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急性髓细胞白血病复发持续四年。白血病细胞产生集落刺激活性且不产生白血病相关抑制因子。

Relapse of acute myeloblastic leukemia lasting for four years. Production by leukemic cells of colony-stimulating activity and non-production of leukemia-associated inhibitor.

作者信息

Giannoulis N, Reizenstein P, Ost A

出版信息

Acta Med Scand. 1981;210(1-2):139-43.

PMID:6945794
Abstract

A 36-year-old woman with acute myeloblastic leukemia (M2) achieved complete remission in Feb. 1973, after ten weeks of chemotherapy with rubidomycin-cytosine arabinoside. She received weekly immunotherapy with bacillus Calmette-Guerin and allogeneic non-irradiated blast cells and monthly chemotherapy with thioguanine-cytosine arabinoside as maintenance. The bone marrow remained normocellular for 20 months. A first relapse occurred after this period. A second remission was achieved by seven courses of different cytostatic combinations. A second relapse, refractory to all cytostatic combinations tried, occurred in June 1976. She was thereafter in relapse until her death in July 1980. Autopsy showed extensive leukemic infiltration in bone marrow, liver, spleen, pericardium, stomach, and lymph nodes. Cytochemistry, surface markers, the capacity to stimulate lymphocytes, the in vitro growth pattern (colony-forming unit culture) of bone marrow and biochemical analyses did not give any remarkable results. In contrast, the peripheral blood cells produced a normal amount of colony-stimulating activity, which is significantly more than that produced by the blood from other leukemia patients. In liquid culture, the peripheral blood cells from this patient also seemed to live longer and mature more than cells from other leukemia patients. Finally, the peripheral leukemic cells from this patient seemed to produce far less leukemia-associated stem cell inhibitor than cells from other leukemia patients. The normal colony-stimulating activity production by leukemic cells and the absence of leukemia-associated stem cell inhibitor may therefore explain the long survival of this patient in relapse.

摘要

一名36岁的急性髓细胞白血病(M2型)女性患者,在接受柔红霉素 - 阿糖胞苷化疗十周后,于1973年2月实现完全缓解。她接受了每周一次的卡介苗和异体未照射原始细胞免疫治疗,以及每月一次的硫鸟嘌呤 - 阿糖胞苷化疗作为维持治疗。骨髓在20个月内保持正常细胞状态。在此期间后首次复发。通过七个疗程的不同细胞抑制剂组合实现了第二次缓解。1976年6月出现第二次复发,对所有尝试的细胞抑制剂组合均耐药。此后她一直处于复发状态,直至1980年7月去世。尸检显示骨髓、肝脏、脾脏、心包、胃和淋巴结有广泛的白血病浸润。细胞化学、表面标志物、刺激淋巴细胞的能力、骨髓的体外生长模式(集落形成单位培养)和生化分析均未得出任何显著结果。相比之下,外周血细胞产生的集落刺激活性正常,明显高于其他白血病患者血液产生的集落刺激活性。在液体培养中,该患者的外周血细胞似乎比其他白血病患者的细胞存活时间更长且成熟度更高。最后,该患者的外周白血病细胞产生的白血病相关干细胞抑制剂似乎比其他白血病患者的细胞少得多。因此,白血病细胞产生正常的集落刺激活性以及缺乏白血病相关干细胞抑制剂可能解释了该患者复发后存活时间较长的原因。

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