Establishment of a Primary Effusion Lymphoma Cell Line (RM-P1) and In Vivo Growth System Using SCID Mice

2002 ◽  
Vol 76 (2) ◽  
pp. 165-172 ◽  
Author(s):  
Jun-ichi Miyagi ◽  
Masato Masuda ◽  
Nobuyuki Takasu ◽  
Akitoshi Nagasaki ◽  
Tetsuharu Shinjyo ◽  
...  
Keyword(s):  
Cell Line ◽  
Primary Effusion Lymphoma ◽  
Scid Mice ◽  
Lymphoma Cell ◽  
Lymphoma Cell Line ◽  
Primary Effusion Lymphoma Cell ◽  
Growth System ◽  
In Vivo Growth

scholarly journals Human Immunodeficiency Virus Replication in a Primary Effusion Lymphoma Cell Line Stimulates Lytic-Phase Replication of Kaposi’s Sarcoma-Associated Herpesvirus

1999 ◽  
Vol 73 (12) ◽  
pp. 10329-10338 ◽  
Author(s):  
Vasundhara Varthakavi ◽  
Philip J. Browning ◽  
Paul Spearman
Keyword(s):  
Human Immunodeficiency Virus ◽  
Cell Line ◽  
Kaposi's Sarcoma ◽  
Primary Effusion Lymphoma ◽  
Kaposi’S Sarcoma ◽  
Lytic Replication ◽  
Lymphoma Cell ◽  
Lymphoma Cell Line ◽  
Primary Effusion Lymphoma Cell ◽  
Immunodeficiency Virus

ABSTRACT Human immunodeficiency virus (HIV) and Kaposi’s sarcoma-associated herpesvirus (KSHV) coinfect many individuals in North America and in parts of Africa. Infection with HIV is a leading risk factor for the development of Kaposi’s sarcoma (KS). In this study, we tested the hypothesis that HIV infection of common or adjacent cells would stimulate replication and spread of KSHV. Infection of a primary effusion lymphoma cell line by vesicular stomatitis virus type G-pseudotyped HIV type 1 led to a rapid induction of lytic-phase KSHV replication. Induction of lytic KSHV replication by HIV required active replication of HIV. The addition of the nucleoside reverse transcriptase inhibitor azidothymidine or the protease inhibitor indinavir to the culture prevented HIV spread and inhibited the associated induction of KSHV lytic replication. Lytic replication occurred in both HIV-infected and HIV-uninfected cells within the culture, and could be induced in uninfected cells via a soluble factor released from the HIV-infected cells. Transmission of infectious KSHV to an uninfected target cell was enhanced by HIV replication and was inhibited by antiretroviral drugs. These results may have implications for the pathogenesis and treatment of KS in individuals coinfected with KSHV and HIV.

scholarly journals In vivo growth of a murine lymphoma cell line alters regulation of expression of HSP72.

1995 ◽  
Vol 15 (2) ◽  
pp. 1071-1078 ◽  
Author(s):  
S Davidson ◽  
P Høj ◽  
T Gabriele ◽  
R L Anderson
Keyword(s):  
Heat Shock ◽  
Cell Line ◽  
B Cell Lymphoma ◽  
Lymphoma Cell ◽  
Lymphoma Cell Line ◽  
Regulation Of Expression ◽  
Heat Shock Element ◽  
Stressed Cells

