Subtype and pathway specific responses to anticancer compounds in breast cancer
- Heiser, LM; Sadanandam, A; Kuo, WL; Benz, SC; Goldstein, TC; Ng, S; Gibb, WJ; Wang, NJ; Ziyad, S; Tong, F; Bayani, N; Hu, Z; Billig, JI; Dueregger, A; Lewis, S; Jakkula, L; Korkola, JE; Durinck, S; Pepin, F; Guan, YH; Purdom, E; Neuvial, P; Bengtsson, H; Wood, KW; Smith, PG; Vassilev, LT; Hennessy, BT; Greshock, J; Bachman, KE; Hardwicke, MA; Park, JW; Marton, LJ; Wolf, DM; Collisson, EA; Neve, RM; Mills, GB; Speed, TP; Feiler, HS; Wooster, RF; Haussler, D; Stuart, JM; Gray, JW; Spellman, PT;
Publication Year 2012-02-21, Volume 109, Issue #8, Page 2724-2729
- Journal Title
- PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Publication Type
- Journal Article
- Breast cancers are comprised of molecularly distinct subtypes that may respond differently to pathway-targeted therapies now under development. Collections of breast cancer cell lines mirror many of the molecular subtypes and pathways found in tumors, suggesting that treatment of cell lines with candidate therapeutic compounds can guide identification of associations between molecular subtypes, pathways, and drug response. In a test of 77 therapeutic compounds, nearly all drugs showed differential responses across these cell lines, and approximately one third showed subtype-, pathway-, and/or genomic aberration-specific responses. These observations suggest mechanisms of response and resistance and may inform efforts to develop molecular assays that predict clinical response.
- NATL ACAD SCIENCES
- TAXOL-INDUCED APOPTOSIS; RAW COPY NUMBERS; CELL-LINES; KINASE INHIBITOR; FOXA1 EXPRESSION; BETA-CATENIN; RESISTANCE; CISPLATIN; ERBB2; CHEMOSENSITIVITY
- WEHI Research Division(s)
- Link To PubMed Central Version
- Publisher's Version
- Rights Notice
- Copyright © 2013 National Academy of Sciences.
Creation Date: 2012-02-21 12:00:00Last Modified: 0001-01-01 12:00:00