Matthew J. Schiewer, PhD
Assistant Professor, Urology & Cancer Biology
Director, Urology Research Laboratory
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Matthew J. Schiewer, PhD
Assistant Professor, Urology & Cancer Biology
Director, Urology Research Laboratory
Education
Education
PhD, Thomas Jefferson University, Philadelphia, PA - 2012
BS, Marian College, Indianapolis, IN - 2003
Most Recent Peer-Reviewed Publications
- A Novel Role for DNA-PK in Metabolism by Regulating Glycolysis in Castration-Resistant Prostate Cancer
- Novel Oncogenic Transcription Factor Cooperation in RB-Deficient Cancer
- Mutant p53 elicits context-dependent pro-tumorigenic phenotypes
- The circadian cryptochrome, CRY1, is a pro-tumorigenic factor that rhythmically modulates DNA repair
- Rb/e2f1 as a master regulator of cancer cell metabolism in advanced disease
Awards
- 2019, Philadelphia Prostate Cancer Biome Project-Pilot Award Program
- 2019, American Cancer Society Institutional Research Grant (ACS-IRG)-Basic & Clinical Research
- 2018, Jefferson Department of Cancer Biology Retreat Pilot Award (in collaboration with Josep Domingo-Domenech, MD, PhD)
- 2016, AACR-Aflac Inc. Scholar in training award
- 2015, DAVA Oncology GU Malignancies Travel Scholarship
- 2013, Gordon Research Conferences Travel Award
- 2013, Jefferson Graduate School of Biomedical Sciences - The Yun Yen, MD, PhD and Sophie Yen Thesis Prize for Distinguished Research in Pathobiology
- 2012, Keystone Symposia Travel Scholarship
- 2012, AACR-Aflac Inc. Scholar-in-Training Award
- 2010, Thomas Jefferson University Alumni Travel Award
- 2008, GLNR Travel Award
- 1999-2003, Marian College Scholarship
Research & Clinical Interests
Dr. Schiewer’s research is focused on understanding mechanisms of disease progression and developing novel treatment strategies for genitourinary malignancies (prostate, bladder). Specifically, he is interested in examining transcriptional regulation by oncogenic transcription factors and hormone receptors; exploring therapeutic targeting of DNA repair enzymes; and understanding cancer-associated cell cycle derangement.