Eren Rafet, Aslan Ceyda, Yokuş Osman, Doğu Mehmet Hilmi, Suyani Elif
Department of Hematology, Istanbul Training and Research Hospital, Fatih, 34098 Istanbul, Turkey.
Mol Clin Oncol. 2016 Aug;5(2):331-332. doi: 10.3892/mco.2016.927. Epub 2016 Jun 13.
T-cell acute lymphoblastic leukemia (ALL) is an aggressive hematological malignancy, accounting for ~25% of all adult cases of ALL. We herein report a case of T-cell ALL exhibiting aberrant CD34, CD56, CD33 and CD117 expression in addition to T-cell markers, which did not respond to induction treatment. A 55-year-old woman was admitted to our hospital with a sore throat unresponsive to medication for 1 month. The laboratory examination revealed pancytopenia and the peripheral blood smear examination revealed blast cells. On flow cytometric analysis, the blast cells were found to be positive for cytoplasmic CD3, CD2, CD5, CD7, CD34, CD56, CD33 and CD117, and negative for myeloperoxidase, CD13, CD11b, CD15, CD19, CD79a, CD22 and CD10. The patient was diagnosed with T-cell ALL according to the 2008 World Health Organisation classification. The patient did not respond to Hyper-cyclophosphamide, vincristine, adriamycin and dexamethasone (CVAD) course A treatment and succumbed to the disease during Hyper-CVAD course B treatment. To the best of our knowledge, this is the first report of aberrant co-expression of the natural killer cell marker CD56, myeloid cell markers CD117 and CD33 and stem cell marker CD34 in a patient with T-cell ALL. This appears to be associated with an unfavorable outcome, despite the use of intensive chemotherapy.
T细胞急性淋巴细胞白血病(ALL)是一种侵袭性血液系统恶性肿瘤,约占所有成人ALL病例的25%。我们在此报告一例T细胞ALL病例,该病例除表达T细胞标志物外,还异常表达CD34、CD56、CD33和CD117,对诱导治疗无反应。一名55岁女性因咽痛1个月,药物治疗无效而入住我院。实验室检查显示全血细胞减少,外周血涂片检查发现原始细胞。流式细胞术分析显示,原始细胞胞质CD3、CD2、CD5、CD7、CD34、CD56、CD33和CD117呈阳性,髓过氧化物酶、CD13、CD11b、CD15、CD19、CD79a、CD22和CD10呈阴性。根据2008年世界卫生组织分类,该患者被诊断为T细胞ALL。患者对环磷酰胺、长春新碱、阿霉素和地塞米松(CVAD)方案A治疗无反应,在CVAD方案B治疗期间死于该病。据我们所知,这是首例T细胞ALL患者异常共表达自然杀伤细胞标志物CD56、髓系细胞标志物CD117和CD33以及干细胞标志物CD34的报告。尽管使用了强化化疗,但这似乎与不良预后相关。