The Beer and Qian lab is developing precise and personalized approaches to prevent and treat advanced prostate cancer. Our research focus is to understand molecular mechanisms underpinning tumor and tumor microenvironment interaction, metastatic progression, and treatment resistance. Our research methods are multidisciplinary, including genomics, bioinformatics, molecular biology, experimental therapeutics, and clinical trial.
A clinical trial-based reverse translation to understand chemoresistance in prostate cancer.
Improving the efficacy of taxane-based chemotherapy is an urgent and unmet need in the treatment of patients with advanced metastatic prostate cancer. We recently determined the temporal change of gene expression in a cohort of high risk prostate cancer patients before and after a neoadjuvant chemotherapy clinical trial. It was found that chemotherapy was associated with an increase in the gene expression mediating multiple oncogenic signaling pathways. Further, some increases were positively associated with chemotherapy failure and disease recurrence, suggesting potential chemoresistance mechanism. Currently, we are using bioinformatics, molecular and cellular biology, and experimental therapeutic approaches to identify genes and proteins that are truly responsible for adapting, surviving, and escaping chemotherapy. We are also actively exploring ways to target these chemoresistance mechanisms in order to improve the efficacy of chemotherapy.
The crosstalk between hypoxia signaling and hormonal signaling determines cancer progression and hormonal therapy resistance.
Hypoxia is a pathological hallmark of cancer microenvironment. For decades, tumor hypoxia is known to be associated with solid tumor progression, treatment resistance, and patient mortality. However, the signaling pathways underpinning these malignant effects are unclear, and therapeutic strategies are poorly developed. Through cDNA microarray analyses, we have recently identified novel interaction / crosstalk between signaling pathways initiated by hypoxia and androgen, the prostate cancer driving hormone. This new information is guiding us to develop novel understanding in how prostate cancers progress to lethal diseases and acquire resistance to hormonal therapy in hypoxic conditions.
Tomasz M. Beer, M.D., F.A.C.P., professor of medicine and Grover C. Bagby Endowed Chair for Prostate Cancer Research in the division of hematology & medical oncology, chief medical officer for the Cancer Early Detection Advanced Research Center, and deputy director of OHSU Knight Cancer Institute, an NCI-designated Cancer Center. Dr. Beer received his medical degree from Johns Hopkins School of Medicine, Baltimore, Maryland, in 1991; and completed his internship and residency in internal medicine and fellowship in hematology and medical oncology at Oregon Health & Science University.
David Qian, Ph.D., Associate Professor and Principal Investigator, is a molecular and cellular cancer biologist. He received a B.S. in Biochemistry from Alma College, Ph.D. in Toxicology from Johns Hopkins University, and postdoctoral training in tumor angiogenesis, hypoxia, epigenetics, and experimental therapeutics from Johns Hopkins Kimmel Cancer Center.
Dr. Qian has been a principal investigator and graduate faculty at OHSU Knight Cancer Institute and School of Medicine since 2010. He is primarily responsible for the research direction of the lab. Dr. Qian is a strong believer of the mechanism-based cancer treatment approach, in particularly through understanding the molecular genetics and biology of tumor hypoxia.
- Hao Geng, Ph.D.
- Changhui Xue, Ph.D.