We have identified a murine B-cell lymphoma cell line, CH1, that has a much-diminished capacity to express increased levels of heat shock proteins in response to heat stress in vitro. In particular, these cells cannot synthesize the inducible 72-kDa heat shock protein (HSP72) which is normally expressed at high levels in stressed cells. We show here that CH1 fails to transcribe HSP72 mRNA after heat shock, even though the heat shock transcription factor, HSF, is activated correctly. After heat shock, HSF from CH1 is found in the nucleus and is phosphorylated, trimerized, and capable of binding the heat shock element. We propose that additional signals which CH1 cells are unable to transduce are normally required to activate hsp72 transcription in vitro. Surprisingly, we have found that when the CH1 cells are heated in situ in a mouse, they show normal expression of HSP72 mRNA and protein. Therefore, CH1 cells have a functional hsp72 gene which can be transcribed and translated when the cells are in an appropriate environment. A diffusible factor present in ascites fluid is capable of restoring normal HSP72 induction in CH1 cells. We conclude that as-yet-undefined factors are required for regulation of the hsp72 gene or, alternatively, that heat shock in vivo causes activation of hsp70 through a novel pathway which the defect in CH1 has exposed and which is distinct from that operating in vitro. This unique system offers an opportunity to study a physiologically relevant pathway of heat shock induction and to biochemically define effectors involved in the mammalian stress response.

scholarly journals High levels of hyaluronan production by a malignant lymphoma cell line with primary effusion lymphoma immunophenotype OHK

2003 ◽  
Vol 120 (6) ◽  
pp. 1055-1057 ◽  
Author(s):  
Hiroko Kuwabara ◽  
Masahiko Yoneda ◽  
Masami Nagai ◽  
Hajime Nishio ◽  
Taizo Tasaka ◽  
...  
Keyword(s):  
Malignant Lymphoma ◽  
Cell Line ◽  
Primary Effusion Lymphoma ◽  
Lymphoma Cell ◽  
Lymphoma Cell Line

Inhibition Effects of baicalin on Lymphoma Cell Line CA46 in Vitro and in Vivo

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5053-5053
Author(s):  
Jian Da Hu ◽  
Yi Huang ◽  
Yingyu Chen ◽  
Tiannan Wei ◽  
Tingbo Liu ◽  
...  
Keyword(s):  
Cell Line ◽  
Biological Effects ◽  
Annexin V ◽  
Lymphoma Cell ◽  
Control Group ◽  
Dependent Manner ◽  
Lymphoma Cell Line ◽  
Proliferation Inhibition

Abstract Baicalin is a traditional Chinese medicine with multiple biological effects. Some researches showed baicalin has anti-tumor effects in solid tumor, such as prostate cancer. In order to investigate its effects on proliferation inhibition and apoptosis induction in human lymphoma cell, we treated Burkitt lymphoma cell line CA46 with baicalin in vitro and in vivo of CA46 xenograft. Baicalin remarkably inhibited the cell proliferation, with an IC50 value of 10μM. Apoptosis was remarkably induced by baicalin in a dose-dependent manner, which was detected by Annexin V FITC/PI double staining analysis, TUNEL labeling method and DNA fragmentation respectively. Furthermore, RT-PCR showed that the mRNA expressions of c-myc and bcl-2 in treated CA46 cell decreased in a time-dependent manner. Western-Blot showed that the protein expressions of c-myc, bcl-2, procaspase-3 and PARP(116KD) in baicalin treated CA46 cell were down-regulated, while the expression of PARP(85KD) increased. Based on the results in vitro, we investigated in vivo efficacy of baicalin, alone or in combination with cytotoxic drug VP16, for treatment in CA46 nude mice xenograft. Baicalin with the dosage of 40mg/kg/d and 80kg/mg/d could remarkably inhibit the growth of the tumor compared with control group. Combination of baicalin and VP16 had better anti-tumor effects. Histological examination of tumor samples showed more necrotic cells in treated groups. And obvious apoptosis could be observed by electron microscope. No adverse events were found in treated groups. From above we could conclude that baicalin could efficiently induce proliferation inhibition and apoptosis of CA46 cells in vitro and in vivo, which may be related with the down-regulation of c-myc and bcl-2 expressions, as well as the up-regulation of caspase-3 activity.

