Eileen White | |
---|---|
Citizenship | American |
Alma mater | Rensselaer Polytechnic Institute, State University of New York, Stony Brook |
Occupation | Scientist, Researcher |
Years active | 1983-present |
Organization(s) | Rutgers Cancer Institute of New Jersey, Rutgers University |
Known for | oncogenes, cancer research, apoptosis in cancer, metabolism in cancer, autophagy in cancer |
Honours | National Academy of Sciences, American Association for Cancer Research |
Eileen White is an American professor and scientist who currently serves as deputy director, chief scientific officer, and associate director for basic science at the Rutgers Cancer Institute of New Jersey. She is also the distinguished professor of molecular biology and biochemistry at Rutgers University. White was elected member of the National Academy of Sciences in 2021. [1] [2]
White received her BS in Biology from Rensselaer Polytechnic Institute in 1977 and a PhD in Biology from SUNY Stony Brook in 1983 in the laboratory of Arnold J. Levine. [1] [3] After receiving her PhD, she served as a Damon Runyon postdoctoral fellow at Cold Spring Harbor Laboratory under Dr. Bruce Stillman from 1983 to 1986. She then worked as a staff investigator at that laboratory until 1990. [4]
White has spent her career researching apoptosis, autophagy, and metabolism in cancer.
White began her career in cancer research at Cold Spring Harbor Laboratory, where she was investigating how genes from tumor adenoviruses cause cancer. She discovered that one of the viral oncogenes was a viral homologue of the gene that encodes Bcl-2, a mammalian protein that inhibits apoptosis, programmed cell death. [1]
She then joined Rutgers University as an assistant professor in 1990 and continued her work researching the role of apoptosis in cancer. There she discovered that oncogenes that deregulate cell growth can also activate apoptosis, which allowed her to establish the role of the p53 tumor suppressor in suppressing cancer via activation of apoptosis and that proteins inhibiting apoptosis promote cancer. Later, her lab found that the BH3-only members of the Bcl-2 protein family suppress tumor growth, and are consequently inhibited in cancerous cells leading to the conclusion that resisting cell death is one of the hallmarks of cancer. This work allowed for the development of Bcl-2 inhibitors as a viable cancer therapy. Her laboratory then researched the role of autophagy in cancer, and found that cancer cells promote autophagy, the recycling of intracellular components and damaged proteins, in order to combat metabolic stress. She is currently focused on developing cancer therapies that inhibit autophagy in tumors. [4] [5]
White currently serves on the board of scientific counselors of the National Cancer Institute, is deputy director, chief scientific officer, and associate director for basic research at the Rutgers Cancer Institute of New Jersey.
She is a distinguished professor of molecular biology and biochemistry at Rutgers University and a member of the Ludwig Institute for Cancer Research in Princeton, New Jersey. [4]
Apoptosis is a form of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, DNA fragmentation, and mRNA decay. The average adult human loses between 50 and 70 billion cells each day due to apoptosis. For an average human child between eight and fourteen years old, approximately twenty to thirty billion cells die per day.
A tumor suppressor gene (TSG), or anti-oncogene, is a gene that regulates a cell during cell division and replication. If the cell grows uncontrollably, it will result in cancer. When a tumor suppressor gene is mutated, it results in a loss or reduction in its function. In combination with other genetic mutations, this could allow the cell to grow abnormally. The loss of function for these genes may be even more significant in the development of human cancers, compared to the activation of oncogenes.
Adenovirus E1B protein usually refers to one of two proteins transcribed from the E1B gene of the adenovirus: a 55kDa protein and a 19kDa protein. These two proteins are needed to block apoptosis in adenovirus-infected cells. E1B proteins work to prevent apoptosis that is induced by the small adenovirus E1A protein, which stabilizes p53, a tumor suppressor.
Inhibitors of apoptosis are a group of proteins that mainly act on the intrinsic pathway that block programmed cell death, which can frequently lead to cancer or other effects for the cell if mutated or improperly regulated. Many of these inhibitors act to block caspases, a family of cysteine proteases that play an integral role in apoptosis. Some of these inhibitors include the Bcl-2 family, viral inhibitor crmA, and IAP's.
