Research Topics
Genomes and Genes | Eileen WhiteSummaryAffiliation: Rutgers University Country: USA Publications
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Publications
Mechanisms of apoptosis regulation by viral oncogenes in infection and tumorigenesisE White
Department of Molecular Biology and Biochemistry, Center for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, NJ 08854, USA
Cell Death Differ 13:1371-7. 2006..Thus, both infected cells and tumor cells require inhibition of the apoptotic host defense mechanism, the insights from which can be exploited for therapy development...- The pims and outs of survival signaling: role for the Pim-2 protein kinase in the suppression of apoptosis by cytokinesEileen White
Howard Hughes Medical Institute, Center for Advanced Biotechnology and Medicine, Department of Molecular Biology and Biochemistry, Cancer Institute of New Jersey, Rutgers University, Piscataway, New Jersey 08854, USA
Genes Dev 17:1813-6. 2003 
Entosis: it's a cell-eat-cell worldEileen White
Center for Advanced Biotechnology and Medicine, Department of Molecular Biology and Biochemistry, Rutgers University, 679 Hoes Lane, Piscataway, NJ 08854, USA
Cell 131:840-2. 2007..Given that surviving detachment from the ECM is an event associated with the progression of epithelial cancers, entosis--along with apoptosis--may contribute to tumor suppression by promoting the elimination of cancer cells...- Autophagy suppresses tumor progression by limiting chromosomal instabilityRobin Mathew
University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA
Genes Dev 21:1367-81. 2007..Identification of this novel role of autophagy may be important for rational chemotherapy and therapeutic exploitation of autophagy inducers as potential chemopreventive agents... - Autophagy promotes tumor cell survival and restricts necrosis, inflammation, and tumorigenesisKurt Degenhardt
Center for Advanced Biotechnology and Medicine, 679 Hoes Lane, Piscataway, New Jersey 08854, USA
Cancer Cell 10:51-64. 2006..Thus, autophagy may function in tumor suppression by mitigating metabolic stress and, in concert with apoptosis, by preventing death by necrosis... - Autophagy mitigates metabolic stress and genome damage in mammary tumorigenesisVassiliki Karantza-Wadsworth
Division of Medical Oncology, Department of Internal Medicine, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA
Genes Dev 21:1621-35. 2007..Therefore, we propose that autophagy limits metabolic stress to protect the genome, and that defective autophagy increases DNA damage and genomic instability that ultimately facilitate breast cancer progression... - Role of the polarity determinant crumbs in suppressing mammalian epithelial tumor progressionCristina M Karp
Department of Molecular Biology and Biochemistry, Center for Advanced Biotechnology and Medicine, Rutgers University, NJ 08854, USA
Cancer Res 68:4105-15. 2008..These findings suggest a role for mammalian polarity determinants in suppressing tumorigenesis that may be analogous to the well-studied polarity tumor suppressor mechanisms in Drosophila... - Caspase-dependent processing activates the proapoptotic activity of deleted in breast cancer-1 during tumor necrosis factor-alpha-mediated death signalingRamya Sundararajan
Rutgers University, 679 Hoes Lane, Room 140, Piscataway, NJ 08854, USA
Oncogene 24:4908-20. 2005..DBC-1, like its homolog cell cycle and apoptosis regulatory protein-1 (CARP-1), may function in the regulation of apoptosis... - Role of autophagy in cancerRobin Mathew
University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA
Nat Rev Cancer 7:961-7. 2007..Recent evidence suggests that autophagy provides a protective function to limit tumour necrosis and inflammation, and to mitigate genome damage in tumour cells in response to metabolic stress... 
