Acquired resistance to combination treatment through loss of synergy with MEK and PI3K inhibitors in colorectal cancer

• Main Authors: Bhattacharya B., Low S.H.H., Chong M.L., Chia D., Koh K.X., Sapari N.S., Kaye S., Hung H., Benoukraf T., Soong R.
• Other Authors: CANCER SCIENCE INSTITUTE OF SINGAPORE
• Format: Article
• Published: 2020
• Subjects: buparlisib; endothelin; endothelin 1; selumetinib; transforming growth factor beta2; antineoplastic agent; mitogen activated protein kinase kinase kinase; phosphatidylinositol 3 kinase; protein kinase inhibitor; acquired resistance; animal experiment; animal model; animal tissue; antineoplastic activity; Article; cancer combination chemotherapy; cancer resistance; cell stimulation; colorectal cancer; controlled study; cross resistance; drug efficacy; drug potentiation; EDN1 gene; gene overexpression; gene silencing; genome analysis; HCT116 cell line; human; human cell; IC50; in vitro study; in vivo study; male; mouse; nonhuman; phenotype; signal transduction; TGFB2 gene; animal; antagonists and inhibitors; colorectal tumor; drug resistance; drug screening; HCT 116 cell line; pathology; physiology; SCID mouse; Animals; Antineoplastic Combined Chemotherapy Protocols; Colorectal Neoplasms; Drug Resistance, Neoplasm; Drug Synergism; HCT116 Cells; Humans; MAP Kinase Kinase Kinases; Mice; Mice, SCID; Phosphatidylinositol 3-Kinases; Protein Kinase Inhibitors; Xenograft Model Antitumor Assays
• Online Access: https://scholarbank.nus.edu.sg/handle/10635/174090
• Institution: National University of Singapore

10.18632/oncotarget.8692