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 DâAgosto
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