HSIEH Wen-Son

With the molecular characteristics of cancers in guiding therapy gaining increasing attention, specific molecular abnormalities predict sensitivity to particular kinase inhibitors in lung cancers and chronic leukemia.

csihws@nus.edu.sg  

Biosketch

Principal Associate, Cancer Science Institute of Singapore, NUS
NUS Visiting Consultant, Department of Otolaryngology, NUH

Year(s) Degree (if applicable) Institute
1988 B.S. Tulane University, New Orleans, LA
1994 M.D. The Johns Hopkins University School of Medicine, Baltimore, MD
Present Principal Associate, Cancer Science Institute of Singapore, National University of Singapore
2011 – present Medical Oncologist, Singapore Oncology Consultants
2008 – present Adjunct Assistant Professor, Johns Hopkins University School of Medicine
2008 – present Visiting Consultant, Department of Head and Neck Surgery National University Hospital
2008 – 2011 Consultant Medical Oncologist and Medical Director, International Cancer Specialists
2001 – 2008 Assistant Professor, Johns Hopkins University School of Medicine
2001 – 2008 Consultant in Oncology, Johns Hopkins-National University Hospital-IMC
2001 – 2006 Investigator, Cancer Epigenetics and Tumor Virology Laboratory, Johns Hopkins Singapore
2002 – 2005 Visiting Consultant, Department of Hematology/Oncology, NUH, Singapore
2005 – 2006 Principal Investigator, Oncology Therapeutics Laboratory, Div of Biomedical Sciences, Johns Hopkins S’pore

Research

Molecular characteristics of certain cancers have allowed specific targeting of genetic and epigenetic abnormalities in certain cancers such as lung cancer and chronic myelogenous leukemia. Our investigations are based on the premise that the presence of the EBV genome or tumor specific genetic and epigenetic abnormalities in nasopharyngeal carcinoma (NPC) may similarly identify tumors that can be specifically targeted. The viral genome is largely transcriptionally silent in these tumors but our investigations have suggested that pharmacologic activation of viral enzyme expression will allow selective targeting of radiopharmaceuticals to these tumors. We are developing targeted therapies for NPC via the induction of silenced Epstein-Barr virus (EBV) and cellular tumor suppressor gene (TSG) expression. Ongoing trials include those testing the clinical and biological effects of valproic acid and Azacitidine/SAHA by standard clinical criteria and molecular characterization of tumor and blood specimens.

In addition, we seek to quantify the viral gene activation associated with several chemotherapy regimens as well as molecularly targeted agents, to characterize the time course of viral activation, and to explore the potential utility of viral gene activation for tumor imaging and to explore the tumor selective targeting of radiopharmaceuticals in an early phase clinical trial.

We are also continuing to develop cell cycle inhibitors for the treatment of NPC. NPC has a number of aberrations in the regulators of the cell cycle. Our previous studies have shown that NPC tumors in vitro and in vivo are sensitive to the effects of cell cycle inhibition. We are currently engaged in preclinical evaluation of a novel cell cycle inhibitor and will proceed to early phase clinical trials once the pharmacodynamics modeling has been completed.

This project will form a part of the translational therapeutic component of CSI while collaborating with clinicians and translational scientists in NUS/NUH, Singapore General Hospital (SGH), and Johns Hopkins University School of Medicine.

Time course of uptake of [125I]FIAU by another EBV(+) Burkitt’s xenograft (Akata) by SPECT-CT in vivo
(Fu et al, Clinical Cancer Research 2006).