Tumor necrosis factor and human acute leukemia.
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.
Elbaz
O
O
Hematology Unit, Faculty of Medicine, Almansoura University, Egypt.
Mahmoud
L A
LA
D000208:Acute Disease; D002455:Cell Division / Q000187:drug effects; D015536:Down-Regulation; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology; D006801:Humans; D007377:Interleukin-3 / Q000494:pharmacology; D007951:Leukemia, Myeloid / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D016188:Receptors, Granulocyte Colony-Stimulating Factor / Q000378:metabolism; D016187:Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / Q000378:metabolism; D016185:Receptors, Interleukin-3 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology / Q000502:physiology*
D007377:Interleukin-3; D016188:Receptors, Granulocyte Colony-Stimulating Factor; D016187:Receptors, Granulocyte-Macrophage Colony-Stimulating Factor; D016185:Receptors, Interleukin-3; D014409:Tumor Necrosis Factor-alpha; D016179:Granulocyte Colony-Stimulating Factor; D016178:Granulocyte-Macrophage Colony-Stimulating Factor