Recurrent activating mutations of PPAR gamma associated with luminal bladder tumors.
Rochel, N., Krucker, C., Coutos-Thevenot, L., Osz, J., Zhang, R., Guyon, E., Zita, W., Vanthong, S., Hernandez, O.A., Bourguet, M., Badawy, K.A., Dufour, F., Peluso-Iltis, C., Heckler-Beji, S., Dejaegere, A., Kamoun, A., de Reynies, A., Neuzillet, Y., Rebouissou, S., Beraud, C., Lang, H., Massfelder, T., Allory, Y., Cianferani, S., Stote, R.H., Radvanyi, F., Bernard-Pierrot, I.(2019) Nat Commun 10: 253-253
- PubMed: 30651555 
- DOI: https://doi.org/10.1038/s41467-018-08157-y
- Primary Citation of Related Structures:  
6FZF, 6FZG, 6FZJ, 6FZP, 6FZY - PubMed Abstract: 
The upregulation of PPAR¦Ã/RXR¦Á transcriptional activity has emerged as a key event in luminal bladder tumors. It renders tumor cell growth PPAR¦Ã-dependent and modulates the tumor microenvironment to favor escape from immuno-surveillance. The activation of the pathway has been linked to PPARG gains/amplifications resulting in PPAR¦Ã overexpression and to recurrent activating point mutations of RXR¦Á. Here, we report recurrent mutations of PPAR¦Ã that also activate the PPAR¦Ã/RXR¦Á pathway, conferring PPAR¦Ã-dependency and supporting a crucial role of PPAR¦Ã in luminal bladder cancer. These mutations are found throughout the protein-including N-terminal, DNA-binding and ligand-binding domains-and most of them enhance protein activity. Structure-function studies of PPAR¦Ã variants with mutations in the ligand-binding domain allow identifying structural elements that underpin their gain-of-function. Our study reveals genomic alterations of PPARG that lead to pro-tumorigenic PPAR¦Ã/RXR¦Á pathway activation in luminal bladder tumors and may open the way towards alternative options for treatment.
Organizational Affiliation: 
Institut de G¨¦n¨¦tique et de Biologie Mol¨¦culaire et Cellulaire (IGBMC), Institut National de La Sant¨¦ et de La Recherche M¨¦dicale (INSERM), U1258/Centre National de Recherche Scientifique (CNRS), UMR7104/Universit¨¦ de Strasbourg, 67404 Illkirch, France. rochel@igbmc.fr.