Characterization of a Novel Human Anaplastic Large Cell Lymphoma Cell Line Tumorigenic in SCID Mice

2002 ◽  
Vol 43 (1) ◽  
pp. 165-172 ◽  
Author(s):  
Hartmut Merz ◽  
Karin Lange ◽  
Timo Gaiser ◽  
Anke Müller ◽  
Ursula Kapp ◽  
...  
Keyword(s):  
Cell Line ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Scid Mice ◽  
Lymphoma Cell ◽  
Lymphoma Cell Line ◽  
Large Cell Lymphoma

scholarly journals Calcium-Carbonate Nanocapsules Improve the Efficacy of BEZ235 in Lymphoma a Cell Line: A Promising New Technology of Drug Delivery

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4851-4851
Author(s):  
Monica Civallero ◽  
Viviana Vergaro ◽  
Cinzia Citti ◽  
Maria Cosenza ◽  
Giuseppe Cannazza ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Cell Line ◽  
Cell Lines ◽  
Free Drug ◽  
Lymphoma Cell ◽  
Intracellular Concentration ◽  
Solid Cancer ◽  
Lymphoma Cell Line ◽  
Biological Studies

Abstract Nanotechnology is a promising branch of the medical field, directed to improve diagnostic and therapeutics strategies, applying nanovectors as drug delivery systems. Efficient encapsulation of anticancer drugs in nanocolloids and microcapsules was recently developed by G. Ciccarella research group (1). Based on our collaboration with the Nantional Nanotechnology Laboratory of the University of Salento and our previous experience with target therapies, we encapsulated BEZ235, a phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin inhibitor (mTOR). BEZ235 efficiently blocks the dysfunctional activation of the PI3K/mTOR pathway in cellular and in vivo settings, thus inhibiting the growth and proliferation of various cancer cells, and phase I/II clinical trials were open in solid cancer. However the scarse solubility limited further development of this promising compound. In order to overcome the solubility issue BEZ235-loaded nanocapsules were generated by the stepwise adsorption of oppositely charged polyelectrolytes into biocompatible CaCO3 cores. First nanocapsules were tested for biocompatibility. The exposition of lymphoma cell lines to empty nanocapsules up to 48 hours, did not induce any cititoxicity, confirming their biocompatibility. Second, encapsulated BEZ235 was compared with free-drug to test the cytotoxicity in a T lymphoma cell line (HUT78) by MTT assay (Fig. 1). The results suggested that nanoencapsulated-BEZ235 was extremely efficient compared with free-BEZ235, reaching IC50 just after 5 hours of exposure compared with an IC65% at 48 hours with the free drug. A validated LC-MS/MS method was developed in order to quantify intracellular concentration of BEZ235 over time. Intracellular concentration of BEZ235 in the lymphoma cell line was consistent with biological results since the internalization kinetic and efficiency was increased by the coating. In order to confirm that the encapsuled-BEZ235 was still effective on cell apoptosis, we tested free BEZ and encapsulated BEZ235 at a concentration of 1µM in T cell lymphoma cell lines. Encapsulated-BEZ235 induced apoptosis evidenced by the cleavage of caspase 8, 9 and 3 at an earlier time point compared with free BEZ235 and at significantly lower concentration. We also confirmed that the encapsulated-BEZ235 maintained its effect on the target mTOR/AKT pathway: p-AKT was dephosphorylated at 5h while the free BEZ235 operates at least after 24 hours at concentrations 100 times higher, as previously demonstrated (2). Keeping in mind a future clinical application of these polymeric particles/capsules, our data can be regarded as a promising new nanotechnology-based strategy to improve the efficacy and bioavailability of old and new drugs. Functional biological studies of BEZ235-encapsulated carrier and its mechanism of internalization are already under way, and animal in vivo studies to evaluated toxicity and distribution of the nanocapsuled compound are ongoing. 1 F. Baldassare et al., Macromolecular Bioscience, Volume 12, Issue 5, pages 656-665, 2012 2 Civallero M, Cosenza M, Marcheselli L, Pozzi S, Sacchi S. Expert Opin Investig Drugs. 2012 Nov;21(11):1597-606. Disclosures No relevant conflicts of interest to declare.

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