scholarly journals Expression of HOXC4, HOXC5, and HOXC6 in human lymphoid cell lines, leukemias, and benign and malignant lymphoid tissue

Blood ◽  
1996 ◽  
Vol 87 (5) ◽  
pp. 1737-1745 ◽  
Author(s):  
J Bijl ◽  
JW van Oostveen ◽  
M Kreike ◽  
E Rieger ◽  
LM van der Raaij-Helmer ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Lines ◽  
Lymphoid Cell ◽  
Lymphoid Cells ◽  
Normal Donor ◽  
Rt Pcr ◽  
Neoplastic Cells ◽  
Human Lymphoid Cell ◽  
Hodgkin's Lymphomas ◽  
Lymphoid Cell Lines

Abstract Besides their regulatory role in embryogenesis, homeobox (HOX) genes are expressed in a specific manner in hematopoietic cell lineages, implying a role in the molecular regulation of hematopoiesis. Some HOX C cluster genes are found to be expressed in lymphoid cells of mice and humans. Their function and expression in normal hematopoiesis are still largely unknown. We have studied the mRNA expression of HOXC4, HOXC5, and HOXC6 in several stages of lymphocyte maturation by reverse transcriptase-polymerase chain reaction (RT-PCR) and RNA in situ hybridization (RISH). We examined CD34+/CD38low and CD34+/CD38high cells obtained from normal donor bone marrow (BM), a panel of 19 lymphoid cell lines, several types of leukemias and non-Hodgkin's lymphomas (NHL), and lymphocytes isolated from tonsillar tissue and peripheral blood (PB). HOXC4 and HOXC6 were found to be expressed during maturation in B- and T-lymphoid cells. The expression of each gene was found to be initiated at different cell maturation stages. HOXC4 transcripts were present in CD34+/CD38low cells, which are thought to comprise stem cells and noncommitted progenitor cells, and in subsequent stages to terminally maturated lymphoid cells. HOXC6 expression is initiated in equivalents of prothymocyte and pre-pre-B cell stage and remains present in mature cells. However, HOXC5 is only expressed in neoplastic cell lines and in neoplastic cells of NHL, but not in CD34+ BM cells, nor in resting or activated lymphoid cells isolated from tonsil, PB, or in leukemia cells. In cell lines, weak expression of HOXC5 is initiated in equivalents of pre-B cell and common thymocyte stage and is continuously expressed in mature cell lines. Semi-quantitative RT-PCR showed that expression levels of HOXC5 were much lower than those of HOXC4 and HOXC6; furthermore an increase of expression of HOXC4, HOXC5, and HOXC6 during lymphoid cell differentiation was demonstrated. Thus, mainly mature lymphoid cell lines and neoplastic cells of NHL do express HOXC5, in contrast to the lack of expression in normal lymphoid cells and leukemias. These findings suggest involvement of HOXC5 in lymphomagenesis.

scholarly journals Expression of HOXC4, HOXC5, and HOXC6 in human lymphoid cell lines, leukemias, and benign and malignant lymphoid tissue

Blood ◽  
1996 ◽  
Vol 87 (5) ◽  
pp. 1737-1745 ◽  
Author(s):  
J Bijl ◽  
JW van Oostveen ◽  
M Kreike ◽  
E Rieger ◽  
LM van der Raaij-Helmer ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Lines ◽  
Lymphoid Cell ◽  
Lymphoid Cells ◽  
Normal Donor ◽  
Rt Pcr ◽  
Neoplastic Cells ◽  
Human Lymphoid Cell ◽  
Hodgkin's Lymphomas ◽  
Lymphoid Cell Lines

