Qi Chen, PhD

Professional Background

Ph.D., Department of Biochemistry, Sun Yet-sen University, China 2003

Postdoctoral Fellow, NIDDK / NIH, USA 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

My research interest is basic and translational 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 differences in pharmacokinetics of oral and intravenous ascorbate. With oral ingestion, vitamin C systematic concentrations are tightly controlled. Whereas oral vitamin C does not kill cancer cells, intravenous administration bypasses its physiological tight control, and establishes pharmacological concentrations, which kills cancer cells and 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. Partially based on our studies, IVC is now 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-like cells (CSCs).
Enrichment of CSCs in pancreatic cancer has been proposed to root the poor treatment outcomes of this disease. 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. Our research effort is in discovering novel agents that comprehensively inhibit EMT and CSCs.

A few highlights of our recent achievements:
Our papers are highly cited – as of January 2025, 14 papers (out of 58) have been cited >100 times each by other researchers, with the highest 3 having 1418, 1153 and 901 citations respectively.

A DOD funded clinical trial ($3.6M, 2024-2028) in muscle-invasive bladder cancer is ongoing using high dose intravenous ascorbate, with KUMC being the primary site (PI: John Taylor).

Collaboration interests:
Intravenous ascorbate (IVC) in CAR-T cell therapy, and in neuroblastoma treatment.
Clinical trials in cancer patients using IVC as adjunctive therapy
Cancer cell metabolism
Cancer immunology
Medicinal chemistry and drug formulation
EMT and CSC mouse models, especially in pancreatic cancer.

• Polireddy K, Dong R, Reed G, Yu J, Chen P, Williamson S, Violet PC, Pessetto Z, Godwin AK, Fan F, Levine M, Drisko JA, 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 MG, Sun AY, Lee JH, Krishna MC, Shacter E, Choyke PL, Pooput C, Kirk KL, Buettner GR, 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 AF, 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