IL-6 Undergoes Transition from in vitro Autocrine Growth Factor to in vivo Growth Inhibitor of B Lymphoma Cells

1997 ◽  
Vol 4 (5) ◽  
pp. 201-207
Author(s):  
Dae-Ho Cho ◽  
Hyung-Sik Kang ◽  
Jung-Jae Ma ◽  
Sung-Sook Kim ◽  
Hwan-Mook Kim ◽  
...  
Keyword(s):  
Growth Factor ◽  
Growth Inhibitor ◽  
Autocrine Growth ◽  
Lymphoma Cells ◽  
B Lymphoma ◽  
Autocrine Growth Factor ◽  
B Lymphoma Cells ◽  
In Vivo Growth

IL-6 undergoes transition from in vitro autocrine growth factor to in vivo growth inhibitor of B lymphoma cells

1997 ◽  
Vol 4 (5) ◽  
pp. 201-207 ◽  
Author(s):  
Dae-Ho Cho ◽  
Hyung-Sik Kang ◽  
Jung-Jae Ma ◽  
Sung-Sook Kim ◽  
Hwan-Mook Kim ◽  
...  
Keyword(s):  
Growth Factor ◽  
Growth Inhibitor ◽  
Autocrine Growth ◽  
Lymphoma Cells ◽  
B Lymphoma ◽  
Autocrine Growth Factor ◽  
B Lymphoma Cells ◽  
In Vivo Growth

CD4+ T cells kill Id+ B-lymphoma cells: FasLigand-Fas interaction is dominant in vitro but is redundant in vivo

2004 ◽  
Vol 53 (12) ◽  
pp. 1135-1145 ◽  
Author(s):  
Katrin U. Lundin ◽  
Valentina Screpanti ◽  
Hilde Omholt ◽  
Peter O. Hofgaard ◽  
Hideo Yagita ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Lymphoma Cells ◽  
B Lymphoma ◽  
B Lymphoma Cells

177Lu-antibody conjugates for single-cell kill of B-lymphoma cells in vitro and for therapy of micrometastases in vivo

2005 ◽  
Vol 32 (3) ◽  
pp. 269-278 ◽  
Author(s):  
Rosana B. Michel ◽  
Philip M. Andrews ◽  
Adriane V. Rosario ◽  
David M. Goldenberg ◽  
M. Jules Mattes
Keyword(s):  
Single Cell ◽  
Lymphoma Cells ◽  
B Lymphoma ◽  
B Lymphoma Cells ◽  
Cell Kill ◽  
Antibody Conjugates

scholarly journals Interleukin-11 acts as an autocrine growth factor for human megakaryoblastic cell lines

Blood ◽  
1993 ◽  
Vol 81 (4) ◽  
pp. 889-893 ◽  
Author(s):  
S Kobayashi ◽  
M Teramura ◽  
I Sugawara ◽  
K Oshimi ◽  
H Mizoguchi
Keyword(s):  
Growth Factor ◽  
Cell Lines ◽  
Antisense Oligonucleotides ◽  
Leukemia Cell ◽  
Dependent Manner ◽  
Autocrine Growth ◽  
Autocrine Loop ◽  
Autocrine Growth Factor ◽  
Interleukin 11

Abstract The cytokine interleukin-11 (IL-11) promotes normal human megakaryocytopoiesis in vitro. However, its role in abnormal megakaryocytopoiesis is not well known. Accordingly, we studied its effects on human megakaryoblastic cell lines CMK and Meg-J. IL-11 stimulated the proliferation of CMK and Meg-J in a dose-dependent manner with maximal growth being achieved at the concentration of 50 and 500 ng/mL, respectively. The growth of the cells was inhibited by anti-IL-11 antibody and IL-11 antisense oligonucleotides. IL-11 transcripts were detected in these two cell lines using a reverse transcriptase-polymerase chain reaction assay. These findings indicate that IL-11 might be an autocrine growth factor for megakaryoblastic cells. IL-11 transcripts also existed in other leukemia cell lines: HL- 60, U937, and K562. However, the growth of these cells was not stimulated by IL-11, and was not inhibited by IL-11 antisense oligonucleotides. These results suggested that IL-11 might regulate malignant cells of the megakaryocytic lineage, in part by an autocrine loop.