Besides their regulatory role in embryogenesis, homeobox (HOX) genes are expressed in a specific manner in hematopoietic cell lineages, implying a role in the molecular regulation of hematopoiesis. Some HOX C cluster genes are found to be expressed in lymphoid cells of mice and humans. Their function and expression in normal hematopoiesis are still largely unknown. We have studied the mRNA expression of HOXC4, HOXC5, and HOXC6 in several stages of lymphocyte maturation by reverse transcriptase-polymerase chain reaction (RT-PCR) and RNA in situ hybridization (RISH). We examined CD34+/CD38low and CD34+/CD38high cells obtained from normal donor bone marrow (BM), a panel of 19 lymphoid cell lines, several types of leukemias and non-Hodgkin's lymphomas (NHL), and lymphocytes isolated from tonsillar tissue and peripheral blood (PB). HOXC4 and HOXC6 were found to be expressed during maturation in B- and T-lymphoid cells. The expression of each gene was found to be initiated at different cell maturation stages. HOXC4 transcripts were present in CD34+/CD38low cells, which are thought to comprise stem cells and noncommitted progenitor cells, and in subsequent stages to terminally maturated lymphoid cells. HOXC6 expression is initiated in equivalents of prothymocyte and pre-pre-B cell stage and remains present in mature cells. However, HOXC5 is only expressed in neoplastic cell lines and in neoplastic cells of NHL, but not in CD34+ BM cells, nor in resting or activated lymphoid cells isolated from tonsil, PB, or in leukemia cells. In cell lines, weak expression of HOXC5 is initiated in equivalents of pre-B cell and common thymocyte stage and is continuously expressed in mature cell lines. Semi-quantitative RT-PCR showed that expression levels of HOXC5 were much lower than those of HOXC4 and HOXC6; furthermore an increase of expression of HOXC4, HOXC5, and HOXC6 during lymphoid cell differentiation was demonstrated. Thus, mainly mature lymphoid cell lines and neoplastic cells of NHL do express HOXC5, in contrast to the lack of expression in normal lymphoid cells and leukemias. These findings suggest involvement of HOXC5 in lymphomagenesis.

scholarly journals Cytotoxicity of farnesyltransferase inhibitors in lymphoid cells mediated by MAPK pathway inhibition and Bim up-regulation

Blood ◽  
2011 ◽  
Vol 118 (18) ◽  
pp. 4872-4881 ◽  
Author(s):  
Husheng Ding ◽  
Jennifer Hackbarth ◽  
Paula A. Schneider ◽  
Kevin L. Peterson ◽  
X. Wei Meng ◽  
...  
Keyword(s):  
Cell Lines ◽  
Lymphoid Cell ◽  
Mapk Pathway ◽  
Lymphoid Cells ◽  
Farnesyltransferase Inhibitors ◽  
Death Domain ◽  
Nucleotide Exchange ◽  
Human Lymphoid Cell ◽  
Induced Apoptosis ◽  
Lymphoid Cell Lines

Abstract The mechanism of cytotoxicity of farnesyltransferase inhibitors is incompletely understood and seems to vary depending on the cell type. To identify potential determinants of sensitivity or resistance for study in the accompanying clinical trial (Witzig et al, page 4882), we examined the mechanism of cytotoxicity of tipifarnib in human lymphoid cell lines. Based on initial experiments showing that Jurkat variants lacking Fas-associated death domain or procaspase-8 undergo tipifarnib-induced apoptosis, whereas cells lacking caspase-9 or overexpressing Bcl-2 do not, we examined changes in Bcl-2 family members. Tipifarnib caused dose-dependent up-regulation of Bim in lymphoid cell lines (Jurkat, Molt3, H9, DoHH2, and RL) that undergo tipifarnib-induced apoptosis but not in lines (SKW6.4 and Hs445) that resist tipifarnib-induced apoptosis. Further analysis demonstrated that increased Bim levels reflect inhibition of signaling from c-Raf to MEK1/2 and ERK1/2. Additional experiments showed that down-regulation of the Ras guanine nucleotide exchange factor RasGRP1 diminished tipifarnib sensitivity, suggesting that H-Ras or N-Ras is a critical farnesylation target upstream of c-Raf in lymphoid cells. These results not only trace a pathway through c-Raf to Bim that contributes to tipifarnib cytotoxicity in human lymphoid cells but also identify potential determinants of sensitivity to this agent.

scholarly journals THE RELATIONSHIP BETWEEN ß2-MICROGLOBULIN AND IMMUNOGLOBULIN IN CULTURED HUMAN LYMPHOID CELL LINES

1973 ◽  
Vol 137 (3) ◽  
pp. 838-843 ◽  
Author(s):  
T. H. Hütteroth ◽  
H. Cleve ◽  
S. D. Litwin ◽  
M. D. Poulik
Keyword(s):  
Cell Surface ◽  
Cell Lines ◽  
Specific Antibody ◽  
Lymphoid Cell ◽  
Lymphoid Cells ◽  
Human Lymphoid Cell ◽  
Membrane Antigens ◽  
The Relationship ◽  
Lymphoid Cell Lines

ß2-microglobulin was detected on the cell surface and in the medium of human lymphoid cells established in long-term culture. The secretion of ß2-microglobulin was relatively uniform when different cell lines were compared, whereas IgG production varied widely. κ- and µ-membrane antigens were modulated by specific antibody; ß2-microglobulin was not modulated. Anti-κ and anti-µ antisera had no effect on the expression of membrane ß2-microglobulin, nor had anti-ß2-microglobulin antiserum any effect on the expression of κ- and µ-membrane antigens.

