Our Science – Cao Website
Liang Cao, Ph.D.
![]() |
|
|||||||||||||||||||||
Biography
Dr. Cao received his Ph.D. from the Department of Biochemistry and Molecular Biology at Harvard University in 1991. Subsequently, he was a Damon Runyon Cancer Research Fellow at the Cancer Center of Massachusetts General Hospital. He has managed research and drug discovery operations in academic and industry labs for 17 years. He is an inventor of over 30 US patents that resulted in novel diagnostics, drug discovery products, and therapeutic molecules in clinical trials.Research
The Molecular Targets Core currently develops technologies and assays that allow clinical investigators to examine the effects of drugs on intended targets and their associated pathways, as well as relevant biomarkers that are indicative of biological responses to the treatment. The Core has expertise in the following areas that are available to the clinical investigators:
1. Biomarker assay development and validation. The Core utilizes highly sensitive immunoassays, mostly based on a unique electrochemiluminescence technology that provides superior sensitivity, specificity, dynamic range and throughput needed for the analysis of clinical specimens. There are a range of biomarker assays available for cell proliferation, tumor angiogenesis, cell signaling, and apoptosis.
2. Implementation of biomarker analysis and correlative studies with clinical investigations at NCI. The Core has the ability to perform biomarker testing and to analyze data for selected endpoints. The Core has an extensive number of engagements on current clinical trials at NCI.
Dr. Cao has research interests on two major areas of translational cancer research:
1. Molecular pathogenesis of pediatric sarcoma to understand the initiation of pathogenic process and to identify cellular targets for targeted therapies. The lab recently performed the genome-wide identification of direct targets for translocated oncogene PAX3-FKHR, using chromatin immunoprecipitation and second generation DNA sequence analysis. Such study will likely facilitate the understanding of the roles of PAX3-FKHR in the development of alveolar rhabdomyosarcoma, and the identification and validation of downstream targets for preclinical evaluation.
2. Preclinical evaluation of novel targeted therapies and identification of predictive biomarkers to be implemented for clinical investigations. The lab focuses on biologics that modulate cellular survival signal and thus, leading to the cancer cell death. The studies are focused on understanding the cellular markers associated with the response of the tumors to these investigational agents and events associated with resistance.
Selected publications:
1. Belinostat phase II study in patients with recurrent or refractory advanced thymic epithelial tumors. Giaccone G, Rajan A, Berman A, Kelly R, Szabo E, Lopez-Chavez A, Trepel J, Lee MJ, Cao L, Espinoza-Delgado I, Spittler J, Loehrer PJ. (in press) J. Clin. Oncol.
2. Insulin-like growth factor 1 receptor antibody induces rhabdomyosarcoma cell death via a process involving AKT and Bcl-x(L). Mayeenuddin LH, Yu Y, Kang Z, Helman LJ, Cao L. (in press) Oncogene.
3. Genome-wide identification of PAX3-FKHR binding sites in rhabdomyosarcoma reveals candidate target genes important for development and cancer. Cao L, Yu Y, Bilke S, Walker RL, Mayeenuddin LH, Pineda M, Azorsa DO, Yang F, Helman LJ, Meltzer PS. (2010) Cancer Res. 70:6497-508.
4. Aminoflavone, a ligand of the Aryl Hydrocarbon Receptor (AhR), inhibits HIF-1α expression in an AhR-independent fashion. Terzuoli E, Puppo M, Rapisarda A, Uranchimeg B, Cao L, Burger AM, Ziche M, Melillo G. (2010) Cancer Res. 70:6837-48.
5. Combination targeted therapy with sorafenib and bevacizumab results in enhanced anti-tumor activity and toxicity. Posadas EM, Azad NS, Kwitkowski VE, Steinberg S. Liel MS, Kotz HL, Minasian L, Sarosy G, Chow C, Premkumar A, Jain L, Cao L, McNally D, Annunziata CM, Chen HX, Wright JJ, and Kohn EC. (2008) J. Clin. Oncol. 26:3709-3714.
6. Addiction to elevated insulin-like growth factor I receptor and initial modulation of the AKT pathway define the responsiveness of rhabdomyosarcoma to the targeting antibody. Cao L, Yu Y, Darko I, Currier D, Mayeenuddin LH, Wan X, Khanna C, Helman LJ. (2008) Cancer Res. 68:8039-8048.
This page was last updated on 5/13/2011.