Suzanne Cory is an Australian molecular biologist. She has worked on the genetics of the immune system and cancer and has lobbied her country to invest in science. She is married to fellow scientist Jerry Adams, also a WEHI scientist, whom she met while studying for her PhD at the University of Cambridge, England.
Karen Heather Vousden, CBE, FRS, FRSE, FMedSci is a British medical researcher. She is known for her work on the tumour suppressor protein, p53, and in particular her discovery of the important regulatory role of Mdm2, an attractive target for anti-cancer agents. From 2003 to 2016, she was the director of the Cancer Research UK Beatson Institute in Glasgow, UK, moving back to London in 2016 to take up the role of Chief Scientist at CRUK and Group Leader at the Francis Crick Institute.
BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 is a protein that in humans is encoded by the BNIP3 gene.
Kun-Liang Guan, is a Chinese-born American biochemist. He won the MacArthur Award in 1998.
Safingol is a lyso-sphingolipid protein kinase inhibitor. It has the molecular formula C18H39NO2 and is a colorless solid. Medicinally, safingol has demonstrated promising anticancer potential as a modulator of multi-drug resistance and as an inducer of necrosis. The administration of safingol alone has not been shown to exert a significant effect on tumor cell growth. However, preclinical and clinical studies have shown that combining safingol with conventional chemotherapy agents such as fenretinide, vinblastine, irinotecan and mitomycin C can dramatically potentiate their antitumor effects. Currently in Phase I clinical trials, it is believed to be safe to co-administer with cisplatin.
Beth Cindy Levine was an American microbiologist. She was an investigator at the Howard Hughes Medical Institute (HHMI), Professor of Internal Medicine and Microbiology, Director of the Center for Autophagy Research and Charles Cameron Sprague Distinguished Chair in Biomedical Sciences at the University of Texas Southwestern Medical Center. She specialized in the field of autophagy; more specifically in its regulation and its role in diverse diseases, including cancer and infectious diseases. Levine was described as a pioneer in the field of modern mammalian autophagy.
Peter K. Vogt is an American molecular biologist, virologist and geneticist. His research focuses on retroviruses and viral and cellular oncogenes.
Craig B. Thompson is an American cell biologist and current president of the Memorial Sloan Kettering Cancer Center.
Maureen E. Murphy, Ph.D., is a researcher at The Wistar Institute in Philadelphia. Her research focuses on the tumor suppressor genes p53 and p14arf.
Joan S. Brugge is the Louise Foote Pfeiffer Professor of Cell Biology and the Director of the Ludwig Center at Harvard Medical School, where she also served as the Chair of the Department of Cell Biology from 2004 to 2014. Her research focuses on cancer biology, and she has been recognized for her explorations into the Rous sarcoma virus, extracellular matrix adhesion, and epithelial tumor progression in breast cancer.
Ed Harlow is an American molecular biologist.
Xin Lu is a Professor of Cancer Biology and Director of the Ludwig Institute for Cancer Research at the University of Oxford. She is known for her discovery of and research on the ASPP family of proteins.
Marcela V. Maus is an Associate Professor of Medicine at Harvard Medical School and Director of the Cellular Immunotherapy Program at Massachusetts General Hospital. She works on immunotherapy for the treatment of cancer, using genetically engineered T cells to target malignancies (cancer).
Carol Jeanne Thiele is an American microbiologist and cancer researcher specialized in the development of novel therapeutic strategies for pediatric tumors. She is chief of the cell and molecular biology section at the National Cancer Institute. She is a founding editor of the journal Cell Death & Differentiation.
Erinna Lee is a Singaporean molecular biologist specializing in apoptosis and autophagy.
Laura Attardi is the Catharine and Howard Avery Professor of the School of Medicine, and professor of radiation oncology and genetics at Stanford University where she leads the Attardi Laboratory. Attardi studies the tumor suppressor protein p53 and the gene that encodes it, TP53, to better understand mechanisms for preventing cancer.