Haobin Chen, M.D., Ph.D.

Assistant Clinical Investigator

Thoracic Surgery Branch


Building 10-CRC, Room 3-5888
Bethesda, MD 20892



Research Topics

Small cell lung cancer (SCLC) is a deadly disease and represents 12-15% of all lung cancers. Little progress has been made in its treatment over the past 30 years. Some obstacles against progress are limited systemic treatment options and rapid development of drug resistance. There is an unmet need to understand resistance mechanisms and to develop novel therapies for SCLC.

Gene expression is controlled by epigenetic machinery in cells. Epigenetic therapy targets critical epigenetic machinery in cancer cells to restore normal gene expression and to stop cancer growth. BET bromodomain proteins are emerging epigenetic targets. The use of small molecule inhibitors to target this family of proteins has generated many promising results in liquid tumors, but this approach has not been tested in solid tumors. One of the focuses of my research is to identify which group of SCLC patients would benefit from this novel epigenetic therapy. The other focus of my research is to uncover drug resistance mechanism in SCLC by using a high-throughput screening approach.


Dr. Chen received his M.D./M.S. degree from Shanghai Medical University (Now Shanghai Medical College Fudan University) in China and his Ph.D. degree from New York University (NYU). He was a research assistant professor at NYU for 4 years, and then completed an internal medicine residency at the Kingsbrook Jewish Medical Center in Brooklyn, NY. He joined the NCI Medical Oncology Branch as a clinical fellow in 2013. He has been a Physician-Scientist Early Investigator in the Thoracic Surgery Branch since 2016.

Selected Publications

  1. Chen H, Giri NC, Zhang R, Yamane K, Zhang Y, Maroney M, Costa M. Nickel ions inhibit histone demethylase JMJD1A and DNA repair enzyme ABH2 by replacing the ferrous iron in the catalytic centers. J Biol Chem. 2010;285(10):7374-83.
  2. Chen H, Ke Q, Kluz T, Yan Y, Costa M. Nickel ions increase histone H3 lysine 9 dimethylation and induce transgene silencing. Mol Cell Biol. 2006;26(10):3728-37.
  3. Chen H, Yan Y, Davidson TL, Shinkai Y, Costa M. Hypoxic stress induces dimethylated histone H3 lysine 9 through histone methyltransferase G9a in mammalian cells. Cancer Res. 2006;66(18):9009-16.

Related Scientific Focus Areas

This page was last updated on Monday, June 13, 2022