Paul Marker

Paul Marker
Associate Professor

Ph.D., Stanford University, 1998
Postdoctoral Research: University of California-San Francisco 

Lab website: http://pharmacy.wisc.edu/marker-lab

Address: 4111 Rennebohm Hall

Telephone: 608-890-2150

E-mail:

Department: Pharmacy

Research Interests

My laboratory investigates prostate cancer, benign prostatic hyperplasia, and normal prostate biology using mouse genetics and human patient samples.

Research Fields

Disease Biology
Development
Gene Expression
Genomics & Proteomics
Human, mouse & rat

Research Description:

Research in the Marker laboratory is focused on understanding the biology of the prostate gland at the molecular level. Interest in understanding the biology of the prostate is driven both by the fascinating nature of the developmental processes that function during organogenesis of the prostate and by the high incidence in humans of prostatic diseases including prostatic adenocarcinoma and benign prostatic hyperplasia. The Marker lab is particularly interested in the role of intercellular communication between epithelial and mesenchymal/stromal cells during prostatic branching morphogenesis and during the progression of prostate cancer. Current projects in the Lab include investigation of the roles of Fibroblast growth factor receptor 2 (Fgfr2) during prostatic development and cancer progression. Large scale sequencing and whole-genome association studies have shown that Fgfr2 is both commonly mutated in human cancers, and single nucleotide polymorphisms in Fgfr2 increase the risk for developing cancer. Data from the Marker lab and others has also shown that the Fgfr2 is a critical mediator of early development in the prostate. Ongoing research in the Marker lab is focused on understanding the mechanisms of Fgfr2 action in the prostate both during mouse development and in human prostate cancer. A second project in the Marker lab is a forward genetic screen in mice to identify new genes involved in prostate cancer progression using transposon-mediated insertional mutagenesis. A secondary screen is used to validate the importance of candidate genes identified using the mouse model by examining the human orthologues of the candidates for altered expression in human prostate cancers. This project has already identified new candidate oncogenes that are also over-expressed in human prostate cancers. Ongoing studies include continued screens for novel prostate cancer genes and functional evaluation of candidate genes to determine their roles in prostate cancer initiation and/or progression. 

Representative Publications:

Search PubMed for more publications by Paul Marker

Joesting MS, Cheever TR, Volzing KG, Yamaguchi T, Wolf V, Naf D, Rubin JS, and Marker PC. Secreted frizzled related protein 1 is a paracrine modulator of epithelial branching morphogenesis, proliferation, and secretory gene expression in the prostate. 2008. Developmental Biology. 317: 161-173. 

Kuslak SL and Marker PC. Fibroblast growth factor receptor signaling through MEK-ERK is required for prostate bud induction. Differentiation. 2007. 75: 638-651. 

Kuslak SL, Thielen JL, and Marker PC. The mouse seminal vesicle shape mutation is allelic with Fgfr2. Development. 2007. 134: 557-565. 

Thielen JL, Volzing KG, Collier LS, Green LE, Largaespada DA, and Marker PC. Markers of prostate region-specific epithelial identity define anatomical locations in the mouse prostate that are molecularly similar to human prostate cancers. Differentiation. 2007. 75: 49-61. 

Joesting MS, Perrin S, Elenbaas B, Fawell SE, Rubin JS, Franco OE, Hayward SW, Cunha GR, and Marker PC. Identification of SFRP1 as a candidate mediator of stromal-to-epithelial signaling in prostate cancer. Cancer Research. 2005. 65:10423-10430.