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作 者:Robert Clarke Brandon C.Jones Catherine M.Sevigny Leena A.Hilakivi-Clarke Surojeet Sengupta
机构地区:[1]The Hormel Institute and Department of Biochemistry,Molecular Biology and Biophysics,University of Minnesota,Austin,MN55912,USA [2]Department of Oncology,Georgetown University Medical Center,Washington,DC 20057,USA [3]The Jackson Laboratory,600 Main Street,Bar Harbor,ME 04609,USA
出 处:《Cancer Drug Resistance》2021年第4期762-783,共22页癌症耐药(英文)
基 金:This work was supported by grants from the from the Department of Defense Breast Cancer Research Program(CA171885);from the National Cancer Institute(U01CA184902)to Dr.Clarke.
摘 要:Breast cancers characterized by expression of estrogen receptor-alpha(ER;ESR1)represent approximately 70%of all new cases and comprise the largest molecular subtype of this disease.Despite this high prevalence,the number of adequate experimental models of ER+breast cancer is relatively limited.Nonetheless,these models have proved very useful in advancing understanding of how cells respond to and resist endocrine therapies,and how the ER acts as a transcription factor to regulate cell fate signaling.We discuss the primary experimental models of ER+breast cancer including 2D and 3D cultures of established cell lines,cell line-and patient-derived xenografts,and chemically induced rodent models,with a consideration of their respective general strengths and limitations.What can and cannot be learned easily from these models is also discussed,and some observations on how these models may be used more effectively are provided.Overall,despite their limitations,the panel of models currently available has enabled major advances in the field,and these models remain central to the ability to study mechanisms of therapy action and resistance and for hypothesis testing that would otherwise be intractable or unethical in human subjects.
关 键 词:Breast cancer experimental models PDX XENOGRAFTS study design
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