scholarly journals Human chronic myelogenous leukemia cell-line with positive Philadelphia chromosome

Blood ◽  
1975 ◽  
Vol 45 (3) ◽  
pp. 321-334 ◽  
Author(s):  
CB Lozzio ◽  
BB Lozzio
Keyword(s):  
Cell Line ◽  
Chronic Myelogenous Leukemia ◽  
Culture Media ◽  
Specific Antigen ◽  
Philadelphia Chromosome ◽  
Experimental Studies ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Chromosome 17 ◽  
Leukemia Cell Line

Abstract A cell-line derived from a patient with chronic myelogenous leukemia (CML) is described. The new cell-line, which has over 175 serial passanges in a 3 1/2-yr period, has the following characteristics: (1) CML cells started to proliferate actively since they were first incubated in culture media. A threefold increase in the total number of cells was observed during the first seven passages; the cell population increased by a factor of 10 to 20 every 7 days from passage 8 through 85; from 20 to 40 times from passage 86 through 150, and more than 40 times after 150 passages. (2) The majority of the nononucleated cells are undifferentiated blasts. (3) The karyotype of all the cells examined show the Philadelphia (Ph1) chromosome and a long acrocentric marker plus aneuploidy. The Giemsa-banding studies identified the Ph1 chromosome as a terminal deletion of the long arm of chromosome 22:del(22)(q12) and the long acrocentric marker as an unbalanced reciprocal translocation of one chromosome 17 and the long arm of one chromosome 15. (4) The CML cells do not produce immunoglobulins, are free of mycoplasma, Epstein-Barr virus, and herpes-like virus particles. (5) CML cells have no alkaline phosphatase and myeloperoxidase activities and did not engulf inert particles. (6) Cultured CML cells provide a constant source of a specific antigen. This CML cell-line represents a unique source of CML cells with meaningful indicators of malignancy for clinical and experimental studies.

scholarly journals Human chronic myelogenous leukemia cell-line with positive Philadelphia chromosome

Blood ◽  
1975 ◽  
Vol 45 (3) ◽  
pp. 321-334 ◽  
Author(s):  
CB Lozzio ◽  
BB Lozzio
Keyword(s):  
Cell Line ◽  
Chronic Myelogenous Leukemia ◽  
Culture Media ◽  
Specific Antigen ◽  
Philadelphia Chromosome ◽  
Experimental Studies ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Chromosome 17 ◽  
Leukemia Cell Line

A cell-line derived from a patient with chronic myelogenous leukemia (CML) is described. The new cell-line, which has over 175 serial passanges in a 3 1/2-yr period, has the following characteristics: (1) CML cells started to proliferate actively since they were first incubated in culture media. A threefold increase in the total number of cells was observed during the first seven passages; the cell population increased by a factor of 10 to 20 every 7 days from passage 8 through 85; from 20 to 40 times from passage 86 through 150, and more than 40 times after 150 passages. (2) The majority of the nononucleated cells are undifferentiated blasts. (3) The karyotype of all the cells examined show the Philadelphia (Ph1) chromosome and a long acrocentric marker plus aneuploidy. The Giemsa-banding studies identified the Ph1 chromosome as a terminal deletion of the long arm of chromosome 22:del(22)(q12) and the long acrocentric marker as an unbalanced reciprocal translocation of one chromosome 17 and the long arm of one chromosome 15. (4) The CML cells do not produce immunoglobulins, are free of mycoplasma, Epstein-Barr virus, and herpes-like virus particles. (5) CML cells have no alkaline phosphatase and myeloperoxidase activities and did not engulf inert particles. (6) Cultured CML cells provide a constant source of a specific antigen. This CML cell-line represents a unique source of CML cells with meaningful indicators of malignancy for clinical and experimental studies.

scholarly journals Group-specific human granulocyte antigens on a chronic myelogenous leukemia cell line with a Philadelphia chromosome marker

