@article{891,
  author = {Junhee Seok and H. Shaw Warren and Alex G. 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 Hennessy and Celeste C. Finnerty and Cecilia M. López and Shari Honari and Ernest E. Moore and Joseph P. Minei and Joseph Cuschieri and Paul E. Bankey and Jeffrey L. Johnson and Jason Sperry and Avery B. Nathens and Timothy R. Billiar and Michael A. West and Marc G. Jeschke and Matthew B. Klein and Richard L. Gamelli and Nicole S. Gibran and Bernard H. Brownstein and Carol 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 David N. Herndon and Ronald W. Davis and Wenzhong Xiao and Ronald G. Tompkins and the Inflammation and Host Response to Injury, Large Scale Collaborative Research Program and Amer Abouhamze and Ulysses G. J. Balis and David G. Camp and Asit K. De and Brian G. Harbrecht and Douglas L. Hayden and Amit Kaushal and Grant E. O’Keefe and Kenneth T. Kotz and Weijun Qian and David A. Schoenfeld and Michael B. Shapiro and Geoffrey M. Silver and Richard D. Smith and John D. Storey and Robert Tibshirani and Mehmet Toner and Julie Wilhelmy and Bram Wispelwey and Wing H Wong},
  title = {Genomic responses in mouse models poorly mimic human inflammatory diseases},
  abstract = {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 responses in corresponding mouse models correlate poorly with the human conditions and also, one another. Among genes changed significantly in humans, the murine orthologs are close to random in matching their human counterparts (e.g., R2 between 0.0 and 0.1). In addition to improvements in the current animal model systems, our study supports higher priority for translational medical research to focus on the more complex human conditions rather than relying on mouse models to study human inflammatory diseases.},
  year = {2013},
  journal = {Proceedings of the National Academy of Sciences},
  volume = {110},
  pages = {3507-3512},
  month = {2013-02-26},
  url = {https://www.pnas.org/doi/10.1073/pnas.1222878110},
  doi = {10.1073/pnas.1222878110},
}