Additional file 1: of Therapeutic potential of combined BRAF/MEK blockade in BRAF-wild type preclinical tumor models Anais Del Curatolo Fabiana Conciatori Ursula Cesta Incani Chiara Bazzichetto Italia Falcone Vincenzo Corbo Sabrina D’Agosto Adriana Eramo Giovanni Sette Isabella Sperduti Teresa De Luca Mirko Marabese Senji Shirasawa Ruggero De Maria Aldo Scarpa Massimo Broggini Donatella Del Bufalo Francesco Cognetti Michele Milella Ludovica Ciuffreda 10.6084/m9.figshare.6796268.v1 https://springernature.figshare.com/articles/journal_contribution/Additional_file_1_of_Therapeutic_potential_of_combined_BRAF_MEK_blockade_in_BRAF-wild_type_preclinical_tumor_models/6796268 Supplementary Methods. Figure S1. RAF inhibition induces BRAF/CRAF heterodimerization in KRAS-mut contexts. Figure S2. Effects of trametinib, dabrafenib and their combination on cell growth and cell cycle distribution in A549 and MiaPaCa2 cells. Figure S3. Effects of trametinib and dabrafenib combination in lung cancer cells. Figure S4. Effects of trametinib and dabrafenib combination in pancreatic cancer cells. Figure S5. Effects of trametinib, dabrafenib and their combination in LCSC. Figure S6. Statistical correlation between KRAS status and pharmacological interactions. Figure S7. Effects of lapatinib in EGFR/HER2 amplified lung cancer cell lines. Table S1. Summary of the genetic status of the cell lines analyzed and response to treatments. (PDF 2519 kb) 2018-07-09 05:00:00 MAPK BRAF MEK Combination therapy Paradoxical effect