The Cancer Institute of New Jersey

Eileen White, PhD

	Associate Director, CINJ, RWJMS The Cancer Institute of New Jersey 195 Little Albany Street New Brunswick, NJ 08901 (732) 235-5329 whiteei@umdnj.edu http://lifesci.rutgers.edu/~molbiosci/faculty/white.html http://news.rutgers.edu/medrel/special-content/2009/nih-challenge-grants-20090929/medrel_generic_content_type_view http://recovery.rutgers.edu/index.php?q=content/dr-eileen-white-awarded-nih-challenge-grant-study-role-cellular-metabolism-cancer http://mbb.rutgers.edu/

Degree

Honors

Publications

Bray, K., Chen, H.-Y., Karp, C. M., May, M., Ganesan, S., Karantza-Wadsworth, V., DiPaola, R. S., and White, E. Bcl-2 modulation to activate apoptosis in prostate cancer. Mol. Cancer Res (in press). 2009;
White, E., and DiPaola, R. S. The double-edged sword of autophagy modulation in cancer. Clinical Cancer Res (in press). 2009; Cited in PubMed; PMID 19706824
Mathew, R., Karp, M. C., Beaudoin, B., Vuong, N., Chen, G., Chen, H.-Y., Bray, K., Reddy, A., Bhanot, G., Gelinas, C., DiPaola, R. S., Karantza-Wadsworth, V., and White, E. Autophagy suppresses tumorigenesis through elimination of p62. Cell . 2009; 137:1062-1075. Cited in PubMed; PMID 19524509
Featured by: Moscat, J. and Diaz-Meco, M. T. p62 at the crossroads of autophagy, apoptosis, and cancer. Cell. 2009; 137:1001-1004.
White, E. and Lowe, S. W. Eating to exit: autophagy enabled senescence revealed. Genes & Dev. 2009; 23:784-787. Cited in PubMed; PMID 19339684
Mathew, R., Karantza-Wadsworth, V., and White. E. Assessing metabolic stress and autophagy status in epithelial tumors. Methods Enzymol. 2009; 453:53-81. Cited in PubMed; PMID 19216902
White, E. Role of metabolic stress responses of apoptosis and autophagy in tumor suppression. Oncogenes Meet Metabolism. Ernst Schering Foundation. 2008; Springer:23-34.
Mathew, R., Degenhardt, K., Haramati, L., Karp, C. M., and White, E. Immortalized mouse epithelial cell models to study the role of apoptosis in cancer. Methods Enzymol. 2008; 446:77-106. Cited in PubMed; PMID 18603117
Karantza-Wadsworth and White, E. A mouse mammary epithelial cell model to identify molecular mechanisms regulating breast cancer progression. Methods Enzymol. 2008; 446:61-76. Cited in PubMed; PMID 18603116
Karp, C. M., Tan, T.-T., Mathew, R., Nelson, D., Mukherjee, C., Degenhardt, K., Karantza-Wadsworth, V., and White, E. Role of the polarity determinant crumbs in suppressing mammalian epithelial tumor progression. Cancer Res. 2008; 68:4105-4115.. Cited in PubMed; PMID 18519669
Jin, S. and White, E. Tumor suppression by autophagy through the management of metabolic stress. Autophagy. 2008; 4:563-566. Cited in PubMed; PMID 18326941
Karantza-Wadsworth, V., and White, E. Programmed Cell Death. Chapter 7, V. T. DeVita, T. S. Lawrence, and S. A. Rosenberg, eds. Cancer: Principles and Practice of Oncology. 2008; 1:93-101.
White, E. Autophagic cell death unraveled: Pharmacologic inhibition of apoptosis and autophagy enables necrosis. Autophagy. 2008; 4:399-401. Cited in PubMed; PMID 18367872
Prives, C. and White E. Does control of mutant p53 by Mdm2 complicate cancer therapy? Genes & Dev. 2008; 22:1259-1264. Cited in PubMed; PMID 18483214
Simmons, M. J., Fan, G., Zong, W.-X., Degenhardt, K., White, E., and Gelinas, C. Bfl-1 /A1 functions, similar to Mcl-1, as a selective tBid and Bak antagonist. Oncogene. 2008; 27:1421-1428. Cited in PubMed; PMID 17724464
Karantza-Wadsworth, V. and White, E. Role of autophagy in breast cancer Autophagy. 2007; 3::610-613.