Blood ◽  
1977 ◽  
Vol 49 (5) ◽  
pp. 715-718 ◽  
Author(s):  
SI Drew ◽  
PI Terasaki ◽  
RJ Billing ◽  
OJ Bergh ◽  
J Minowada ◽  
...  
Keyword(s):  
Cell Line ◽  
Chronic Myelogenous Leukemia ◽  
B Lymphocyte ◽  
Philadelphia Chromosome ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Leukemia Cell Line ◽  
Chromosomal Marker ◽  
Chronic Myelogenous Leukemia Cell ◽  
Chromosome Marker

Group-specific human granulocyte antigens are serologically detectable with granulocytotoxic-positive human alloantisera on a cell line, K562, of chronic myelogenous leukemia origin which bears a Philadelphia chromosomal marker. The same cell line lacks serologically detectable HLA, B2 microglobulin, and B-lymphocyte antigens. Granulocyte antigens are important cell markers for cell lines of suspected myeloid lineage.

scholarly journals Group-specific human granulocyte antigens on a chronic myelogenous leukemia cell line with a Philadelphia chromosome marker

Blood ◽  
1977 ◽  
Vol 49 (5) ◽  
pp. 715-718 ◽  
Author(s):  
SI Drew ◽  
PI Terasaki ◽  
RJ Billing ◽  
OJ Bergh ◽  
J Minowada ◽  
...  
Keyword(s):  
Cell Line ◽  
Chronic Myelogenous Leukemia ◽  
B Lymphocyte ◽  
Philadelphia Chromosome ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Leukemia Cell Line ◽  
Chromosomal Marker ◽  
Chronic Myelogenous Leukemia Cell ◽  
Chromosome Marker

Abstract Group-specific human granulocyte antigens are serologically detectable with granulocytotoxic-positive human alloantisera on a cell line, K562, of chronic myelogenous leukemia origin which bears a Philadelphia chromosomal marker. The same cell line lacks serologically detectable HLA, B2 microglobulin, and B-lymphocyte antigens. Granulocyte antigens are important cell markers for cell lines of suspected myeloid lineage.

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.

2′,5′-Oligoadenylate-Antisense Chimeras Cause RNase L to Selectively Degrade bcr/abl mRNA in Chronic Myelogenous Leukemia Cells

Blood ◽  
1998 ◽  
Vol 92 (11) ◽  
pp. 4336-4343 ◽  
Author(s):  
Avudaiappan Maran ◽  
Cornelius F. Waller ◽  
Jayashree M. Paranjape ◽  
Guiying Li ◽  
Wei Xiao ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cell Line ◽  
Chronic Myelogenous Leukemia ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Leukemia Cell Line ◽  
Leukemia Cells ◽  
Mrna Levels ◽  
Rnase L ◽  
Hematopoietic Stem

We report an RNA targeting strategy, which selectively degrades bcr/abl mRNA in chronic myelogenous leukemia (CML) cells. A 2′,5′-tetraadenylate activator (2-5A) of RNase L was chemically linked to oligonucleotide antisense directed against either the fusion site or against the translation start sequence in bcr/abl mRNA. Selective degradation of the targeted RNA sequences was demonstrated in assays with purified RNase L and decreases of p210bcr/abl kinase activity levels were obtained in the CML cell line, K562. Furthermore, the 2-5A-antisense chimeras suppressed growth of K562, while having substantially reduced effects on the promyelocytic leukemia cell line, HL60. Findings were extended to primary CML cells isolated from bone marrow of patients. The 2-5A-antisense treatments both suppressed proliferation of the leukemia cells and selectively depleted levels of bcr/abl mRNA without affecting levels of β-actin mRNA, determined by reverse transcriptase-polymerase chain reaction (RT-PCR). The specificity of this approach was further shown with control oligonucleotides, such as chimeras containing an inactive dimeric form of 2-5A, antisense lacking 2-5A, or chimeras with altered sequences including several mismatched nucleotides. The control oligonucleotides had either reduced or no effect on CML cell growth and bcr/abl mRNA levels. These findings show that CML cell growth can be selectively suppressed by targeting bcr/abl mRNA with 2-5A-antisense for decay by RNase L and suggest that these compounds should be further explored for their potential as ex vivo purging agents of autologous hematopoietic stem cell transplants from CML patients.

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.

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