Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
5R01CA078312-02
Application #
6174220
Study Section
Reproductive Endocrinology Study Section (REN)
Program Officer
Freeman, Colette S
Project Start
1999-07-01
Project End
2002-06-30
Budget Start
2000-07-01
Budget End
2001-06-30
Support Year
2
Fiscal Year
2000
Total Cost
$222,778
Indirect Cost
Name
University of Wisconsin Madison
Department
Biology
Type
Schools of Veterinary Medicine
DUNS #
161202122
City
Madison
State
WI
Country
United States
Zip Code
53715
Asher, Jennifer M; O'Leary, Kathleen A; Rugowski, Debra E et al. (2012) Prolactin promotes mammary pathogenesis independently from cyclin D1. Am J Pathol 181:294-302
Arendt, Lisa M; Rugowski, Debra E; Grafwallner-Huseth, Tara A et al. (2011) Prolactin-induced mouse mammary carcinomas model estrogen resistant luminal breast cancer. Breast Cancer Res 13:R11
Carver, Kristopher C; Piazza, Timothy M; Schuler, Linda A (2010) Prolactin enhances insulin-like growth factor I receptor phosphorylation by decreasing its association with the tyrosine phosphatase SHP-2 in MCF-7 breast cancer cells. J Biol Chem 285:8003-12
Sakamoto, K; Triplett, A A; Schuler, L A et al. (2010) Janus kinase 2 is required for the initiation but not maintenance of prolactin-induced mammary cancer. Oncogene 29:5359-69
Arendt, Lisa M; Grafwallner-Huseth, Tara L; Schuler, Linda A (2009) Prolactin-growth factor crosstalk reduces mammary estrogen responsiveness despite elevated ERalpha expression. Am J Pathol 174:1065-74
Carver, Kristopher C; Arendt, Lisa M; Schuler, Linda A (2009) Complex prolactin crosstalk in breast cancer: new therapeutic implications. Mol Cell Endocrinol 307:1-7
Piazza, Timothy M; Lu, Juu-Chin; Carver, Kristopher C et al. (2009) SRC family kinases accelerate prolactin receptor internalization, modulating trafficking and signaling in breast cancer cells. Mol Endocrinol 23:202-12
Arendt, Lisa M; Evans, Lindsay C; Rugowski, Debra E et al. (2009) Ovarian hormones are not required for PRL-induced mammary tumorigenesis, but estrogen enhances neoplastic processes. J Endocrinol 203:99-110
Carver, Kristopher C; Schuler, Linda A (2008) Prolactin does not require insulin-like growth factor intermediates but synergizes with insulin-like growth factor I in human breast cancer cells. Mol Cancer Res 6:634-43
Arendt, Lisa M; Schuler, Linda A (2008) Prolactin drives estrogen receptor-alpha-dependent ductal expansion and synergizes with transforming growth factor-alpha to induce mammary tumors in males. Am J Pathol 172:194-202

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