scholarly journals Induction of erythropoietic colonies in a human chronic myelogenous leukemia cell line

Blood ◽  
1979 ◽  
Vol 54 (5) ◽  
pp. 1182-1187 ◽  
Author(s):  
R Hoffman ◽  
MJ Murnane ◽  
EJ Jr Benz ◽  
R Prohaska ◽  
V Floyd ◽  
...  
Keyword(s):  
Cell Line ◽  
Chronic Myelogenous Leukemia ◽  
Sodium Butyrate ◽  
K562 Cell ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Leukemia Cell Line ◽  
Erythroid Cell ◽  
K562 Cell Line ◽  
Chronic Myelogenous Leukemia Cell

The ability of cells derived from the K562 cell line to generate erythropoietic colonies was studied. The K562 cell line was derived from a patient with chronic myelogenous leukemia 8 yr ago by Lozzio and Lozzio. Rare benzidine-positive colonies formed when these cells were cloned in plasma clots (3 +/- 1/10(4) cells), and their number was not substantially increased by the addition of erythropoietin (9.5 +/- 1/10(4) cells). Sodium butyrate was capable of markedly enhancing the number of benzidine-positive colonies (19.5 +/- 1/10(4) cells) formed, while the combination of sodium butyrate plus erythropoietin exerted a synergistic effect on erythropoietic colony formation (57 +/- 4/10(4) cells). The K562 cell line is a long-term culture system that contains human erythropoietic stem cells. This cell line should be useful in future studies on the cellular and molecular events associated with human erythroid cell differentiation.

scholarly journals Induction of erythropoietic colonies in a human chronic myelogenous leukemia cell line

Blood ◽  
1979 ◽  
Vol 54 (5) ◽  
pp. 1182-1187 ◽  
Author(s):  
R Hoffman ◽  
MJ Murnane ◽  
EJ Jr Benz ◽  
R Prohaska ◽  
V Floyd ◽  
...  
Keyword(s):  
Cell Line ◽  
Chronic Myelogenous Leukemia ◽  
Sodium Butyrate ◽  
K562 Cell ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Leukemia Cell Line ◽  
Erythroid Cell ◽  
K562 Cell Line ◽  
Chronic Myelogenous Leukemia Cell

Abstract The ability of cells derived from the K562 cell line to generate erythropoietic colonies was studied. The K562 cell line was derived from a patient with chronic myelogenous leukemia 8 yr ago by Lozzio and Lozzio. Rare benzidine-positive colonies formed when these cells were cloned in plasma clots (3 +/- 1/10(4) cells), and their number was not substantially increased by the addition of erythropoietin (9.5 +/- 1/10(4) cells). Sodium butyrate was capable of markedly enhancing the number of benzidine-positive colonies (19.5 +/- 1/10(4) cells) formed, while the combination of sodium butyrate plus erythropoietin exerted a synergistic effect on erythropoietic colony formation (57 +/- 4/10(4) cells). The K562 cell line is a long-term culture system that contains human erythropoietic stem cells. This cell line should be useful in future studies on the cellular and molecular events associated with human erythroid cell differentiation.

Analysis of Histone Deacetylase Inhibitor, FK228, Effect on Chronic Myelogenous Leukemia Cell Line.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4675-4675
Author(s):  
Seiichi Okabe ◽  
Testuzo Tauchi ◽  
Akihiro Nakajima ◽  
Goro Sashida ◽  
Masahiki Sumi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Clinical Trial ◽  
Cell Line ◽  
Chronic Myelogenous Leukemia ◽  
Glycogen Synthase ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Leukemia Cell Line ◽  
Parental Cell Line ◽  
Chronic Myelogenous Leukemia Cell

Abstract Chronic myelogenous leukemia (CML) results from transformation of hematopoietic cells by the BCR/ABL gene. Although high rates of hematologic responses to imatinib therapy, the acquired resistance to imatinib has been recognized as a major problem in the treatment of CML Histone deacetylases (HDACs) and histone acetyltransferases (HATs) regulate gene expression and cell growth. Recently, HDAC inhibitors have known as a new class of anti-cancer drugs. One of the HDAC inhibitor, FK228 (FR901228, depsipeptide) is now doing the clinical trial for the treatment of patients, such as peripheral T-cell lymphoma, but there was not known to the CML. In this study, we used the TF-1 BCR-ABL cell line, which were transfected BCR/ABL gene to the leukemia cell line, TF-1. We show here that FK228 potently induced apoptosis of TF-1 BCR-ABL cells, compare to the parental cell line, TF-1, in a dose and time depend fashion. BCR-ABL, intracellular molecular chaperone, heat shock protein 90 (HSP90), and p53 which regulate cell cycle, were acetylated after FK228 treatment, but not glycogen synthase kinase-3 β(GSK-3β) and signal-transducing activators of transcription 5 (STAT5). Histone H4 is also acetylated after FK228 treatment. In a cell cycle analysis, TF-1 BCR-ABL cells were stopped at G2-M phase after FK228 treatment. The activity of MAPK and Src kinases were blocked after FK228 treatment in a time and dose depend fashion, but p38 was activated. Inhibitor of apoptosis proteins (c-IAPs) have prevented cell death by inhibiting effectors caspases. IAPs were inhibited by FK228 and caspase3, caspase9 and poly (ADP-ribose) polymerase (PARP) were activated in a time and dose depend manner. Histone acetylation and caspase activitation were not blocked by treatment of p38 inhibitor, SB203580. Our study supports the future clinical trial of FK228 in the management of CML patients.

Deciphering the cross-talking of human competitive endogenous RNAs in K562 chronic myelogenous leukemia cell line

2016 ◽  
Vol 12 (12) ◽  
pp. 3633-3642 ◽  
Author(s):  
Kamalika Sen ◽  
Arijita Sarkar ◽  
Ranjan Kumar Maji ◽  
Zhumur Ghosh ◽  
Sanjib Gupta ◽  
...  
Keyword(s):  
Cell Line ◽  
Chronic Myelogenous Leukemia ◽  
Leukemia Cell ◽  
Myeloproliferative Disorder ◽  
Myelogenous Leukemia ◽  
Leukemia Cell Line ◽  
Chronic Myelogenous Leukemia Cell ◽  
Competitive Endogenous Rnas ◽  
Abnormal Accumulation ◽  
Line P

Chronic myelogenous leukemia (CML) is a myeloproliferative disorder characterized by increased proliferation or abnormal accumulation of the granulocytic cell line without the depletion of their capacity to differentiate.

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