A New Death Receptor 3 Isoform: Expression in Human Lymphoid Cell Lines and Non-Hodgkin's Lymphomas

1998 ◽  
Vol 242 (2) ◽  
pp. 376-379 ◽  
Author(s):  
Krzysztof Warzocha ◽  
Patricia Ribeiro ◽  
Carole Charlot ◽  
Nathalie Renard ◽  
Bertrand Coiffier ◽  
...  
Keyword(s):  
Cell Lines ◽  
Lymphoid Cell ◽  
Death Receptor ◽  
Human Lymphoid Cell ◽  
Isoform Expression ◽  
Death Receptor 3 ◽  
Hodgkin's Lymphomas ◽  
Lymphoid Cell Lines

scholarly journals Effect of cell cycle position on dexamethasone binding by mouse and human lymphoid cell lines: correlation between an increase in dexamethasone binding during S phase and dexamethasone sensitivity

Blood ◽  
1984 ◽  
Vol 63 (1) ◽  
pp. 105-113
Author(s):  
CW Distelhorst ◽  
BM Benutto ◽  
RA Bergamini
Keyword(s):  
Cell Cycle ◽  
Cell Lines ◽  
Lymphoid Cell ◽  
S Phase ◽  
Lymphoid Cells ◽  
Cell Protein ◽  
G1 Phase ◽  
Cycle Phase ◽  
Human Lymphoid Cell ◽  
Lymphoid Cell Lines

We determined the effect of cell cycle position on the amount of dexamethasone that was specifically bound by mouse and human lymphoid cell lines. Cell lines that were either sensitive or resistant to growth inhibition by dexamethasone were compared. Exponentially growing cells were separated by centrifugal elutriation into fractions that corresponded to different positions in the cell cycle. The cell cycle phase distribution of each fraction was estimated by flow cytometry and autoradiography. The amount of dexamethasone bound per cell in each fraction was measured by a whole cell binding assay. In three dexamethasone-sensitive cell lines (two mouse and one human), we found that the amount of dexamethasone bound per cell increased 2–4-fold between G1 phase and S phase, and then decreased during G2/M phase. Results were the same when the amount of dexamethasone bound per milligram of cell protein was measured. Binding affinity was the same during G1 phase and S phase, but the proportion of bound dexamethasone that translocated to the nucleus was greater during S phase. In contrast, we found that the amount of dexamethasone bound per cell by three dexamethasone-resistant cell lines (two mouse and one human) did not increase during S phase. Our results indicate that cell cycle changes in dexamethasone binding are not simply related to changes in cell protein or cell volume during the cell cycle. An increase in dexamethasone binding during S phase may be required for dexamethasone to inhibit cell growth, and a failure of dexamethasone binding to increase during S phase might represent a new mechanism of dexamethasone resistance in lymphoid cells.

scholarly journals Effect of cell cycle position on dexamethasone binding by mouse and human lymphoid cell lines: correlation between an increase in dexamethasone binding during S phase and dexamethasone sensitivity

Blood ◽  
1984 ◽  
Vol 63 (1) ◽  
pp. 105-113 ◽  
Author(s):  
CW Distelhorst ◽  
BM Benutto ◽  
RA Bergamini
Keyword(s):  
Cell Cycle ◽  
Cell Lines ◽  
Lymphoid Cell ◽  
S Phase ◽  
Lymphoid Cells ◽  
Cell Protein ◽  
G1 Phase ◽  
Cycle Phase ◽  
Human Lymphoid Cell ◽  
Lymphoid Cell Lines