Immortalized mouse epithelial cell models to study the role of apoptosis in cancerRobin Mathew
University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey, USA
Methods Enzymol 446:77-106. 2008..Applying this technology to other mouse models can provide insight into additional aspects of oncogenesis...- DNA damage response and MCL-1 destruction initiate apoptosis in adenovirus-infected cellsAndrea Cuconati
Howard Hughes Medical Institute, Cancer Institute of New Jersey, Rutgers University, Piscataway, New Jersey 08854, USA
Genes Dev 17:2922-32. 2003.... - Autophagy suppresses tumorigenesis through elimination of p62Robin Mathew
University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA
Cell 137:1062-75. 2009.... - Akt-dependent expression of NAIP-1 protects neurons against amyloid-{beta} toxicitySylvain Lesne
UMR CNRS 6185, Universite de Caen, Bd H Becquerel BP5229, 14074 Caen, France and Howard Hughes Medical Institute, Rutgers University, Piscataway, New Jersey 08854, USA
J Biol Chem 280:24941-7. 2005..Together, these findings demonstrate that NT-3 signaling counters Abeta-dependent neuronal cell death and may represent an innovative therapeutic intervention to limit neuronal death in Alzheimer disease... - Key roles of BIM-driven apoptosis in epithelial tumors and rational chemotherapyTing Ting Tan
Center for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, New Jersey 08854, USA
Cancer Cell 7:227-38. 2005.... - Role of autophagy in breast cancerVassiliki Karantza-Wadsworth
Division of Medical Oncology, Department of Medicine, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey, USA
Autophagy 3:610-3. 2007.... - Defective ubiquitin-mediated degradation of antiapoptotic Bfl-1 predisposes to lymphomaGaofeng Fan
Center for Advanced Biotechnology and Medicine, University of Medicine and Dentistry of New Jersey UMDNJ Robert Wood Johnson Medical School, Piscataway, USA
Blood 115:3559-69. 2010..Furthermore, because bfl-1 is up-regulated in many human hematopoietic tumors, this finding suggests that strategies to promote Bfl-1 ubiquitination may improve therapy... - Metabolic catastrophe as a means to cancer cell deathShengkan Jin
Department of Pharmacology, Robert Wood Johnson Medical School, 675 Hoes Lane, Piscataway, NJ 08854, USA
J Cell Sci 120:379-83. 2007..The challenge now is to induce metabolic catastrophe therapeutically as an approach to killing the unkillable cells... - Hypoxia and defective apoptosis drive genomic instability and tumorigenesisDeirdre A Nelson
Howard Hughes Medical Institute, Rutgers University, Piscataway, New Jersey 08854, USA
Genes Dev 18:2095-107. 2004.... - A mouse model system to genetically dissect the molecular mechanisms regulating tumorigenesisKurt Degenhardt
Center for Advanced Biotechnology and Medicine, Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, New Jersey 08854 and Cancer Institute of New Jersey, New Brunswick, New Jersey, USA
Clin Cancer Res 12:5298-304. 2006..We have applied this model to establish the role of apoptosis in epithelial solid tumor progression and in treatment response, which has provided novel opportunities for cancer therapies in humans... - Rationally designed treatment for solid tumors with MAPK pathway activation: a phase I study of paclitaxel and bortezomib using an adaptive dose-finding approachJanice M Mehnert
Department of Medicine, Division of Medical Oncology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey, USA
Mol Cancer Ther 10:1509-19. 2011.... - Autophagy regulates keratin 8 homeostasis in mammary epithelial cells and in breast tumorsSameera Kongara
Cancer Institute of New Jersey, 195 Little Albany Street, New Brunswick, NJ 08903, USA
Mol Cancer Res 8:873-84. 2010..High phospho(Ser73)-K8 expression may be a marker of autophagy functional status in breast tumors and, as such, could have therapeutic implications for breast cancer patients... - A mouse mammary epithelial cell model to identify molecular mechanisms regulating breast cancer progressionVassiliki Karantza-Wadsworth
Division of Medical Oncology, Department of Medicine, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey, USA
Methods Enzymol 446:61-76. 2008.... - NBK/BIK antagonizes MCL-1 and BCL-XL and activates BAK-mediated apoptosis in response to protein synthesis inhibitionTsutomu Shimazu
