TUMOR-NECROSIS-FACTOR AND HUMAN ACUTE-LEUKEMIA

被引：14

作者：

ELBAZ, O

MAHMOUD, LA

机构：

[1] Hematology Unit, Faculty of Medicine, Almansoura University, Almansoura

来源：

LEUKEMIA & LYMPHOMA | 1994年 / 12卷 / 3-4期

关键词：

TNF; AML; GM-CSF; G-CSF; IL-3; RECEPTORS;

D O I：

10.3109/10428199409059589

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：191 / 195

页数：5

共 38 条

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