Inhibition of insulin like growth factor II autocrine growth of Wilms' tumor by suramin in vitro and in vivo

1996 ◽  
Vol 103 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Timothy S. Vincent ◽  
Debra J. Hazen-Martin ◽  
A.Julian Garvin
Keyword(s):  
Growth Factor ◽  
Wilms Tumor ◽  
Insulin Like Growth Factor ◽  
Autocrine Growth ◽  
Factor Ii

Vascular endothelial growth factor (VEGF) is an autocrine growth factor for VEGF receptor–positive human tumors

Blood ◽  
2001 ◽  
Vol 98 (6) ◽  
pp. 1904-1913 ◽  
Author(s):  
Rizwan Masood ◽  
Jie Cai ◽  
Tong Zheng ◽  
D. Lynne Smith ◽  
David R. Hinton ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tumor Cell ◽  
Cell Lines ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Autocrine Growth ◽  
Autocrine Growth Factor ◽  
Endothelial Growth Factor

Abstract Angiogenesis is required for the progression of tumors from a benign to a malignant phenotype and for metastasis. Malignant tumor cells secrete factors such as vascular endothelial growth factor (VEGF), which bind to their cognate receptors on endothelial cells to induce angiogenesis. Here it is shown that several tumor types express VEGF receptors (VEGFRs) and that inhibition of VEGF (VEGF antisense oligonucleotide AS-3) or VEGFRs (neutralizing antibodies) inhibited the proliferation of these cell lines in vitro. Furthermore, this effect was abrogated by exogenous VEGF. Thus, VEGF is an autocrine growth factor for tumor cell lines that express VEGFRs. A modified form of VEGF AS-3 (AS-3m), in which flanking 4 nucleotides were substituted with 2-O-methylnucleosides (mixed backbone oligonucleotides), retained specificity and was active when given orally or systemically in vitro and in murine tumor models. In VEGFR-2–expressing tumors, VEGF inhibition may have dual functions: direct inhibition of tumor cell growth and inhibition of angiogenesis.

TNFα therapy activates human B-lymphoma cells in vivo and may protect myelopoiesis

1992 ◽  
Vol 16 (8) ◽  
pp. 769-773 ◽  
Author(s):  
B. Heilig ◽  
M. Mapara ◽  
R. Bargou ◽  
C. Fiehn ◽  
B. Dörken
Keyword(s):  
Lymphoma Cells ◽  
B Lymphoma ◽  
B Lymphoma Cells

Biologic response of B lymphoma cells to anti-CD20 monoclonal antibody rituximab in vitro: CD55 and CD59 regulate complement-mediated cell lysis

Blood ◽  
2000 ◽  
Vol 95 (12) ◽  
pp. 3900-3908 ◽  
Author(s):  
Josée Golay ◽  
Luisella Zaffaroni ◽  
Thomas Vaccari ◽  
Manuela Lazzari ◽  
Gian-Maria Borleri ◽  
...  
Keyword(s):  
B Cells ◽  
Cell Lines ◽  
Low Grade ◽  
Lymphoma Cells ◽  
B Lymphoma Cells ◽  
Biologic Response ◽  
Anti Cd20 ◽  
Hodgkin's Lymphomas

Abstract The chimeric anti-CD20 MAb rituximab has recently become a treatment of choice for low-grade or follicular non-Hodgkin's lymphomas (FL) with a response rate of about 50%. In this report, we have investigated the mechanism of action of rituximab on 4 FL and 1 Burkitt's lymphoma (BL) cell lines, 3 fresh FL samples and normal B cells in vitro. Rituximab efficiently blocks the proliferation of normal B cells, but not that of the lymphoma lines. We did not detect significant apoptosis of the cell lines in response to rituximab alone. All cell lines were targets of antibody-dependent cellular cytotoxicity (ADCC). On the other hand, human complement-mediated lysis was highly variable between cell lines, ranging from 100% lysis to complete resistance. Investigation of the role of the complement inhibitors CD35, CD46, CD55, and CD59 showed that CD55, and to a lesser extent CD59, are important regulators of complement-mediated cytotoxicity (CDC) in FL cell lines as well as in fresh cases of FL: Blocking CD55 and/or CD59 function with specific antibodies significantly increased CDC in FL cells. We conclude that CDC and ADCC are major mechanisms of action of rituximab on B-cell lymphomas and that a heterogeneous susceptibility of different lymphoma cells to complement may be at least in part responsible for the heterogeneity of the response of different patients to rituximab in vivo. Furthermore, we suggest that the relative levels of CD55 and CD59 may become useful markers to predict the clinical response.

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