Department of Biochemistry, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA
Genes Dev 21:929-41. 2007..Although NBK/BIK is dispensable for development, it is the BH3-only protein targeted for inactivation by viruses, suggesting that it plays a role in pathogen/toxin response through apoptosis activation... - Production of membrane proteins for NMR studies using the condensed single protein (cSPP) production systemLili Mao
New York Center on Membrane Protein Structure, Rutgers, The State University of New Jersey, Piscataway, NJ, 08854, USA
J Struct Funct Genomics 10:281-9. 2009.... - Grm5 expression is not required for the oncogenic role of Grm1 in melanocytesYARI E MARIN
Susan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, 213, Ernest Mario School of Pharmacy, Rutgers University, 164 Frelinghuysen Road, Piscataway, NJ 08854, USA
Neuropharmacology 49:70-9. 2005..Taken together, these results indicate that Grm1 can act as an oncogene in melanocytes independently of Grm5 expression... - Assessing metabolic stress and autophagy status in epithelial tumorsRobin Mathew
University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey, USA
Methods Enzymol 453:53-81. 2009..Additionally these cell lines provide an efficient way to perform biochemical analyses, and high throughput screening for modulators of autophagy for potential use in cancer therapy and prevention... - Induction of apoptosis by diterpenes from the soft coral Xenia elongataEric H Andrianasolo
Center for Marine Biotechnology, Institute of Marine and Coastal Sciences, Rutgers, The State University of New Jersey, Piscataway, New Jersey 08901 8521, USA
J Nat Prod 70:1551-7. 2007..The diterpenes induce apoptosis in micromolar concentrations. This is the first report of apoptosis induction by marine diterpenes in xenicane skeletons... - A sesquiterpenelactone from Inula britannica induces anti-tumor effects dependent on Bcl-2 phosphorylationMohamed M Rafi
Department of Food Science, New Jersey Agricultural Experimentation Station, Cook College, Rutgers University, New Brunswick, New Jersey 08901 8520, USA
Anticancer Res 25:313-8. 2005..Although initially active in clinical studies, current anti-microtubule agents are only temporarily effective and the discovery of new agents is warranted... - BH3-only proteins in control: specificity regulates MCL-1 and BAK-mediated apoptosisCeline Gelinas
Center for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, New Jersey 08854, USA
Genes Dev 19:1263-8. 2005 - Therapeutic targeting of death pathways in cancer: mechanisms for activating cell death in cancer cellsTing Ting Tan
Center for Advanced Biotechnology and Medicine and Rutgers University, Piscataway, NJ 08854, USA
Adv Exp Med Biol 615:81-104. 2008..This chapter summarizes the current knowledge of the apoptotic pathways and provides a selective review on the development of drugs that target the apoptotic machinery... - Why sick cells produce tumors: the protective role of autophagyRobin Mathew
University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey, USA
Autophagy 3:502-5. 2007..The protective role of autophagy may be exploited in developing novel autophagy modulators as rational chemotherapeutic as well as chemopreventive agents... - Role of autophagy in cancer: management of metabolic stressShengkan Jin
Department of Pharmacology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, 675 Hoes Lane, Newark, NJ 08854, USA
Autophagy 3:28-31. 2007.... - ASAP, a novel protein complex involved in RNA processing and apoptosisChristian Schwerk
Howard Hughes Medical Institute and Division of Nucleic Acids Enzymology, Department of Biochemistry, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA
Mol Cell Biol 23:2981-90. 2003..Importantly, after induction of apoptosis the ASAP complex disassembles. Taken together, our results suggest an important role for the ASAP complexes in linking RNA processing and apoptosis... - Viral homologs of BCL-2: role of apoptosis in the regulation of virus infectionAndrea Cuconati
Howard Hughes Medical Institute, Center for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, New Jersey 08854, USA
Genes Dev 16:2465-78. 2002 - Tumor suppression by autophagy through the management of metabolic stressShengkan Jin
