明,与原发性急性白血病相比,CML急变期在早期出现分化停滞。这从以下事实尤其明显可见:在大多数具有髓系分化的患者中,MPO仅能在超微结构水平或用抗MPO抗体显示。预计利用包括免疫球蛋白和T细胞受体基因重排以及髓过氧化物酶的mRNA表达等分子研究,将能更好地洞察目前无法分类的CML急变期病例的分化水平。