Truncating Prolactin Receptor Mutations Promote Tumor Growth in Murine Estrogen Receptor-Alpha Mammary Carcinomas
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- 作者：Obi L. Griffith1 ; 2 ; 3 ; 9 ; Szeman Ruby Chan4 ; 8 ; 9 ; Malachi Griffith1 ; 3 ; 5 ; Kilannin Krysiak1 ; 2 ; Zachary L. Skidmore1 ; Jasreet Hundal1 ; Julie A. Allen4 ; Cora D. Arthur4 ; Daniele Runci4 ; Mattia Bugatti7 ; Alexander P. Miceli4 ; Heather Schmidt1 ; Lee Trani1 ; Krishna-Latha Kanchi1 ; Christopher A. Miller1 ; 2 ; David E. Larson1 ; 5 ; Robert S. Fulton1 ; 5 ; William Vermi4 ; 7 ; Richard K. Wilson1 ; 2 ; 3 ; 5 ; Robert D. Schreiber4 ; 6 ; 10 ; schreiber@immunology.wustl.edu" class="auth_mail" title="E-mail the corresponding author ; Elaine R. Mardis1 ; 2 ; 3 ; 5 ; emardis@wustl.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：breast cancer ; estrogen-receptor positive ; luminal ; STAT1 ; mouse model ; whole genome sequencing ; PRLR
- 刊名：Cell Reports
- 出版年：2016
- 出版时间：27 September 2016
- 年：2016
- 卷：17
- 期：1
- 页码：249-260
- 全文大小：1922 K
文摘
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Mice lacking Stat1 develop mammary tumors that model human ERα+ breast cancer
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DNA sequencing finds a Prlr truncating mutation hotspot in 100% of Stat1−/− tumors
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At least 77.8% of DCIS examined also contain PRLR truncating mutations
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Co-expression of truncated and full-length PRLR promote tumor growth in MEFs
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