Expression of the neural cell adhesion molecule CD56 is associated with short remission duration and survival in acute myeloid leukemia with t(8;21)(q22;q22)
Expression of the neural cell adhesion molecule CD56 is associated with short remission duration and survival in acute myeloid leukemia with t(8;21)(q22;q22)
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DOI：
10.1182/blood.v90.4.1643.1643_1643_1648
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发表时间：
1997-08-15
期刊：
影响因子：
20.3
通讯作者：
Bloomfield, CD
中科院分区：
文献类型：
--
作者：
Baer, MR;Stewart, CC;Bloomfield, CD
尽管 t(8;21) (q22;q22) 的急性髓系白血病 (AML) 与较高的完全缓解 (CR) 率和延长的无病生存期相关，但治疗结果并非普遍有利。识别预测治疗结果的因素可能有助于根据风险优化治疗。 t(8;21) 的 AML 具有独特的免疫表型，其特征是表达骨髓和干细胞抗原 CD13、CD15、CD34 和 HLADr，以及频繁表达 B 细胞抗原 CD19 和神经细胞粘附分子 CD56（一种自然杀伤细胞/干细胞抗原）。由于 CD56 表达与髓外白血病和多药耐药性相关，因此我们试图将 CD56 表达与 t(8;21) 的 AML 治疗结果相关联。作为成人 AML 前瞻性免疫表型研究 (CALGB 8361) 的一部分，通过多参数流式细胞术对 29 名接受癌症和白血病 B 组 (CALGB) 方案治疗的 t(8;21) 成人新发 AML 患者的预处理白血病细胞进行免疫表型分析。 CD56在16例（55%）中表达。 CD56 表达与年龄、性别、白细胞计数、粒细胞计数、其他细胞遗传学异常的存在或诊断时髓外疾病的存在之间没有相关性。对于有和没有 CD56 表达的病例，标准剂量阿糖胞苷和柔红霉素的 CR 率相似（88% vs 92%；P = 1.0）。 CR 后治疗包括至少一个疗程的大剂量阿糖胞苷，26 名达到 CR 的患者中有 24 名患者接受了至少一个疗程的高剂量阿糖胞苷治疗；在有和没有 CD56 表达的情况下，所施用的疗程数相似。尽管 CR 后治疗没有差异，但与不表达 CD56 的病例相比，有 CD56 表达的病例的 CR 持续时间显着缩短（中位为 8.7 个月 vs 未达到；P = .01），生存期也是如此（中位为 16.5 个月 vs 未达到；P = .008）。我们得出结论，t(8;21) AML 中 CD56 的表达与 CR 持续时间和生存期显着缩短相关。我们的结果表明 CD56 表达可能有助于对该 AML 亚型进行分层治疗。 (C) 1997 年，美国血液学会。
Although acute myeloid leukemia (AML) with t(8;21) (q22;q22) is associated with a high complete remission (CR) rate and prolonged disease-free survival, treatment outcome is not universally favorable. Identifying factors that predict for treatment outcome might allow therapy to be optimized based on risk. AML with t(8;21) has a distinctive immunophenotype, characterized by expression of the myeloid and stem cell antigens CD13, CD15, CD34, and HLADr, and frequent expression of the B-cell antigen CD19 and the neural cell adhesion molecule CD56, a natural killer cell/stem cell antigen. Because CD56 expression has been associated with both extramedullary leukemia and multidrug resistance, we sought to correlate CD56 expression with treatment outcome in AML with t(8;21). Pretreatment leukemia cells from 29 adult de novo AML patients with t(8;21) treated on Cancer and Leukemia Group B (CALGB) protocols were immunophenotyped by multiparameter flow cytometry as part of a prospective immunophenotyping study of adult AML (CALGB 8361). CD56 was expressed in 16 cases (55%). There was no correlation between CD56 expression and age, sex, white blood cell count, granulocyte count, the presence of additional cytogenetic abnormalities, or the presence of extramedullary disease at diagnosis. The CR rate to standard-dose cytarabine and daunorubicin was similar for cases with and without CD56 expression (88% v 92%; P = 1.0). Post-CR therapy included at least one course of high-dose cytarabine in 24 of 26 patients who achieved CR; numbers of courses administered were similar in cases with and without CD56 expression. Although post-CR therapy did not differ, CR duration was significantly shorter in cases with CD56 expression compared with those without (median, 8.7 months v not reached; P = .01), as was survival (median, 16.5 months v not reached; P = .008). We conclude that CD56 expression in AML with t(8;21) is associated with significantly shorter CR duration and survival. Our results suggest that CD56 expression may be useful in stratifying therapy for this subtype of AML. (C) 1997 by The American Society of Hematology.