Elbaz O, Mahmoud L A
Hematology Unit, Faculty of Medicine, Almansoura University, Egypt.
Leuk Lymphoma. 1994 Jan;12(3-4):191-5. doi: 10.3109/10428199409059589.
Tumor necrosis factor (TNF) is a major regulator of AML growth in vitro and markedly enhances AML growth induced by GM-CSF/IL-3. TNF, on the other hand, suppresses the G-CSF stimulated AML cell proliferation and serves as a modulator of growth factor receptors on AML cells. It upregulates GM-CSF and IL-3 receptors by a mechanism which depends on new protein synthesis and downregulates G-CSF receptors by activation of protein kinase C (PCK). The leukemic cells from patients with acute or chronic leukemias have similar TNF receptor structures (MW 76 kD). Serum TNF levels increase in patients with both acute and chronic leukemias especially in those with advanced disease. The clinical application of TNF in association with GM-CSF or IL-3 may be of value for patients with AML.
肿瘤坏死因子（TNF）是急性髓系白血病（AML）体外生长的主要调节因子，能显著增强GM-CSF/IL-3诱导的AML生长。另一方面，TNF抑制G-CSF刺激的AML细胞增殖，并作为AML细胞上生长因子受体的调节剂。它通过一种依赖新蛋白质合成的机制上调GM-CSF和IL-3受体，并通过激活蛋白激酶C（PCK）下调G-CSF受体。急性或慢性白血病患者的白血病细胞具有相似的TNF受体结构（分子量76 kD）。急性和慢性白血病患者的血清TNF水平都会升高，尤其是晚期疾病患者。TNF与GM-CSF或IL-3联合应用对AML患者可能具有价值。
