Common Reactivity of Bovine and Human Sera towards Bovine Lymphoid Tumor Cells

2015 ◽  
pp. 232-234
Author(s):  
Z. Trainin ◽  
R. Meirom ◽  
A. Barnea ◽  
H. Ungar-Waron
Keyword(s):  
Tumor Cells ◽  
Lymphoid Tumor ◽  
Human Sera

Cross-linking CTX, a novel thymocyte-specific molecule, inhibits the growth of lymphoid tumor cells in xenopus

1997 ◽  
Vol 34 (2) ◽  
pp. 133-143 ◽  
Author(s):  
Jacques Robert ◽  
Isabelle Chretien ◽  
Chantal Guiet ◽  
Louis Du Pasquier
Keyword(s):  
Tumor Cells ◽  
Cross Linking ◽  
Lymphoid Tumor

scholarly journals Simultaneous Inactivation of the p16, p15 and p14 Genes Encoding Cyclin-Dependent Kinase Inhibitors in Canine T-Lymphoid Tumor Cells

2013 ◽  
Vol 75 (6) ◽  
pp. 733-742 ◽  
Author(s):  
Aki FUJIWARA-IGARASHI ◽  
Yuko GOTO-KOSHINO ◽  
Hiroyuki MOCHIZUKI ◽  
Shingo MAEDA ◽  
Yasuhito FUJINO ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Kinase Inhibitors ◽  
Cyclin Dependent Kinase ◽  
Lymphoid Tumor ◽  
Genes Encoding

scholarly journals Receptor-selective TRAIL Mutants Target Lymphoid Tumor cells for Apoptosis via TRAIL-R1: Implications for Therapy

Toxicology ◽  
2008 ◽  
Vol 253 (1-3) ◽  
pp. 6-7 ◽  
Author(s):  
Marion MacFarlane ◽  
Susan L. Kohlhaas ◽  
Michael J. Sutcliffe ◽  
Martin J.S. Dyer ◽  
Gerald M. Cohen
Keyword(s):  
Tumor Cells ◽  
Lymphoid Tumor

scholarly journals The Fine Structure of Lymphosarcoma in Cattle

1969 ◽  
Vol 6 (1) ◽  
pp. 15-29 ◽  
Author(s):  
Yuttaka Fujimoto ◽  
Janice Miller ◽  
C. Olson
Keyword(s):  
Endoplasmic Reticulum ◽  
Fine Structure ◽  
Tumor Cells ◽  
Multivesicular Bodies ◽  
Heterogeneous Mixture ◽  
Nuclear Inclusion ◽  
Cell Type ◽  
Lymphoid Tumor ◽  
Cytoplasmic Membranes ◽  
Predominant Cell Type

Nine cases of bovine lymphosarcoma were classified by light microscopy as lymphoid or reticulum according to the predominant cell type, or as lymphoreticular when there was a heterogeneous mixture of lymphoid and reticulum tumor cells. Typical ultrastructural features of these cells were as follows. Lymphoid tumor cells had smoothly contoured nuclear and cytoplasmic membranes and few cytoplasmic organelles. Reticulum tumor cells had large interchromatin spaces and irregular nuclear and cytoplasmic outlines. They often had multivesicular bodies, lysosomal vesicles, and much smooth-surfaced endoplasmic reticulum in the cytoplasm and were frequently surrounded by extracellular microfibrils and collagen libers. Nuclear inclusion-like masses of cytoplasm were common in both types of tumor cells. No structure was observed which could be recognized as virus.

scholarly journals Growth-inhibitory activity of lymphoid cell plasma membranes. I. Inhibition of lymphocyte and lymphoid tumor cell growth.

1984 ◽  
Vol 99 (4) ◽  
pp. 1221-1226 ◽  
Author(s):  
K C Stallcup ◽  
A Dawson ◽  
M F Mescher
Keyword(s):  
Plasma Membrane ◽  
Tumor Cell ◽  
Growth Inhibition ◽  
Tumor Cells ◽  
Inhibitory Activity ◽  
Calf Serum ◽  
Lymphoid Cells ◽  
Spleen Cells ◽  
Lymphoid Tumor ◽  
Normal Spleen

Membranes isolated from normal spleen cells or lymphoid tumor cells were found to inhibit in vitro growth of several murine tumor cell lines including a B cell hybridoma, a thymoma, and a mastocytoma. 50% inhibition occurred at membrane protein concentrations of 60-100 micrograms/ml. A similar concentration dependence was found for inhibition of [3H]-thymidine incorporation by tumor cells and for the lipopolysaccharide-induced mitogenic response of normal spleen cells. The inhibitory activity co-purified with the plasma membrane upon fractionation of crude membranes. Membrane solubilization with deoxycholate followed by dialysis to remove the detergent gave good recovery of inhibitory activity in the resulting reconstituted membranes. Membrane-mediated growth inhibition resulted from a decreased rate of proliferation and not from increased cell death. A toxic effect of the membranes was further ruled out by the finding that increasing the fetal calf serum content of the medium could substantially reverse the growth inhibition. Thus, the plasma membrane of lymphoid cells contains a component that can slow or stop the growth of cells in culture. This membrane component may have a role in cell contact-mediated regulation of growth.

