Using novel genome-wide ChIP-on-chip and computational approaches, researchers identified a core set of metabolic genes that must be repressed in normal cells in order to prevent the aberrant growth characteristic of human tumors (Mol Cell. 2004 Nov 5;16(3):399-411 and Genes Dev. 2005 Mar 1;19(5):553-69).
We successfully employed antisense oligonucleotide ablation of STAT3 expression to revert lymphoma growth in a mouse xenograft model (Nat Med. 2005 Jun;11(6):623-9).
Our scientists showed that blood-borne Sindbis vectors can systemically and specifically deliver apoptotic vectors to most primary and/or metastasized tumor cells (Nat Biotechnol. 2004 Jan;22(1):70-7).
Investigators targeted the ®Trcp1 locus in mice by homologous recombination. They discovered a new and unexpected role for ®Trcp1 in regulating cell cycle division by targeting for degradation Emi1, an inhibitor of the anaphase promoting complex. They have also shown that ®Trcp1 behaves as an oncogene in the breast epithelium (Dev Cell. 2003 Jun;4(6):799-812 and Mol Cell Biol. 2004 Sep;24(18):8184-94).
Scientists described a new pathway for K-Ras in which this oncogene is phosphorylated and discharged from the plasma membrane and promotes apoptosis after association with mitochondria (Mol Cell. 2006 Feb 17;21(4):481-93). In a related subject, researchers described a new positive feedback loop for Ras activation that involves the binding of GTP-bound Ras to an allosteric site on the exchange factor SOS (Curr Biol. 2006 Nov 7;16(21):2173-9).
Our investigators developed an animal model for glioblastoma multiforme and found that the invading cells downregulate MHC and, in collaboration with breast cancer researchers at Perlmutter Cancer Center, showed that radiation augmented immunotherapy by inducing re-expression of MHC (Cell Cycle. 2006 Jan;5(1):93-9 and Clin Cancer Res. 2006 Aug 1;12(15):4730-7).
We have elucidated the details of the unfolded protein response (UPR), including the control of ER-stress-mediated eIF2a phosphorylation and de-phosphorylation, and established its relevance to cancer (J Cell Biol. 2004 Oct 11;167(1):27-33).
Researchers in our laboratories identified a mechanism by which the Kaposi's sarcoma-associated herpesvirus (KSHV) replication and transcriptional activator (RTA) protein contributes to the initial establishment of viral latency (J Virol. 2005 Jul;79(13):8493-505).
Researchers determined the crystal structures of the catalytic domain of human Dot1 (hDot1), a histone H3 lysine 79-specific HMT that plays a pivotal role in the development of leukemias involving mixed lineage leukemia (MLL) fusion proteins (Cell. 2003 Mar 7;112(5):711-23).