Research Topics
Genomes and Genes
| Leif W EllisenSummaryAffiliation: Harvard University Country: USA Publications
| Collaborators
|
Detail Information
Publications
Hypoxia regulates TSC1/2-mTOR signaling and tumor suppression through REDD1-mediated 14-3-3 shuttlingMaurice Phillip DeYoung
Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA 02114, USA
Genes Dev 22:239-51. 2008..Together, these findings define a molecular mechanism of signal integration by TSC1/2 that provides insight into the ability of REDD1 to function in a hypoxia-dependent tumor suppressor pathway...- Growth control under stress: mTOR regulation through the REDD1-TSC pathwayLeif W Ellisen
Harvard Medical School, MGH Cancer Center, Boston, Massachusettes 02114, USA
Cell Cycle 4:1500-02. 2005.... - Tumor-specific p73 up-regulation mediates p63 dependence in squamous cell carcinomaMaurice Phillip DeYoung
Massachusetts General Hospital Cancer Center, Boston, MA 02114, USA
Cancer Res 66:9362-8. 2006..Together, these findings define a specific molecular mechanism of p63 dependence through p73 up-regulation, and they provide a rationale for targeting the p63 pathway as a therapeutic strategy in SCCs... - BRCA1-associated epigenetic regulation of p73 mediates an effector pathway for chemosensitivity in ovarian carcinomaNageatte Ibrahim
Massachusetts General Hospital Cancer Center and Harvard Medical School, Vincent Center for Reproductive Biology, Massachusetts General Hospital, Boston, Massachusetts, USA
Cancer Res 70:7155-65. 2010..TAp73 might represent a response predictor and potential therapeutic target for enhancing chemosensitivity in this disease... - The integrin alpha(v)beta(3-5) ligand MFG-E8 is a p63/p73 target gene in triple-negative breast cancers but exhibits suppressive functions in ER(+) and erbB2(+) breast cancersChuanwei Yang
Cancer Research Center at Massachusetts General Hospital, Boston, Massachusetts 02114, USA
Cancer Res 71:937-45. 2011..Its potential use as a serum biomarker that contributes to the pathogenesis of triple-negative breast cancers urges continued evaluation of its differential functions... - The p63/p73 network mediates chemosensitivity to cisplatin in a biologically defined subset of primary breast cancersChee Onn Leong
Massachusetts General Hospital Cancer Center and Harvard Medical School, 55 Fruit Street, Boston, MA 02114, USA
J Clin Invest 117:1370-80. 2007.... - A microRNA-dependent program controls p53-independent survival and chemosensitivity in human and murine squamous cell carcinomaBenjamin Ory
Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, Massachusetts 02114, USA
J Clin Invest 121:809-20. 2011..Thus, we have identified a direct, microRNA-dependent regulatory circuit mediating inducible chemoresistance, whose inhibition may provide a new therapeutic opportunity in p53-deficient tumors... - Negative feedback control of HIF-1 through REDD1-regulated ROS suppresses tumorigenesisPeter Horak
Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA 02114, USA
Proc Natl Acad Sci U S A 107:4675-80. 2010..Furthermore, they define REDD1 as a key metabolic regulator that suppresses tumorigenesis through distinct effects on mTORC1 activity and mitochondrial function... - p63 and p73: life and death in squamous cell carcinomaJames W Rocco
Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts, USA
Cell Cycle 5:936-40. 2006..Specific chemotherapeutic agents and future targeted approaches may be able to exploit this pathway to therapeutic advantage... - Physical association of HDAC1 and HDAC2 with p63 mediates transcriptional repression and tumor maintenance in squamous cell carcinomaMatthew R Ramsey
Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, Massachusetts 02114, USA
Cancer Res 71:4373-9. 2011..In addition, our findings offer a rationale to apply HDAC inhibitors for SCC treatment... - Regulation of mTOR and cell growth in response to energy stress by REDD1Avi Sofer
Massachusetts General Hospital Cancer Center and Harvard Medical School, GRJ 904, 55 Fruit Street, Boston, Massachusetts 02114, USA
Mol Cell Biol 25:5834-45. 2005..These results define REDD1 as a critical transducer of the cellular response to energy depletion through the TSC-mTOR pathway... - Efficacy of neoadjuvant Cisplatin in triple-negative breast cancerDaniel P Silver
Dana Farber Cancer Institute, Department of Medical Oncology, Smith 209, 1 Jimmy Fund Way, Boston, MA 02115, USA
J Clin Oncol 28:1145-53. 2010..CONCLUSION Single-agent cisplatin induced response in a subset of patients with TNBC. Decreased BRCA1 expression may identify subsets of TNBCs that are cisplatin sensitive. Other biomarkers show promise in predicting cisplatin response... - Feedback control of p53 translation by REDD1 and mTORC1 limits the p53-dependent DNA damage responseDouangsone D Vadysirisack
