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Kenneth J. Pienta
Department Affiliation: Primary: Urology;
Secondary: Pharmacology and Molecular Sciences; Oncology
Degree: M.D., Johns Hopkins University School of Medicine
Telephone Number : 410-502-3137
Fax Number: 410-955-0833
E-mail address: firstname.lastname@example.org
School of Medicine Address: Marburg 121, 600 N. Wolfe Street, Baltimore, MD 21205
The ecology of cancer, tumor microenvironment, metastasis, biomarker development, novel therapeutic development.
Dr. Pienta's laboratory has championed the concept that cancer tumorigenesis and metastasis can best be understood utilizing the principles of Ecology. Ecologists have studied the population biology of invasive species for decades and have documented their impact on local environments as well as the global ecosystem as a whole. Invasive species start as a native population within a defined community and are then transported by some means to a new environment. In this new environment, the invader either then dies off or enters a period of time during which it establishes itself (lag period). It then begins to spread and have impact on the local environment, disrupting the ecosystem as a whole. This disruption has broad implications for the native species and the broader ecosystem. Biologic traits that result in a robust invasive species include rapid proliferative capacity, adaptation to environmental stress (phenotypic plasticity) and high tolerance to environmental heterogeneity. The life cycle of invasive species is directly analogous to the study of cancer metastasis. Cancer must grow in a primary site, extravasate and survive in the circulation to then intravasate at a target organ (invasive species survival in transport). Cancer cells often lay dormant at their metastatic site for a long period of time (lag period) before proliferating (invasive spread). Proliferation in the new site has an impact on the target organ microenvironment (ecological impact) and eventually the human host (biosphere impact). Successful treatment of cancer with a single agent is rarely enough to cure a patient without strategically modifying the support systems conducive to survival of cancer. The Pienta laboratory works to develop new treatments for cancer utilizing network disruption.
- Grasso, C.S., Wu, Y.M., Robinson, D.R., Cao, X., Dhanasekaran, S.M., Khan, A.P., Quist, M.J., Jing, X., Lonigro, R.J., Brenner, J.C., Asangani, I.A., Ateeq, B., Chun, S.Y., Siddiqui, J., Sam, L., Anstett, M., Mehra, R., Prensner, J.R., Palanisamy, N., Ryslik, G.A., Vandin, F., Raphael, B.J., Kunju, L.P., Rhodes, D.R., Pienta, K.J., Chinnaiyan, A.M., and Tomlins, S.A. The mutational landscape of lethal castration-resistant prostate cancer. Nature, 487(7406):239-43. Pub Med Reference
- Park, S.I., Liao, J., Berry, J.E., Li, X., Koh, A.J., Michalski, M.E., Eber, M.R., Soki, F.N., Sadler, D., Sud, S., Tisdelle, S., Daignault, S.D., Nemeth, J.A., Snyder, L.A., Wronski, T.J., Pienta, K.J., and McCauley, L.K. Cyclophosphamide creates a receptive microenvironment for prostate cancer skeletal metastasis. Cancer Res. 72(10):2522-32, 2012. Pub Med Reference
- Mishra, A., Wang, J., Shiozawa, Y., McGee, S., Kim, J., Jung, Y., Joseph, J., Berry, J.E., Havens, A., Pienta, K.J, and Taichman, R.S. Hypoxia stabilizes GAS6/AXl signaling in metastatic prostate cancer. Mol Cancer Res. 10(6):703-12, 2012. Pub Med Reference
- Pienta, K.J. and Camacho D.F. Disrupting the networks of cancer. Clin Cancer Res. 18(10):2801-8, 2012. Pub Med Reference
- Elbez, R., McNaughton, B.H., Patel, L., Pienta, K.J., and Kopelman, R. Nanoparticle induced cell magneto-rotation: monitoring morphology, stress and drug sensitivity of a suspended single cancer cell. PLoS One 6(12):e28475, 2011. Pub Med Reference
- Mehra, R., Kumar-Sinha, C., Shankar, S., Lonigro, R.J., Jing, X., Philips, N.E., Siddiqui, J., Han, B., Cao, X., Smith, D.C., Shah, R.B., Chinnaiyan, A.M. and Pienta, K.J. Characterization of bone metastases from rapid autopsies of prostate cancer patients. Clin Cancer Res. 17(12):3924-32, 2011. Pub Med Reference
- Shiozawa, Y., Pedersen, E.A., Havens, A.M., Jung, Y., Mishra, A., Joseph, J., Kim, J.K., Patel, L.R., Ying, C., Ziegler, A.M., Pienta, M.J., Song, J., Wang, J., Loberg, R.D., Krebsbach, P.H., Pienta, K.J., and Taichman, R.S. Human prostate cancer metastases target the hematopoietic stem cell niche to establish footholds in mouse bone marrow. J Clin Invest. 121(4):1298-312, 2011. Pub Med Reference