Genomic responses in mouse models poorly mimic human inflammatory diseases.

@article{Seok2013GenomicRI,
  title={Genomic responses in mouse models poorly mimic human inflammatory diseases.},
  author={Junhee Seok and Howland Shaw Warren and Alex Gervacio Cuenca and Michael N. Mindrinos and Henry V Baker and Weihong Xu and Daniel R. Richards and Grace P. McDonald-Smith and Hong Gao and Laura E Hennessy and Celeste C. Finnerty and Christine M. Lopez and Shari Honari and Ernest Eugene Moore and Joseph P. Minei and Joseph Cuschieri and Paul E. Bankey and Jeffrey R. Johnson and Jason Lee Sperry and Avery B Nathens and Timothy R Billiar and Michael Anthony West and Marc G Jeschke and Matthew Brady Klein and Richard L. Gamelli and Nicole S. Gibran and Bernard H. Brownstein and Carol L. Miller-Graziano and Steve E. Calvano and Philip H. Mason and J. Perren Cobb and Laurence G Rahme and Stephen F. Lowry and Ronald V. Maier and Lyle L. Moldawer and DavidN. Herndon and Ronald W. Davis and Wenzhong Xiao and Ronald G. Tompkins},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2013},
  volume={110 9},
  pages={
          3507-12
        }
}
A cornerstone of modern biomedical research is the use of mouse models to explore basic pathophysiological mechanisms, evaluate new therapeutic approaches, and make go or no-go decisions to carry new drug candidates forward into clinical trials. Systematic studies evaluating how well murine models mimic human inflammatory diseases are nonexistent. Here, we show that, although acute inflammatory stresses from different etiologies result in highly similar genomic responses in humans, the… CONTINUE READING

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