Massachusetts General Hospital Cancer Center, GRJ 904, 55 Fruit Street, Boston, MA 02114, USA
Mol Cell Biol 31:4356-65. 2011..This work therefore defines a role for REDD1 in the control of p53 in vivo, with potential therapeutic implications for cancer and for the variety of genetic diseases involving TOR pathway signaling components... - Bcl-2 blocks cisplatin-induced apoptosis and predicts poor outcome following chemoradiation treatment in advanced oropharyngeal squamous cell carcinomaWilliam A Michaud
Massachusetts General Hospital MGH Cancer Center, Department of Surgery, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
Clin Cancer Res 15:1645-54. 2009.... - p63 regulates an adhesion programme and cell survival in epithelial cellsDanielle K Carroll
Department of Cell Biology, Harvard Medical School, 240 Longwood Ave, Boston, MA 02115, USA
Nat Cell Biol 8:551-61. 2006..Our results implicate p63 as a key regulator of cellular adhesion and survival in basal cells of the mammary gland and other stratified epithelial tissues... - A microRNA-dependent circuit controlling p63/p73 homeostasis: p53 family cross-talk meets therapeutic opportunityBenjamin Ory
Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA 02114, USA
Oncotarget 2:259-64. 2011..Additionally, we suggest that inducible chemoresistance mediated by this miR-dependent mechanism might be an attractive target for therapeutic intervention... - PARP Inhibitors in Cancer Therapy: Promise, Progress, and PuzzlesLeif W Ellisen
Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA, 02114, USA
Cancer Cell 19:165-7. 2011..provides evidence that a treatment strategy aimed at inducing DNA damage with chemotherapy while simultaneously disabling repair using a PARP inhibitor might offer hope for patients with a treatment-refractory form of breast cancer... - REDD1, a developmentally regulated transcriptional target of p63 and p53, links p63 to regulation of reactive oxygen speciesLeif W Ellisen
Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
Mol Cell 10:995-1005. 2002..Thus, REDD1 encodes a shared transcriptional target that implicates ROS in the p53-dependent DNA damage response and in p63-mediated regulation of epithelial differentiation... - The histone deacetylase Sirt6 regulates glucose homeostasis via Hif1alphaLei Zhong
The Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA 02114, USA
Cell 140:280-93. 2010..Our studies uncover a role for the chromatin factor SIRT6 as a master regulator of glucose homeostasis and may provide the basis for novel therapeutic approaches against metabolic diseases, such as diabetes and obesity... - p63 mediates survival in squamous cell carcinoma by suppression of p73-dependent apoptosisJames W Rocco
Massachusetts General Hospital Center for Cancer Research and Harvard Medical School, Boston, Massachusetts 02114, USA
Cancer Cell 9:45-56. 2006..Together, these data define a pathway whereby deltaNp63alpha promotes survival in squamous epithelial malignancy by repressing a p73-dependent proapoptotic transcriptional program... - Regulation of mTOR function in response to hypoxia by REDD1 and the TSC1/TSC2 tumor suppressor complexJames Brugarolas
Dana Farber Cancer Institute and Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Genes Dev 18:2893-904. 2004..Inhibition of mTOR function by hypoxia is likely to be important for tumor suppression as TSC2-deficient cells maintain abnormally high levels of cell proliferation under hypoxia... - Tissue-specific signatures of activating PIK3CA and RAS mutations in carcinosarcomas of gynecologic originWhitfield B Growdon
Vincent Center for Reproductive Biology, MGH Vincent Department of Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA 02114, USA
Gynecol Oncol 121:212-7. 2011..Therefore, broad genotyping was performed to identify tissue-specific somatic mutational profiles that may help direct targeted therapies in this complex neoplasia... - mTOR activity under hypoxiaDouangsone D Vadysirisack
Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA, USA
Methods Mol Biol 821:45-58. 2012..These methodologies will serve as valuable tools for researchers seeking to understand mTORC1 dysregulation in the context of hypoxic stress... - Dexamethasone represses signaling through the mammalian target of rapamycin in muscle cells by enhancing expression of REDD1Hongmei Wang
Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA
J Biol Chem 281:39128-34. 2006..Overall, the data support the conclusion that REDD1 functions upstream of Tuberin and Rheb to down-regulate mTOR signaling in response to dexamethasone...