Arf and Ink4a Are Critical Factors Determining the Cell of Origin and Therapeutic Sensitivity in Myc-Induced Mouse Lymphoid Tumor

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2448-2448
Author(s):  
Eiji Sugihara ◽  
Takatsune Shimizu ◽  
Kensuke Kojima ◽  
Jo Ishizawa ◽  
Michael Andreeff ◽  
...  
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
Tumor Cells ◽  
Mononuclear Cells ◽  
Preventive Therapy ◽  
Bone Marrow Mononuclear Cells ◽  
Cell Of Origin ◽  
Wild Type ◽  
Lymphoid Tumor ◽  
Cells Of Origin

Abstract Abstract 2448 Understanding the cell of origin of tumors is important not only for elucidating detailed mechanisms of tumorigenesis but also for characterizing the context in which tumor cells develop, both of which provide valuable information that can inform preventive therapy and therapeutic strategies in the clinical setting. However, the cell of origin and the factors determining the cell of origin remain unclear. In this study, a mouse model of precursor-B acute lymphoblastic leukemia/lymphoma (pre-B ALL/LBL: B220+CD19+CD43+/–IgM−) was established by retroviral transduction of Myc oncogenes (N-Myc or c-Myc) into mouse bone marrow mononuclear cells. To identify the cell of origin of this tumor, we fractionated N-Myc-transduced hematopoietic stem cells (HSCs), common lymphoid progenitors (CLPs), myeloid progenitors (MPs) and committed progenitor B cells, and then transplanted into recipient mice in a limiting dilution manner. As a result, HSCs showed the highest susceptibility to N-Myc-induced pre-B ALL/LBL versus CLPs and MPs. Frequencies of tumor-initiating cells originated from HSCs, CLPs and MPs were 1/184, 1/558 and 1/9286, respectively. Although N-Myc was unable to induce any tumor directly from committed progenitor B cells, N-Myc was able to induce pre-B ALL/LBL directly from those cells in the absence of Ink4a and Arf genes whose expression is normally maintained at low levels for endowing self-renewal capacity to HSCs. Furthermore, we found that N-Myc induced pre-B ALL/LBL directly from Arf deficient progenitor B cells. Since Arf was expressed significantly higher in progenitor B cells than Ink4a, Arf might play a predominant role in the determination of the cell of origin. In our mouse model, there is no significant difference between two types of Myc oncogenes, N-Myc and c-Myc, in respect to tumorigenic activities of the induced tumors, suggesting similar impacts of Myc family genes on lymphoid tumor. Next, we analyzed chemotherapeutic sensitivities of tumor cells derived from distinct cells of origin, wild-type HSCs and Ink4a/Arf−/− progenitor B cells. Tumor cells derived from Ink4a/Arf−/− progenitor B cells were significantly more resistant to Ara-C treatment than those derived from wild-type HSCs in vivo and in vitro. To eradicate Ink4a/Arf−/−-derived tumor cells, the Mdm2 inhibitor Nutlin-3 was used because Nultin-3 was assumed to be able to replace the role of Arf which inhibits Mdm2 to block p53 degradation. As a result, Nutlin-3 restored p53 and thereby induced massive apoptosis in tumor cells derived from Ink4a/Arf−/− progenitor B cells. In contrast, Nutlin-3 did not induce apoptosis in tumor cells derived from wild-type HSCs due to p53 mutations. Furthermore, Nutlin-3 effectively induced apoptosis in human B-ALL cell lines with wild-type p53 and lacking Ink4a and Arf expression. In addition, tumor cells derived from Ink4a/Arf−/− cells were more sensitive to Nutlin-3 treatment than normal bone marrow mononuclear cells. Therefore, Mdm2 inhibition can be a novel and promising therapeutic approach to the treatment of Ink4a/Arf deficient pre-B ALL/LBL, such as is frequently found in Ph+ B-ALL and relapsed B-ALL. Collectively these findings suggest that Ink4a and Arf are critical determining factors of the cell of origin of pre-B ALL/LBL, and that tumor cells derived from distinct cells of origin showed different drug sensitivities to Ara-C and Nutlin-3, which provides a novel insight into preventive therapy and different therapeutic approaches depending on genetic background of tumor cells. Disclosures: Saya: Kyowa Hakko Kirin, Co., Ltd.: Research Funding.

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