Abstract We determined the effect of cell cycle position on the amount of dexamethasone that was specifically bound by mouse and human lymphoid cell lines. Cell lines that were either sensitive or resistant to growth inhibition by dexamethasone were compared. Exponentially growing cells were separated by centrifugal elutriation into fractions that corresponded to different positions in the cell cycle. The cell cycle phase distribution of each fraction was estimated by flow cytometry and autoradiography. The amount of dexamethasone bound per cell in each fraction was measured by a whole cell binding assay. In three dexamethasone-sensitive cell lines (two mouse and one human), we found that the amount of dexamethasone bound per cell increased 2–4-fold between G1 phase and S phase, and then decreased during G2/M phase. Results were the same when the amount of dexamethasone bound per milligram of cell protein was measured. Binding affinity was the same during G1 phase and S phase, but the proportion of bound dexamethasone that translocated to the nucleus was greater during S phase. In contrast, we found that the amount of dexamethasone bound per cell by three dexamethasone-resistant cell lines (two mouse and one human) did not increase during S phase. Our results indicate that cell cycle changes in dexamethasone binding are not simply related to changes in cell protein or cell volume during the cell cycle. An increase in dexamethasone binding during S phase may be required for dexamethasone to inhibit cell growth, and a failure of dexamethasone binding to increase during S phase might represent a new mechanism of dexamethasone resistance in lymphoid cells.

scholarly journals Identification of human lymphoma cells by antisera to malignancy- associated nucleolar antigens

Blood ◽  
1984 ◽  
Vol 63 (3) ◽  
pp. 559-565
Author(s):  
RJ Ford ◽  
M Cramer ◽  
FM Davis
Keyword(s):  
Lymphoid Cell ◽  
B Lymphocyte ◽  
Cell Types ◽  
Lymphoid Cells ◽  
Lymphoma Cells ◽  
Neoplastic Cells ◽  
Human Lymphoid Cell ◽  
Definition Of ◽  
Hodgkin's Lymphomas

Abstract The non-Hodgkin's lymphomas (NHL) are a diverse group of human lymphoid neoplasms that have long presented pathologists with formidable diagnostic challenges. These tumors of the immune system are thought to represent neoplastic transformations of most of the recognized stages in T and B lymphocyte ontogeny. Lymphoma cells, however, often simulate their normal lymphocytic counterparts both morphologically and cell surface phenotypically, creating difficulties in discriminating normal from neoplastic lymphocytes. We have used heteroantisera to the human malignancy-associated nucleolar antigen (HMNA) to prospectively evaluate its efficacy in identifying the morphologically neoplastic cells in NHL lesions. In 65 cases of T and B cell histopathologic types of NHL, the antisera reacted with nucleoli in the morphologically and cytogenetically neoplastic lymphoma cells, but not with normal- appearing lymphoid and other cell types present in the lesions. Control specimens from normal and hyperplastic lymphoid tissue also failed to react with anti-HMNA antibodies. Normal activated lymphoid cells in vitro and growth-factor-dependent normal lymphoid cell lines also failed to express the nucleolar antigen(s). These data suggest that the HMNA is a valuable tumor cell marker for neoplastic human lymphoid cell populations and can be used with other types of cell markers for a better definition of the neoplastic cells in NHL.

Identification of human lymphoma cells by antisera to malignancy- associated nucleolar antigens

Blood ◽  
1984 ◽  
Vol 63 (3) ◽  
pp. 559-565
Author(s):  
RJ Ford ◽  
M Cramer ◽  
FM Davis
Keyword(s):  
Lymphoid Cell ◽  
B Lymphocyte ◽  
Cell Types ◽  
Lymphoid Cells ◽  
Lymphoma Cells ◽  
Neoplastic Cells ◽  
Human Lymphoid Cell ◽  
Definition Of ◽  
Hodgkin's Lymphomas

The non-Hodgkin's lymphomas (NHL) are a diverse group of human lymphoid neoplasms that have long presented pathologists with formidable diagnostic challenges. These tumors of the immune system are thought to represent neoplastic transformations of most of the recognized stages in T and B lymphocyte ontogeny. Lymphoma cells, however, often simulate their normal lymphocytic counterparts both morphologically and cell surface phenotypically, creating difficulties in discriminating normal from neoplastic lymphocytes. We have used heteroantisera to the human malignancy-associated nucleolar antigen (HMNA) to prospectively evaluate its efficacy in identifying the morphologically neoplastic cells in NHL lesions. In 65 cases of T and B cell histopathologic types of NHL, the antisera reacted with nucleoli in the morphologically and cytogenetically neoplastic lymphoma cells, but not with normal- appearing lymphoid and other cell types present in the lesions. Control specimens from normal and hyperplastic lymphoid tissue also failed to react with anti-HMNA antibodies. Normal activated lymphoid cells in vitro and growth-factor-dependent normal lymphoid cell lines also failed to express the nucleolar antigen(s). These data suggest that the HMNA is a valuable tumor cell marker for neoplastic human lymphoid cell populations and can be used with other types of cell markers for a better definition of the neoplastic cells in NHL.

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