Molecular Biology and
Associate Director for Basic Science
Cancer Institute of NJ
195 Little Albany Street
New Brunswick, NJ 08901
Oncogenes, tumor suppressor genes, apoptosis, autophagy, cancer metabolism
Dr. Eileen White received her Bachelor of Science degree from Rensselaer Polytechnic Institute followed by a Ph.D. in Biology from SUNY Stony Brook. She went on as a Damon Runyon Postdoctoral fellow in the laboratory of Dr. Bruce Stillman and then to a Staff Investigator at Cold Spring Harbor Laboratory. There she discovered that one of the oncogenes of the DNA tumor virus adenovirus encoded an inhibitor of programmed cell death or apoptosis that was a viral homologue of Bcl-2. She went on to establish that oncogene activation that deregulates cell growth also activates apoptosis, and that inhibition of apoptosis is an important cancer-promoting function. These findings revealed roles for the p53 tumor suppressor in activating apoptosis and suppressing cancer and the Bcl-2-related anti-apoptotic proteins in blocking apoptosis and promoting cancer.
Dr. White continued her work defining the role and mechanisms of apoptosis regulation in cancer at Rutgers University where she is currently the Associate Director for Basic Science and Program Leader of the Cell Death and Survival Signaling Program at the Cancer Institute of New Jersey, and is Professor of Molecular Biology and Biochemistry at Rutgers University, and Adjunct Professor of Surgery at RWJMS-UMDNJ. Dr. White has served on the Board of Scientific Counselors of the National Cancer Institute and other review panels for the National Institutes of Health. She is the recipient of numerous awards including a MERIT award from the National Cancer Institute, the Red Smith award from the Damon Runyon Cancer Research Foundation, and is a Fellow of the American Society of Microbiology. Dr. White is also a member of the Board of Directors of the American Association for Cancer Research, the Scientific Review Boards for the Starr Cancer Consortium, the Damon Runyon Cancer Research Foundation, and the Cancer Prevention and Research Institute of Texas. She serves on the Editorial Boards of Genes & Development, the Journal of Cell Biology, Oncogene, Cancer Prevention Research, Molecular Cancer Research, Autophagy, and Cell Death and Disease. She is also an investigator on cancer clinical trials, and is a consultant to the pharmaceutical industry for anti-cancer drug discovery. Current research of the White Laboratory at the Cancer Institute of New Jersey is focused translational research modulating the apoptosis pathway for cancer therapy and on the role of metabolism and autophagy in cancer progression and treatment.
Recent work on apoptosis focuses on the role of the Bcl-2 family of apoptosis regulators in controlling cancer cell survival and death. They have established that specific proapoptotic BH3-only members of the Bcl-2 family function in tumor suppression and that their activity is suppressed in cancers. Similarly, cancer cells often gain the function of anti-apoptotic Bcl-2 family members, which promotes cancer. They are defining these mechanisms of apoptosis deregulation in cancers and developing therapeutic strategies to inhibit Bcl-2-related apoptosis inhibitors for clinical benefit.
The White laboratory established that tumor cells with defects in apoptosis tolerate metabolic stress by activating the catabolic process of autophagy. Autophagy is a form of cellular self-cannibalism where cells capture and then digest their own cytoplasm and organelles in lysosomes. They have shown that this cellular self-eating allows cells to recycle intracellular components for macromolecular synthesis to sustain metabolism during periods of starvation. Autophagy also is required for the removal of damaged proteins and organelles to prevent their accumulation in stress, thereby reducing oxidative stress and cellular damage. Thus autophagy is a survival mechanism that sustains metabolism and mitigates damage in cancer cells, and current efforts are to therapeutically block autophagy to reduce the stress tolerance and survival of cancer cells in cancer therapy.