Year arrived at BSU: 1997
Department of Biology
Boise State University
Boise, ID 83725-1515Office Location: Science Building, Room 227
Office Number: 208-426-4287
Office Fax: 208-426-4267
E-Mail Address: firstname.lastname@example.org
B.S. in Biology, Pennsylvania State University, State College, PA, 1983
Ph.D. in Biology, The Johns Hopkins University, Baltimore, MD, 1991
Postdoctoral Fellowship, Intramural Research Training Award, National Cancer Institute, National Institutes of Health, 1992-1997
BIOL 301 Cell Biology
BIOL 343 Genetics
BIOL 344/344G Molecular Cell & Genetics Laboratory
BIOL 441/541 Molecular Biology of Cancer
BIOL 465/565 Advanced Topics in Molecular Biological Techniques
BIOL 466/566 Molecular Studies of Cancer
BIOL 595 Readings and Discussion: Cancer Biology
My laboratory’s research interests are directed towards elucidation of the molecular mechanisms that promote tumor progression. We have been working on the effects of the cytokine Oncostatin M (OSM) on breast tumor progression and metastasis. Oncostatin M (OSM), an IL-6 family cytokine, is produced by breast cancer cells and tumor-associated cells of the immune system, including macrophages and neutrophils. OSM has been shown to inhibit the proliferation of breast cancer cells, and this effect initially focused much attention on OSM as a potential breast cancer therapy. Data from our lab, however, suggests that OSM could actually contribute to tumor progression and the development of a metastatic state. We have shown that OSM induces vascular endothelial cell growth factor (VEGF), cyclooxygenase-2 (COX-2), cell detachment, and invasive capacity in vitro. In vivo studies involving the role of OSM in breast, prostate, and colon cancer progression are underway.
Jorcyk, C.L., Holzer, R.G., and Ryan, R.E.: Oncostatin induces detachment and enhanced metastatic capacity in T-47D human breast carcinoma cells. Cytokine in press.
Queen, M.M., Ryan, R.E., Holzer, R.G., Keller-Peck, C.R., and Jorcyk, C.L.: Breast cancer cells stimulate neutrophils to produce Oncostatin M: potential implications for tumor progression. Cancer Research 65: 8896-8904, 2005.
MacDougall, C.A., Ide, A., Soares, C., Vargas, M., Holzer, R.G., and Jorcyk, C.L.: Involvement of the hepatocyte growth factor-met receptor signaling loop with the classical “3M” pathways in tumor progression of mouse prostate adenocarcinoma cells. The Prostate 64: 139-149, 2005.
Holzer, R.G., Tommack, M., Schlekeway, E., Ryan, R.E, and Jorcyk, C.L: Oncostatin M induces the detachment of a reservoir of invasive mammary carcinoma cells: the role of cyclooxygenase-2. Clinical and Experimental Metastasis 21:167-176, 2004.
Holzer, R.G., MacDougall, C., Atwood, C., Green, J.E., and Jorcyk, C.L. 2003. Development and characterization of a progressive series of hormone-responsive mammary adenocarcinoma cell lines derived from the C3(1)/SV40 Large T-antigen transgenic mouse model. Breast Cancer Research and Treatment 77:65-76.
Soares, C., Shibata, M.-A., Green, J.E. and Jorcyk, C.L.: 2002. Development of PIN and prostate adenocarcinoma cell lines: a model system for multistage tumor progression. Neoplasia 4: 112-120.
Calvo, A., Xiao, N., Simon, R., Kang, J., Best, C., Emmert-Buck, M., Jorcyk, C.L., and Green, J.E. 2002. Identification of genes in prostate tumor progression by cDNA microarray analysis in an in vitro model derived from C3(1)/T-antigen transgenic mice: down-regulation of selenoprotein-P in mouse and human prostate cancer. Cancer Research 62: 5325-35.
Wigginton, J.M., Park, J.W., Gruys, M.E., Young, H.A., Jorcyk, C.L., Back, T.C., Brunda, M.J., Strieter, R.M., Ward, J., Green, J.E. and Wiltrout, R.H. 2001. Complete regression of established spontaneous mammary carcinoma and the therapeutic prevention of genetically programmed neoplastic transition by IL-12/pulse IL-2: induction of local T cell infiltration, fas/fas ligand gene expression, and mammary epithelial apoptosis. J. Immunol. 166: 1156-1168.
Green, J.E., Shibata, M.A., Yoshidome, K., Kiu, M.L., Jorcyk, C., Anver, M.R., Wigginton, J., Wiltrout, R., Shibata, E., Kaczmarczyk, S., Wang, W., Liu, Z.Y., Calvo, A. and Couldrey, C. 200. The C3(1)/SV40 T-antigen transgenic mouse model of mammary cancer: ductal epithelial cell targeting with multistage progression to carcinoma. Oncogene 19: 1020-1027.
Shibata, M.-A., Yoshidome, K., Shibata, E., Jorcyk, C.L. and Green, J.E. 2000. Suppression of mammary carcinoma growth in vitro and in vivo by inducible expression of the Cdk inhibitor p21. Cancer Gene Therapy 1: 1-10.
Maroulakou, I. G., Shibata, M.-A., Anver, M., Jorcyk, C. L., Liu, M.-L., Roche, N., Roberts, A. B., Tsarfaty, I., Reseau, J., Ward, J., and Green, J. E. 1999. Heterotopic endochondrial ossification with mixed tumor formation in C3(1)/Tag transgenic mice is associated with elevated TGF-beta1 and BMP-2 expression. Oncogene 18: 5435-5447.
Ward, J., Konishi, N., Ohshima, M., Lamb, P.L., Jorcyk, C. and Barrett, J. 1998. Kai1 expression in paraffin embedded sections of prostate cell lines and normal, hyperplastic and neoplastic human prostate. Pathology International 48: 87-92.
Shibata, M.-A., Jorcyk, C. L., Devor, D., Yoshidome, K., Rulong, S., Resau, J., Roche, N., Roberts, A., Ward, J., and Green, J. E. 1998. Altered expression of transforming growth factor ˜s during urethral and bulbourethral gland tumor progression in transgenic mice carrying the androgen-responsive C3(1) 5’ flanking region fused to SV40 large T antigen. Carcinogenesis 19: 195-205.
Shibata, M.-A., Jorcyk, C. L., Liu, M.-L., Yoshidome, K., Gold, L., Green, J. E. 1998. The C3(1)/SV40 T antigen transgenic mouse model of prostate and mammary cancer. Toxicologic Pathology 26: 177-182.
Yoshidome, K., Shibata, M.-A., Maroulakou, I. G., Liu, M.-L., Jorcyk, C. L., Gold, L. G., Welch, V. N., and Green, J. E. 1998. Genetic alterations in the development of mammary and prostate cancer in the C(3)1/Tag transgenic mouse model (Review). International Journal of Oncology 12: 449-453.
Liu, M.-L., Von Lintig, F. C., Liyange, M., Shibata, M.-A., Jorcyk, C. L., Ried, T., Boss, G. R. and Green, J. E. 1998. Amplification of Ki-ras and elevation of MAP kinase activity during mammary tumor progression in C3(1)/SV40 tag transgenic mice. Oncogene 18: 2403-2411.
Jorcyk, C. L., Liu, M.-L., Maroulakou, I. G., Shibata, M.-A., Komschlies, K. L., McPhaul, M. J., Resau, J. H. and Green, J. E. 1998. Development and characterization of a mouse prostate adenocarcinoma cell line: ductal formation determined by extracellular matrix. The Prostate 34: 10-22.