Department of Pharmacology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA
Autophagy 4:563-6. 2008..Furthermore, we need to be able to identify human tumors with deficient autophagy, and to develop rational cancer therapies that take advantage of the altered metabolic state and stress responses inherent to this autophagy defect... - E1A sensitizes cells to tumor necrosis factor alpha by downregulating c-FLIP SDenise Perez
Center for Advanced Biotechnology and Medicine, Department of Molecular Biology and Biochemistry, Rutgers University, 679 Hoes Lane, Piscataway, NJ 08854, USA
J Virol 77:2651-62. 2003.... - Augmentation of apoptosis by the combination of bleomycin with trifluoperazine in the presence of mutant p53Gregory F Sullivan
University of Medicine and Dentistry of New Jersey/Robert Wood Johnson Medical School, Cancer Institute of New Jersey, USA
J Exp Ther Oncol 2:19-26. 2002..These results indicate that the enhancement of bleomycin induced DNA damage by trifluoperazine is mediated, at least in part, through the induction of apoptosis... - Targeting tumor metabolism with 2-deoxyglucose in patients with castrate-resistant prostate cancer and advanced malignanciesMark Stein
Cancer Institute of New Jersey, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, New Jersey 08901, USA
Prostate 70:1388-94. 2010.... - Exploiting different ways to dieDeirdre A Nelson
Howard Hughes Medical Institute and Center for Advanced Biotechnology and Medicine, Department of Molecular Biology and Biochemistry, Cancer Institute of New Jersey, Rutgers University, Piscataway, New Jersey 08854, USA
Genes Dev 18:1223-6. 2004 - BAX and BAK mediate p53-independent suppression of tumorigenesisKurt Degenhardt
Center for Advanced Biotechnology and Medicine, Department of Molecular Biology and Biochemistry, Rutgers University, 679 Hoes Lane, Room 140, Piscataway, NJ 08854, USA
Cancer Cell 2:193-203. 2002..Thus, BAX and BAK function to suppress tumorigenesis, and their deficiency was selected for in vivo... - FLIPping the balance between apoptosis and proliferation in thyroid cancerRobin Mathew
Center for Advanced Biotechnology and Medicine, Rutgers University, USA
Clin Cancer Res 12:3648-51. 2006 - Bak and Bax function to limit adenovirus replication through apoptosis inductionAndrea Cuconati
Howard Hughes Medical Institute Department of Molecular Biology, Rutgers University, Piscataway, New Jersey 08854, USA
J Virol 76:4547-58. 2002..Thus, Bax- and Bak-mediated apoptosis severely limits adenoviral replication, demonstrating that Bax and Bak function as an antiviral response at the cellular level... - Regulation of the mitochondrial checkpoint in p53-mediated apoptosis confers resistance to cell deathHolly Henry
Howard Hughes Medical Institute, 679 Hoes Lane, Piscataway, New Jersey, NJ 08854, USA
Oncogene 21:748-60. 2002..Thus, p53 induces apoptosis in part through Bax and Bak, and even an incomplete inhibition of this mitochondrial checkpoint may be sufficient to confer resistance to cell death... - Bax and Bak independently promote cytochrome C release from mitochondriaKurt Degenhardt
Department of Molecular Biology, The Cancer Institute of New Jersey, Rutgers University, Piscataway, New Jersey 08854, USA
J Biol Chem 277:14127-34. 2002..Thus, either Bax or Bak is required for death signaling through mitochondria in response to TNF-alpha, but both are dispensable for p53-dependent transformation inhibition... - The adenovirus E1A proteins induce apoptosis, which is inhibited by the E1B 19-kDa and Bcl-2 proteinsL Rao
Center for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, NJ 08854
Proc Natl Acad Sci U S A 89:7742-6. 1992..High-frequency transformation requires a second function encoded by the E1B 19-kDa protein to block apoptosis... - The 19-kilodalton adenovirus E1B transforming protein inhibits programmed cell death and prevents cytolysis by tumor necrosis factor alphaE White
Center for Advanced Biotechnology and Medicine, Piscataway, New Jersey 08854
Mol Cell Biol 12:2570-80. 1992.... - Tumor necrosis factor-alpha induces Bax-Bak interaction and apoptosis, which is inhibited by adenovirus E1B 19KR Sundararajan
Rutgers University, Piscataway, New Jersey 08854, USA
