Our Science – Kwong Website

King F. Kwong, M.D.

Surgery Branch Thoracic Oncology Section Investigator NIH/NCI Bldg. 10, CRC 4W-3940 10 Center Drive, MSC 1201 Bethesda, MD 20892-1201 Phone:   301-496-2127 Fax:   301-451-6934 E-Mail:   kwongk2@mail.nih.gov

Biography

Dr. Kwong graduated with honors from Amherst College and received his M.D. from the George Washington University School of Medicine. He completed the Surgical Internship and General Surgery Residency at the George Washington University Medical Center and his research fellowship at Barnes Hospital, Washington University School of Medicine in St. Louis. He then completed the Cardiothoracic Surgery residency at the University of Miami Hospitals.

Following his surgical training, Dr. Kwong was recruited to the full-time academic faculty at the University of Maryland School of Medicine, where he was active in clinical and translational research of thoracic cancers until joining the Thoracic Oncology Section at the NCI. He is an elected fellow of both the American College of Surgeons and the American College of Chest Physicians. He is a member of ACOSOG, ASCO, American College of Surgeons (ACS), American College of Chest Physicians (ACCP), IASLC, and AACR. Dr. Kwong is board-certified in Cardiothoracic Surgery and General Surgery.

Research

The cancer research laboratory is focused on identifying key alterations in the apoptosis pathways contributing to tumor survival, from the earliest stages of tumorigenesis to advanced disease such as metastasis, and the development of novel targeted agents directed toward the apoptosis pathways to render cancer cell arrest, and ultimately cancer cell death. Currently, the contribution of abnormal apoptosis regulation to cancer cell viability and tumor progression in thoracic cancers is not well-defined.

Programmed cell death, or apoptosis, is a highly phylogenetically conserved intracellular process. The proteins and regulatory elements of apoptosis are found in many cell types; but in the cancer cell, apoptosis regulation may be altered by genetic changes or selection to render less effective its intrinsic ability to keep host cells in check and to destroy cells potentially detrimental to the host organism. Fundamentally, apoptosis is an efficient method to eliminate cells that disrupt the homeostasis of the organism. Apoptotic cell death is characterized morphologically by an orderly sequence of proteolytic destruction of DNA degradation, nuclear fragmentation, and cytoplasmic involution. Homologues of the members of the apoptosis pathway, such as those in the caspase family and the inhibitors of apoptosis (IAPs), have been identified in organisms ranging from C. elegans to H. sapiens (humans), thus reinforcing the importance of an intact, properly functioning, apoptosis system.

Current work in the laboratory is directed at better understanding of how the inhibitors of apoptosis proteins (IAPs) fundamentally prevent induction of programmed cell death in non-small cell lung cancer and to determine ways to overcome these molecular barriers in order to translate novel therapeutic regimens into the clinical setting. Additionally, investigations are being conducted to better understand the mechanisms leading to the development of lung cancer metastasis and to identify new methods of potential clinical intervention for metastatic disease.

This page was last updated on 6/20/2009.