Triple combination targeting PI3K,ER,and CDK4/6 inhibits growth of ER-positive breast cancer resistant to fulvestrant and CDK4/6 or PI3K inhibitor  

作　　者：Mikkel G.Terp Martina Tuttolomondo Neil Portman Sidse Ehmsen Lene E.Johansen Martin Bak Elgene Lim Henrik J.Ditzel 

机构地区：[1]Department of Cancer and Inflammation Research,Institute of Molecular Medicine,University of Southern Denmark,Odense,Denmark [2]Garvan Institute of Medical Research,Darlinghurst,Sydney,New SouthWales,Australia [3]St.Vincent’s Clinical School,Faculty of Medicine,University of New SouthWales Sydney,Sydney,New South Wales,Australia [4]Department of Oncology,Institute of Clinical Research,Odense University Hospital,Odense,Denmark [5]Department of Pathology,Sydvestjysk Sygehus,Esbjerg,Denmark [6]Academy of Geriatric Cancer Research(AgeCare),Odense University Hospital,Odense,Denmark

出　　处：《Cancer Communications》2023年第6期720-725,共6页癌症通讯（英文）

基　　金：funded in part by grants from the Danish Cancer Society(to Henrik J.Ditzel);Health Insurance“Denmark”(to Henrik J.Ditzel);Academy of Geriatric Cancer Research(AgeCare)(to Henrik J.Ditzel);Pink Tribute(to Henrik J.Ditzel).

摘　　要：Dear Editor,Despite the improved outcome of advanced estrogen receptor-positive(ER+)breast cancer patients treated with endocrine therapy in combination with either a cyclindependent kinase 4/6 inhibitor(CDK4/6i)or a phosphoinositide 3-kinase inhibitor(PI3Ki),the disease will eventually progress,and the optimal treatment strategy upon progression remains undefined[1-4].To address this,we developed MCF-7-and T47D-derived PIK3CAmutated breast cancer cell lines[5]resistant to combined CDK4/6i palbociclib and fulvestrant(MPF-R and TPFR)or combined PI3Ki alpelisib and fulvestrant(MAF-R and TAF-R),respectively(Supplementary Materials and Methods).Drug-sensitive isogenic cells(M-S and T-S)grown in parallel with MPF-R and TPF-R cells and the original MCF-7/S0.5 and T47D cells were analyzed for comparison.

关 键 词：PIK3CA BREAST cancer 

分 类 号：R737.9[医药卫生—肿瘤]