@article{3098708,
    title = "Nuclear factor-kappa B affects tumor progression in a mouse model of
malignant pleural effusion",
    author = "Stathopoulos, GT and Zhu, ZW and Everhart, MB and Kalomenidis, I and and Lawson, WE and Bilaceroglu, S and Peterson, TE and Mitchell, D and Yull, and FE and Light, RW and Blackwell, TS",
    journal = "American Journal of Respiratory Cell and Molecular Biology: An Official Journal of the American Thoracic Society, Medical Section of the American Lung Association",
    year = "2006",
    volume = "34",
    number = "2",
    pages = "142-150",
    publisher = "AMER THORACIC SOC",
    issn = "1044-1549, 1535-4989",
    doi = "10.1165/rcmb.2005-0130OC",
    keywords = "Lewis lung cancer; lung; adenocarcinoma; bioluminescence; luciferase",
    abstract = "We developed a novel mouse model of malignant pleural effusion (MPE) by
injecting Lewis lung cancer (LLC) cells directly into the pleural space
of syngeneic C57B/6 mice. The pleural effusions in this model share
common cellular and biochemical features with human MPEs. Implantation
and growth of pleural tumors triggers a host inflammatory response
characterized by a mixed inflammatory cell influx into the pleural
fluid. LLC cells exhibited high basal nuclear factor (NF)-kappa B
activity in vitro and in vivo, which we used to drive expression of a
NF-kappa B-dependent green fluorescent protein-firefly luciferase fusion
reporter construct. NF-kappa B-dependent reporter expression allowed
intravital tracing of pleural tumors. Inhibition of NF-kappa B in LLC
cells did not affect cell viability in culture; however, injection of
LLC cells expressing a dominant NF-kappa B inhibitor resulted in
decreased tumor burden, decreased pleural effusion volume, and decreased
pleural effusion TNF-alpha levels. These studies indicate that tumor
NF-kappa B activity regulates pleural tumor progression. This
reproducible model of MPE can be used to further study the influence of
specific host and tumor factors on the pathogenesis of MIRE and evaluate
new therapeutic strategies."
}