Qi Chen, PhD
Associate Professor, Pharmacology, Toxicology & Therapeutics
qchen@kumc.eduMore:
Professional Background
Ph.D., Department of Biochemistry, Sun Yet-sen University, China 2003
Postdoctoral Fellow, NIDDK / NIH , 2008
Assistant Professor, Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, 2008-2017
Associate Professor, Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, 2017- present
Research
Overview
We are in the field of basic and translational research in cancer medicine, with current focuses in:
1) translational research with high-dose intravenous ascorbate (vitamin C) in cancer treatment.
Our research has made primary contribution to the paradigm shifting discoveries that established the scientific basis for using high-dose intravenous ascorbate (IVC) in cancer treatment. We have revealed the different pharmacokinetic behaviors of oral and intravenous ascorbate. With oral ingestion, vitamin C systematic concentrations are tightly controlled. Intravenous administration bypasses its physiological tight control, and establishes pharmacological concentrations, which kills cancer cells but spear normal cells. We have discovered the pro-oxidative actions of pharmacological ascorbate in killing cancers, which is in contrast to its known anti-oxidant effects. We have also documented benefits of combining IVC with conventional cancer therapies. Currently, IVC treatment is in Phase II clinical trials in multiple centers in the US and worldwide.
2) small molecule inhibitors for cancer epithelial-mesenchymal transition (EMT) and cancer stem cells (CSCs).
Enrichment of stem-like cancer cells (CSCs) in pancreatic cancer has been proposed to root the poor prognosis and treatment outcomes of this disease. The presence of CSCs is highly associated with cancer cell epithelial-mesenchymal transition (EMT) that contributes to chemo resistant tumors prone to metastasis and recurrence. It is well accepted that EMT is an important initial step during the complicated process of cancer cell dissemination and metastasis. Therefore, inhibiting cancer cell EMT and CSC has emerged to be an important strategy for ultimate elimination of cancer cell populations.
A few highlights of our recent achievements (since 2020):
A DOD funded clinical trial ($1.6M) in muscle-invasive bladder cancer is ongoing using high dose intravenous ascorbate, with KUMC being the primary site (PI: John Taylor).
Our papers are highly cited – 14 papers (out of 58) have been cited >100 times each by other researchers, with the highest 3 having 1334, 1091 and 851 citations respectively.
Collaboration interests:
Intravenous ascorbate in CAR-T cell therapy, and in neuroblastoma treatment.
Cancer cell metabolism.
Cancer immunology.
EMT and CSC mouse models, especially in pancreatic cancer.
Selected Publications
- Polireddy, K, Dong, R, Reed, G, Yu, J, Chen, P, Williamson, S, Violet, P., C, Pessetto, Z, Godwin, A., K, Fan, F, Levine, M, Drisko, J., A, Chen, Q. 2017. High Dose Parenteral Ascorbate Inhibited Pancreatic Cancer Growth and Metastasis: Mechanisms and a Phase I/IIa study. (Top 100 most downloaded article of the journal in 2017). Scientific reports, 7 (1), 17188
- Chen, Q, Espey, M., G, Sun, A., Y, Lee, J., H, Krishna, M., C, Shacter, E, Choyke, P., L, Pooput, C, Kirk, K., L, Buettner, G., R, Levine, M. 2007. Ascorbate in pharmacologic concentrations selectively generates ascorbate radical and hydrogen peroxide in extracellular fluid in vivo.. Proceedings of the National Academy of Sciences of the United States of America, 104 (21), 8749-54
- Ma, Y, Chapman, J, Levine, M, Polireddy, K, Drisko, J, Chen, Q. 2014. High-dose parenteral ascorbate enhanced chemosensitivity of ovarian cancer and reduced toxicity of chemotherapy. (Featured with a commentary article. National media coverage.). Science translational medicine, 6 (222), 222ra18
- Ma, Y, Chen, P, Drisko, J, Godwin, A., F, Chen, Q. 2020. Pharmacologic Ascorbate Induces “BRCAness” and Enhances Effects of Poly(ADP-Ribose) Polymerase Inhibitors against BRCA1/2 Wild-type Ovarian Cancer. Oncology Lett. https://doi.org/10.3892/ol.2020.11364