scholarly journals Lung Tumor Development and Spontaneous Regression in Lambs Coinfected With Jaagsiekte Sheep Retrovirus and Ovine Lentivirus

2010 ◽  
Vol 47 (1) ◽  
pp. 148-162 ◽  
Author(s):  
S. F. Hudachek ◽  
S. L. Kraft ◽  
D. H. Thamm ◽  
H. Bielefeldt-Ohmann ◽  
J. C. DeMartini ◽  
...  
Keyword(s):  
Spontaneous Regression ◽  
Lung Tumor ◽  
Tumor Development ◽  
Jaagsiekte Sheep Retrovirus ◽  
Ovine Lentivirus

scholarly journals Retrovirus Vectors Bearing Jaagsiekte Sheep Retrovirus Env Transduce Human Cells by Using a New Receptor Localized to Chromosome 3p21.3

2000 ◽  
Vol 74 (10) ◽  
pp. 4698-4704 ◽  
Author(s):  
Sharath K. Rai ◽  
James C. DeMartini ◽  
A. Dusty Miller
Keyword(s):  
Host Range ◽  
Chemokine Receptors ◽  
Lung Tumor ◽  
High Titer ◽  
Leukemia Virus ◽  
Human Infection ◽  
Human Cells ◽  
Careful Examination ◽  
Chromosome 3 ◽  
Jaagsiekte Sheep Retrovirus

ABSTRACT Jaagsiekte sheep retrovirus (JSRV) is a type D retrovirus associated with a contagious lung tumor of sheep, ovine pulmonary carcinoma. Other than sheep, JSRV is known to infect goats, but there is no evidence of human infection. Until now it has not been possible to study the host range for JSRV because of the inability to grow this virus in culture. Here we show that the JSRV envelope protein (Env) can be used to pseudotype Moloney murine leukemia virus (MoMLV)-based retrovirus vectors and that such vectors can transduce human cells in culture. We constructed hybrid retrovirus packaging cells that express the JSRV Env and the MoMLV Gag-Pol proteins and can produce JSRV-pseudotype vectors at titers of up to 106 alkaline phosphatase-positive focus-forming units/ml. Using this high-titer virus, we have studied the host range for JSRV, which includes sheep, human, monkey, bovine, dog, and rabbit cells but not mouse, rat, or hamster cells. Considering the inability of the JSRV-pseudotype vector to transduce hamster cells, we used the hamster cell line-based Stanford G3 panel of whole human genome radiation hybrids to phenotypically map the JSRV receptor (JVR) gene within the p21.3 region of human chromosome 3. JVR is likely a new retrovirus receptor, as none of the previously identified retrovirus receptors localizes to the same position. Several chemokine receptors that have been shown to serve as coreceptors for lentivirus infection are clustered in the same region of chromosome 3; however, careful examination shows that the JSRV receptor does not colocalize with any of these genes.

Chemopreventive Potential of α-Carotene Against Mouse Liver and Lung Tumor Development: Comparison with β-Carotene and α-Tocopherol

1997 ◽  
pp. 529-532 ◽  
Author(s):  
Hiroyuki Tsuda ◽  
Yoshio Iwahori ◽  
Takaaki Hori ◽  
Makoto Asamoto ◽  
Hiroyasu Baba-Toriyama ◽  
...  
Keyword(s):  
Mouse Liver ◽  
Lung Tumor ◽  
Tumor Development ◽  
Β Carotene

scholarly journals Decreased Lung Tumor Development in SwAPP Mice through the Downregulation of CHI3L1 and STAT 3 Activity via the Upregulation of miRNA342-3p

2019 ◽  
Vol 16 ◽  
pp. 63-72 ◽  
Author(s):  
Dong Hun Lee ◽  
Ki Cheon Kim ◽  
Chul Ju Hwang ◽  
Kyung Ran Park ◽  
Young Suk Jung ◽  
...  
Keyword(s):  
Lung Tumor ◽  
Tumor Development

scholarly journals Jaagsiekte Sheep Retrovirus Proviral Clone JSRVJS7, Derived from the JS7 Lung Tumor Cell Line, Induces Ovine Pulmonary Carcinoma and Is Integrated into the Surfactant Protein A Gene

2001 ◽  
Vol 75 (9) ◽  
pp. 4239-4246 ◽  
Author(s):  
James C. DeMartini ◽  
Jeanette V. Bishop ◽  
Thomas E. Allen ◽  
F. A. Jassim ◽  
J. Michael Sharp ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Line ◽  
Lung Tumor ◽  
Protein A ◽  
Tumor Cell Line ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Jaagsiekte Sheep Retrovirus ◽  
Pulmonary Carcinoma ◽  
Lung Tumor Cell

ABSTRACT Ovine pulmonary carcinoma (OPC) is a contagious neoplasm of alveolar epithelial type II (ATII) or Clara cells caused by a type D/B chimeric retrovirus, jaagsiekte sheep retrovirus (JSRV). Here we report the isolation, sequencing, pathogenicity, and integration site of a JSRV provirus isolated from a sheep lung tumor cell line (JS7). The sequence of the virus was 93 to 99% identical to other JSRV isolates and contained all of the expected open reading frames. To produce virions and test its infectivity, the JS7 provirus (JSRVJS7) was cloned into a plasmid containing a cytomegalovirus promoter and transfected into 293T cells. After intratracheal inoculation with virions from concentrated supernatant fluid, JSRV-associated OPC lesions were found in one of four lambs, confirming that JSRVJS7 is pathogenic. In JS7-cell DNA, the viral genome was inserted in the protein-coding region for the surfactant protein A (SP-A) gene, which is highly expressed in ATII cells, in an orientation opposite to the direction of transcription of the SP-A gene. No significant transcription was detected from either the viral or the SP-A gene promoter in the JS7 cell line at passage level 170. The oncogenic significance of the JSRV proviral insertion involving the SP-A locus in the JS7 tumor cell line is unknown.