Mathew, R. and White, E. Why sick cells produce tumors: The protective role of autophagy. Autophagy. 2007; 3:502-505..
Ewings, K. E., Hadfield-Moorhouse, K., Wiggins, C. M., Wickenden, J. A., Balmanno, K., Gilley, R., Degenhardt, K., White, E., and Cook, S. J. ERK1/2-dependent phosphorylation of Bim EL promotes its rapid dissociation from MCL-I and BCL-XL. EMBO J.. 2007; 26:2856-2867.
Jin, S. and White, E. Role of autophagy in cancer: Management of metabolic stress. Autophagy. 2007; 3:28-31.
White, E. Entosis: It’s a cell-eat-cell world. Cell . 2007; 131:840-842.
Mathew, R., Kongara, S., Beaudoin, B., Karp, C. M., Bray, K., Degenhardt, K., Chen, G., Jin, S., and White, E. Autophagy suppresses tumor progression by limiting chromosomal instability. Genes & Dev. . 2007; 21:1367-1381.. Cited in PubMed; PMID PMC1877749
Mathew, R., Karantza-Wadsworth, V., and White, E. Role of autophagy in cancer. Nature Rev. Cancer . 2007; 7:961-967. Cited in PubMed; PMID 17972889
Jin, S., DiPaola, R. S., Mathew, R., and White, E. Metabolic catastrophe as a means to cancer cell death. J. Cell Sci. . 2007; 120:379-383..
Featured by: McCarthy, N. Surviving the tumor suppressor. Nature Rev. Cancer . 2007; 7:490-491.
Shimazu, T., Degenhardt, K., Nur-E-Kamal, A., Zhang, J., Yoshida, T., Zhang, Y., Mathew, R., White, E., and Inouye, M. NBK/BIK antagonizes MCL-1 and BCL-XL, and activates BAK-mediated apoptosis in response to protein synthesis inhibition. Genes & Dev.. 2007; 21:929-941.
Karantza-Wadsworth, V., Patel, S., Kravchuk, O., Chen, G., Mathew, R., Jin, S., and White, E. Autophagy mitigates metabolic stress and genome damage in mammary tumorigenesis. Genes & Dev. . 2007; 21:1621-1635. Cited in PubMed; PMID PMC1899472
Degenhardt, K. and White, E. A mouse model system to genetically dissect the molecular mechanisms regulating tumorigenesis. Clin. Cancer Res. . 2006; 12:5298-5304. .
Degenhardt, K., Mathew, R., Beaudoin, B., Bray, K., Anderson, D., Chen, G. Chen, H.-Y., Mukherjee, Gelinas, C., Fan, Y., Nelson, D. A., Jin, S., and White E. Autophagy promotes tumor cell survival and restricts necrosis, inflammation, and tumorigenesis. Cancer Cell . 2006; 10:51-64.
White, E. Mechanisms of apoptosis regulation by viral oncogenes in infection and tumorigenesis. Cell Death Diff. . 2006; 13:1371-1377.
Mathew, R. and White, E. FLIPping the balance between apoptosis and proliferation in thyroid cancer. Clin. Cancer Res. . 2006; 12:3648-3651.
Tan, T.-T., Degenhardt, K., Nelson, D. A., Beaudoin, B., Nieves-Neira, W., Bouillet, P., Villunger, A., Adams, J. M., and White E. Key roles of BIM-driven apoptosis in epithelial tumors and rational chemotherapy. Cancer Cell . 2005; 7:227-238.
Sundararajan, R., Chen, G., Mukherjee, C., and White, E. Caspase-dependent processing activates the pro-apoptotic activity of deleted in breast cancer-1 during tumor necrosis factor-alpha-mediated death signaling. Oncogene . 2005; 24:4908-4920.
Gelinas, C. and White, E. BH3-only proteins in control: Specificity regulates MCL-1 and BAK-mediated apoptosis. Genes & Dev. . 2005; 19:1263-1268.
Nelson, D. A. and White, E. Exploiting different ways to die. Genes & Dev. . 2004; 18:1223-1226.
Nelson, D. A., Tan T.-T., Rabson, A. B., Anderson, D., Degenhardt, K., and White, E. Hypoxia and defective apoptosis drive genomic instability and tumorigenesis. Genes & Dev. . 2004; 18:2095-2107.

Research

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.

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