scholarly journals Acidic isoferritins (leukemia-associated inhibitory activity) fail to inhibit blast proliferation in acute myelogenous leukemia

Blood ◽  
1981 ◽  
Vol 58 (3) ◽  
pp. 653-657 ◽  
Author(s):  
R Taetle
Keyword(s):  
Inhibitory Activity ◽  
Acute Myelogenous Leukemia ◽  
Blood Cells ◽  
Leukemia Cell ◽  
S Phase ◽  
Myelogenous Leukemia ◽  
Leukemia Cell Line ◽  
Acute Myelogenous ◽  
Blast Cells ◽  
Leukemic Clone

Abstract Cell-free extracts of bone marrow and blood cells from patients with leukemia contain an inhibitor of normal granulocyte/macrophage progenitor (CFU-GM) proliferation (leukemia-associated inhibitory activity, LIA) identified as acidic isoferritins. A comparison was made of the action of crude LIA prepared from frozen-thawed leukemic blood cells and purified spleen ferritin from a patient with chronic myelogenous leukemia, on the proliferation of blast progenitors from patients with acute myelogenous leukemia (AML), and on the promyelocytic leukemia cell line, HL-60. Crude LIA showed no inhibition of blast progenitor or HL-60 proliferation at low concentrations, but inhibited the proliferation of CFU-GM. At higher concentrations, crude LIA inhibited both blast cells and CFU-GM. Purified spleen ferritin failed to inhibit blast progenitors or HL-60 cells at any concentration tested, but inhibited both 70-day and 14-day CFU-GM. Using the thymidine “suicide„ technique, the action of LIA was confirmed as being on CFU-GM in S-phase, but it failed to affect the proliferation of blast cell in S-phase. It is concluded that acidic isoferritins inhibit normal CFU-GM but not blast cells from patients with AML. Acidic isoferritins could confer a proliferative advantage of the leukemic clone over its normal counterparts.

scholarly journals Acidic isoferritins (leukemia-associated inhibitory activity) fail to inhibit blast proliferation in acute myelogenous leukemia

Blood ◽  
1981 ◽  
Vol 58 (3) ◽  
pp. 653-657
Author(s):  
R Taetle
Keyword(s):  
Inhibitory Activity ◽  
Acute Myelogenous Leukemia ◽  
Blood Cells ◽  
Leukemia Cell ◽  
S Phase ◽  
Myelogenous Leukemia ◽  
Leukemia Cell Line ◽  
Acute Myelogenous ◽  
Blast Cells ◽  
Leukemic Clone

Cell-free extracts of bone marrow and blood cells from patients with leukemia contain an inhibitor of normal granulocyte/macrophage progenitor (CFU-GM) proliferation (leukemia-associated inhibitory activity, LIA) identified as acidic isoferritins. A comparison was made of the action of crude LIA prepared from frozen-thawed leukemic blood cells and purified spleen ferritin from a patient with chronic myelogenous leukemia, on the proliferation of blast progenitors from patients with acute myelogenous leukemia (AML), and on the promyelocytic leukemia cell line, HL-60. Crude LIA showed no inhibition of blast progenitor or HL-60 proliferation at low concentrations, but inhibited the proliferation of CFU-GM. At higher concentrations, crude LIA inhibited both blast cells and CFU-GM. Purified spleen ferritin failed to inhibit blast progenitors or HL-60 cells at any concentration tested, but inhibited both 70-day and 14-day CFU-GM. Using the thymidine “suicide„ technique, the action of LIA was confirmed as being on CFU-GM in S-phase, but it failed to affect the proliferation of blast cell in S-phase. It is concluded that acidic isoferritins inhibit normal CFU-GM but not blast cells from patients with AML. Acidic isoferritins could confer a proliferative advantage of the leukemic clone over its normal counterparts.