The Effects of Dietary Myoinositol on Lung Tumor Development in Tobacco Smoke-Exposed Mice

2004 ◽  
Vol 16 (4) ◽  
pp. 195-201 ◽  
Author(s):  
Hanspeter Witschi ◽  
Imelda Espiritu ◽  
Man Ly ◽  
Dale Uyeminami
Keyword(s):  
Tobacco Smoke ◽  
Lung Tumor ◽  
Tumor Development

Enhancement of N-bis(2-hydroxypropyl)nitrosamine-initiated lung tumor development in rats by bleomycin and N-methyl-N-nitrosourethane

1984 ◽  
Vol 25 (1) ◽  
pp. 25-31 ◽  
Author(s):  
Tomoyuki Shirai ◽  
Atsuko Masuda ◽  
Masao Hirose ◽  
Etsuo Ikawa ◽  
Nobuyuki Ito
Keyword(s):  
Lung Tumor ◽  
Tumor Development

scholarly journals Overexpression of PRDX4 Modulates Tumor Microenvironment and Promotes Urethane-Induced Lung Tumorigenesis

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Jianbo Zheng ◽  
Xin Guo ◽  
Yuka Nakamura ◽  
Xiaolei Zhou ◽  
Reimon Yamaguchi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Tumor Microenvironment ◽  
Tumor Cell ◽  
Lung Tumor ◽  
Interleukin 1 ◽  
Tumor Development ◽  
Tumor Model ◽  
Tumor Formation ◽  
Tumor Diameter

Peroxiredoxin 4 (PRDX4), initially reported as an antioxidant, is overexpressed in lung cancer and participates in its progression. However, its role in the urethane-induced lung tumor model is undetermined. The aim of this study was to investigate the effect of PRDX4 overexpression on carcinogen-induced lung tumor development. Human PRDX4 overexpression transgenic (Tg) mice (hPRDX4+/+) and non-Tg mice were intraperitoneally injected with urethane to induce lung tumor. After 6 months, tumor formation was compared between groups and possible mechanisms for the difference in tumor development were investigated. The serum and lung PRDX4 expressions were enhanced after urethane stimulation in Tg mice. Both the average number of tumors (≥0.5 mm) and tumor diameter per mouse in the Tg group were significantly larger than in non-Tg controls, while body weight was lower in the Tg group. Compared with non-Tg controls, tumor cell proliferation was enhanced, while tumor cell apoptosis was suppressed in Tg mice. Systemic oxidative stress and oxidative stress in lung tumors were inhibited by PRDX4 overexpression. The balance of prooxidant enzymes and antioxidant enzymes was also shifted to a decreased level in Tg tumor. In lung tumor tissue, the density of microvessel penetrated into tumor was higher in the Tg group; macrophage infiltration was enhanced in Tg tumors, while there was no difference in T lymphocyte infiltration; the expressions of cytokines, including interleukin-1 beta (IL-1β) and matrix metallopeptidase 9 (MMP9), were elevated in Tg tumors, which resulted from enhanced phosphorylation of nuclear factor-κB p65 (NF-κB p65) and c-Jun, respectively. In conclusion, PRDX4 overexpression modulated tumor microenvironment and promoted tumor development in the mouse urethane-induced lung cancer model.

scholarly journals Dexmedetomidine Associated Lung Cancer Proliferation and Tumor Growth is Prevented by β-Caryophyllene: Role of AMPK Activation and PGC-1α/TFAM Over Expression

2022 ◽  
Author(s):  
Dan Wang ◽  
Dazhi Long ◽  
Jiegang Zhou ◽  
Ziqiang Dong ◽  
Guiming Huang
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Lung Tumor ◽  
Apoptotic Cell ◽  
Tumor Development ◽  
A549 Cells ◽  
Treated Group ◽  
Metastatic Progression ◽  
Cancer Proliferation

Background: Dexmedetomidine has been reported to induce anti-apoptotic effects and metastatic progression in lung cancer. In the current investigation, the effect of β-Caryophyllene on dexmedetomidine induced cell proliferation and apoptosis of lung cancer cells and tumor growth in mice was studied. Methods: A549 cell line was cultured with either dexmedetomidine alone or together with β-Caryophyllene for 24 h and analysed for cell proliferation with MTT assay. ELISA based kit was used to determine apoptotic DNA fragmentation. Western blotting was used to determine expression levels of target proteins. The induction of experimental lung tumor in rat model was achieved through the injection of A549 tumor cells subcutaneously into the middle left side of the mice after anesthetization with pentobarbital (35 mg/kg) at 2.8 × 106 cells in 400 μl of PBS. Result: We found that β-Caryophyllene exerts the anti-proliferative effects on A549 cells. Furthermore, β-Caryophyllene significantly prevents apoptotic cell death and causes up-regulation of PGC-1α and TFAM compared to dexmedetomidine treated cells. We observed that β-Caryophyllene suppressed tumor development in mice significantly compared to dexmedetomidine treated group without changing body weight.

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