Special Interests:Anti-cancer drug discovery, development and mechanism of action studies Mechanisms of drug resistance and how to overcome them Targeted cancer treatment and personalized/precision medicine through NGS technologies
About Fengzhi Li
Roswell Park Comprehensive Cancer Center
- Associate Professor of Oncology
- Department of Pharmacology and Therapeutics
- Member, Molecular Pharmacology and Cancer Therapeutics Graduate Program
- Member, Developmental Therapeutics Cancer Center Support Grant Program
- Member, GI Disease Site Research Group at Roswell Park Cancer Institute
I was initially involved in characterization of the anti-apoptotic protein survivin during my postdoctoral studies at Yale Medical School (Li et al., Nature, 396: 580-584, 1998; Li et al., Nature Cell Biol, 1: 461-466, 1999). Survivin is a novel member in the inhibitor of apoptosis (IAP) family and is a treatment (radiation, chemotherapy) resistant factor. Survivin is aberrantly expressed in all types of cancer, while undetectable or with very low level expression in normal tissues.
Since I established my own research laboratory in 2001 at Roswell Park Cancer Institute, my basic cancer research interest has gradually extended into translational cancer research by focusing on discovery and development of low toxic, high efficacy anti-cancer drugs and their mechanism of action studies. My laboratory research is mainly sponsored through NIH/NCI, DOD and many private/public foundations such as the Susan G Komen Breast Cancer Foundation and the Concern Foundation.
Featured on Cancer Talk
- Westover D, Ling X, Lam H, Welch J, Jin C, Gongora C, Del Rio M, Wani M, Li F: FL118, a novel camptothecin derivative, is insensitive to ABCG2 expression and shows improved efficacy in comparison with irinotecan in colon and lung cancer models with ABCG2-induced resistance, Molecular Cancer 2015 (http://www.molecular-cancer.com/content/14/1/92)
- Ling X, Xu C, Fan C, Zhong K, Li F, Wang X: FL118 Induces p53-Dependent Senescence in Colorectal Cancer Cells by Promoting Degradation of MdmX, Cancer Research 2014, 74:7487-7497
- Zhao J, Ling X, Cao S, Liu X, Wan S, Jiang T, Li F: Antitumor activity of FL118, a survivin, Mcl-1, XIAP, cIAP2 selective inhibitor, is highly dependent on its primary structure and steric configuration. Molecular Pharmaceutics, 11 (2): 457-467, 2014
- Ling X and Li F, An intravenous (i.v.) route-compatible formulation of FL118, a survivin, Mcl-1, XIAP, and cIAP2 selective inhibitor, improves FL118 antitumor efficacy and therapeutic index (TI). American Journal of Translational Research, 3(2): 139-154, 2013
- Ling X, Cao S, Cheng Q, Keefe JT, Rustum, YM and Li F, A Novel Small Molecule FL118 That Selectively Inhibits Survivin, Mcl-1, XIAP and cIAP2 in a p53-Independent Manner, Shows Superior Antitumor Activity, PLOS ONE, 2012;7:e45571