J Biol Chem 276:45120-7. 2001.... - The E1B 19K protein blocks apoptosis by interacting with and inhibiting the p53-inducible and death-promoting Bax proteinJ Han
Center for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, New Jersey 08854 USA
Genes Dev 10:461-77. 1996..With the death pathway disabled, induction of growth arrest by p53 can then be manifested... - ERK1/2-dependent phosphorylation of BimEL promotes its rapid dissociation from Mcl-1 and Bcl-xLKatherine E Ewings
Laboratory of Molecular Signalling, The Babraham Institute, Babraham Research Campus, Cambridge, UK
EMBO J 26:2856-67. 2007..These results provide new insights into the role of Bim in cell death and its regulation by the ERK1/2 survival pathway... - Association of Bax and Bak homo-oligomers in mitochondria. Bax requirement for Bak reorganization and cytochrome c releaseValery Mikhailov
Department of Pathology, The University of Texas Health Science Center, San Antonio, Texas 78229, USA
J Biol Chem 278:5367-76. 2003..These results suggest a degree of functional cooperation between Bax and Bak in this form of cell injury, but also demonstrate an absolute requirement of Bax for mitochondrial permeabilization... - Therapeutic starvation and autophagy in prostate cancer: a new paradigm for targeting metabolism in cancer therapyRobert S DiPaola
Department of Medicine, University of Medicine and Dentistry of New Jersey UMDNJ Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA
Prostate 68:1743-52. 2008..The understanding of autophagy, as either a mechanism of resistance to therapies that induce metabolic stress, or as a means to cell death, is rapidly expanding and supportive of a new paradigm of therapeutic starvation... - Apoptosis-inducing galactolipids from a cultured marine diatom, Phaeodactylum tricornutumEric H Andrianasolo
Center for Marine Biotechnology, Institute of Marine and Coastal Sciences, Rutgers, The State University of New Jersey, New Brunswick, New Jersey 08901 8521, USA
J Nat Prod 71:1197-201. 2008..The galactolipids induce apoptosis in micromolar concentrations. This is the first report of apoptosis induction by galactolipids... - Epothilone induced cytotoxicity is dependent on p53 status in prostate cellsMargarita L Ioffe
The Cancer Institute of New Jersey, Robert Wood Johnson Medical School/UMDNJ, New Brunswick, New Jersey 08901, USA
Prostate 61:243-7. 2004..These data provide a basis for further study of p53, and the phosphorylation status of cdc-2, as markers for epothilone sensitivity in clinical studies... - Does control of mutant p53 by Mdm2 complicate cancer therapy?Carol Prives
Department of Biological Sciences, Columbia University, New York, New York 10027, USA
Genes Dev 22:1259-64. 2008..Once stabilized, mutant p53 promotes metastasis. Therefore, therapies that release p53 from Mdm2 might have unwanted consequences when cells have sustained a mutation in p53... - A novel proteomic coculture model of prostate cancer cell growthDmitri Dvorzhinski
The Cancer Institute of New Jersey, New Brunswick, New Jersey 08901, USA
Proteomics 4:3268-75. 2004..These data, therefore, demonstrate a novel coculture model for further study of agents that target proteins in pathways of paracrine or autocrine stimulated cell growth... - Nutlin-3 protects kidney cells during cisplatin therapy by suppressing Bax/Bak activationMan Jiang
Department of Cellular Biology and Anatomy, Medical College of Georgia and Veterans Affairs Medical Center, Augusta, Georgia 30912, USA
J Biol Chem 282:2636-45. 2007..Importantly, it blocked both Bax and Bak oligomerization under these conditions. Together, the results have uncovered a new pharmacological function of nutlins, i.e. suppression of Bax and Bak, two critical mediators of apoptosis... - Autophagic cell death unraveled: Pharmacological inhibition of apoptosis and autophagy enables necrosisEileen White
Autophagy 4:399-401. 2008..1) This radically alters the interpretation of earlier findings reporting induction of autophagic cell death by zVAD,(2) instead, suggests that autophagy functions to promote cell survival...
Research Grants
- FUNCTION OF THE ADENOVIRUS E1B ONCOGENEEileen White; Fiscal Year: 2007..Knowledge gained from this approach will be useful in the development of new anti-viral and anti-cancer regimens. ..