Effect of Thalidomide and Arsenic Trioxide On the Release of Tumor Necrosis Factor – α (TNF-α) and Vascular Endothelial Growth Factor (VEGF) From the KG-1a Human Acute Myelogenous Leukemia Cell Line.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4165-4165
Author(s):  
Erian Girgis ◽  
John Mahoney ◽  
Rafaat Khalil ◽  
Magdi Soliman
Keyword(s):  
Cell Line ◽  
Arsenic Trioxide ◽  
Acute Myelogenous Leukemia ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Leukemia Cell Line ◽  
Acute Myelogenous Leukemia Cell ◽  
Tnf Α ◽  
Significant Difference ◽  
Acute Myelogenous

Abstract Abstract 4165 Although the exact mechanism of action of thalidomide is still unknown, it has been suggested that it may affect TNF-α in addition to its possible anti-angiogenic and immunomodulatory properties. Studies conducted in our lab have indicated that thalidomide cytotoxicity in KG-1a human acute myelogenous leukemia cell line was enhanced by combining it with arsenic trioxide. So, the current investigation was conducted in order to evaluate the effect of thalidomide either alone or in combination with arsenic trioxide on the release of TNF-α and VEGF from this cell line in an attempt to clarify its possible cytotoxic mechanism. Human acute myelogenous leukemia cell line KG-1a (obtained from American Type Culture Collection, ATCC) grown in complete medium containing Iscove's modified Dulbecco's medium and fetal bovine albumin were used in this study. The cells were cultured for 48 hours in a 12 well-culture plates in duplicates at a concentration of 2×106 cells/ml in the presence or absence of thalidomide (5 mg/L) [Tocris bioscience, Ellisville, Mo] and or arsenic trioxide (4 μM) [Sigma-Aldrich, Inc., St. Louis, MO]. Cells were harvested by centrifugation and the levels of TNF-α and VEGF in the supernatant were determined by ELISA using the Quantikine TNF-α and VEGF kits respectively (R&D Systems, Minneapolis, MN). Results obtained indicate that the levels of TNF-α in the supernatant of KG-1a cell cultures incubated with both thalidomide and arsenic trioxide, whether alone or in combination were statistically lower than those observed in the supernatant of control cells (2.89 pg/ml in thalidomide treated cells supernatant, 5.07 pg/ml in arsenic trioxide treated cells supernatant and 4.15 pg/ml in case of the combined treatment with thalidomide and arsenic trioxide versus 16.88 pg/ml in the supernatant of control cells, p<0.05). However, the levels of VEGF in the supernatant of thalidomide treated cells were statistically higher than those in the supernatant of control cells (69.61 pg/ml versus 11.48 pg/ml, p< 0.001). Of note, that arsenic trioxide whether alone or in combination with thalidomide did not produce any statistically significant difference in the levels of VEGF as compared to control or thalidomide treated cell supernatant. These findings clearly indicate that both thalidomide and arsenic trioxide inhibition of TNF-α production by KG-1a cells may play an important role in their cytotoxic effect. However the increase in VEGF levels in the supernatants of thalidomide treated KG-1a cells may reflect a compensatory mechanism of cells which have survived thalidomide cytotoxicity (Supported by NIH grant RR03020). Disclosures: No relevant conflicts of interest to declare.

scholarly journals An undifferentiated variant derived from the human acute myelogenous leukemia cell line (KG-1)

Blood ◽  
1980 ◽  
Vol 56 (2) ◽  
pp. 265-273 ◽  
Author(s):  
HP Koeffler ◽  
R Billing ◽  
AJ Lusis ◽  
R Sparkes ◽  
DW Golde
Keyword(s):  
Cell Line ◽  
Acute Myelogenous Leukemia ◽  
Cellular Response ◽  
Leukemia Cell ◽  
Hla Antigens ◽  
Myelogenous Leukemia ◽  
Leukemic Cells ◽  
Leukemia Cell Line ◽  
Acute Myelogenous

Abstract A variant subline (KG-1a) of the human acute myelogenous leukemia (AML) cell line (KG-1) has been isolated. The cells retain the same constitutive markers as the parent line, including HLA antigens, isoenzymes, and karyotype. The cells from the subline are morphologically and histochemically undifferentiated blast cells, while the parent cells and several of its clones are at the myeloblast and promyelocyte stages of development. The variant cells do not respond to colony-stimulating factor (CSF), and they do not express the human la antigen, nor a recently characterized AML antigen. The parent KG-1 cells are stimulated to proliferate in the presence of CSF and the cells express the la and AML antigen. Variant AML cell lines, such as KG-1a, will be useful in vitro models for investigating cellular response to CSF and for studying antigen expression in leukemic cells.

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