Department of Pharmacology and Therapeutics
Roswell Park Cancer Institute
Elm and Carlton Streets
Buffalo NY USA 14263
Tel: 716-845-1260
FAX: 716-845-8857
E-mail: barbara.foster@roswellpark.org

Dr. Barbara A. Foster joined the staff of Roswell Park Cancer Institute (RPCI) in 2002, as Assistant Member in the Department of Pharmacology & Therapeutics. She also is an Assistant Professor in the Molecular Pharmacology & Cancer Therapeutics Program, Roswell Park Graduate Division, University at Buffalo.

She earned her doctoral degree in Anatomy at the University of California, San Francisco, and completed a postdoctoral fellowship in Cell Biology at Baylor College of Medicine, Houston, TX. Dr. Foster comes to RPCI from the Department of Urology at the University of Pittsburgh, PA.

Dr. Foster’s research interests focus on the understanding of the molecular mechanism of prostatic development and of prostate cancer initiation and progression as well as the utilization of animal models to test novel strategies of chemoprevention and therapy for prostate cancer.

Dr. Foster is a member of the American Association for Cancer Research, Society for Basic Urologic Research and Women in Cancer Research. She has authored or co-authored more than 30 journal articles, abstracts and book chapters.

Current Program
Prostate cancer
Transgenic mouse models
Preclinical testing of new therapeutic approaches

Description of Research

Our laboratory uses animal models to understand the molecular mechanism of prostate cancer initiation and progression in order to rationally design therapeutic approaches for the prevention and treatment of the disease. The ultimate goal of the laboratory is to use preclinical testing of putative therapeutic agents to rapidly identify promising effective agents and facilitate the rapid movement of these compounds from the benchtop to the bedside.
The laboratory extensively uses the transgenic adenocarcinoma of mouse prostate (TRAMP) model. This model uses the probasin promoter to express the potent oncogene SV 40 T antigen (Tag) specifically in the secretory epithelial cells of the prostate. The prostate develops normally. However, at puberty the transgene is expressed and with time TRAMP animals develop progressive prostate cancer culminating in poorly differentiated metastatic disease. We have established multiple cell lines from TRAMP that represent different stages of the disease ranging from non-tumorigenic to tumorigenic and metastatic. These cell lines can be grown in immune intact syngenic hosts and have been used to screen compounds and test immune based therapies for prostate cancer.

Prostate cancer has a high propensity to metastasize to bone. However, our understanding of this process has been severely impeded by the lack of animal models that recapitulate this aspect of the human disease. Recently a TRAMP mouse presented with hind leg paralysis. Upon necropsy it was discovered that this animal had a bone metastasis to the base of the spine. Cell lines were established from this tumor, TRAMP-BC. These cell lines are tumorigenic and metastasize to bone when injected into an immune intact syngenic male host. The TRAMP-BC lines are being used to investigate the molecular mechanism of prostate cancer/bone interactions.

Current compounds and approaches being tested in the lab include low calcemic vitamin D analogs and selenium compounds for chemoprevention, isothiocynates as a nutritional supplement for prevention, and dendritic cell vaccine approaches for treatment and prevention. In addition we are interested in the molecular mechanisms of prostatic development and mesenchymal-epithelial interactions involved in normal and diseased prostatic biology.

Key Publications

 

• Foster BA, Gingrich FR, Kwon ED, Madias C, Greenberg NM (1997). Characterization of prostatic epithelial cell lines derived form transgenic adenocarcinoma of the mouse prostate (TRAMP) model. Cancer Research 57:3325-2230.
  Kwon ED, Hurwitz AA, Foster BA, Madias C, Feldhaus F, Allison J, Greenberg NM, Burg M (1997). Manipulation of T cell costimulatory and inhibitory signals for prostate cancer immunotherapy. PNAS 94:8099-8103.
• Gingrich JR, Barrios RJ, Foster BA, Greenberg NM (1999). Pathologic progression of authochthonous prostate cancer in the TRAMP model. Prostatic Diseases 6:1-6.
• Foster BA, Kaplan PJ, Greenberg NM (1999). Characterization of the FGF axis and identification of a novel FGFRiiic isoform during prostate cancer progression in the TRAMP model. Prostate Cancer and Prostatic Diseases 2:76-82
• Kwon ED, Foster BA, Hurwitz AA, Madias CM, Allison JP, Greenberg NM, Burg MB (2000). Elimination of residual metastatic prostate cancer following surgery and adjunctive CTLA-4 blockade immunotherapy. PNAS 96:15074-15079.
• Hurwitz AA, Foster BA, Kwon ED, Truong T, Choi EM, Greenberg NM, Burg MB, Allison JP (2000). Combination immunotherapy of primary prostate cancer in a transgenic mouse model using CTLA-4 blockade. Cancer Research 60(9):2444-2448.
• Guangzhou H, Foster BA, Mistry S, Buchanan G, Harris JM, Tilley WD, Greenberg NM (2001). Hormone status selects for spontaneous somatic androgen receptor variants that demonstrate specific ligand and cofactor dependent activities in autochthonous prostate cancer. J Biol Chem 276(14):11204-11213.