- OVERALL The overall goal of this Program is to understand how basic cellular processes are altered and co-opted by cancer cells to promote tumor initiation and progression, and to apply this knowledge towards development of new therapeutic approaches. During the past 46 years, the strong underlying basic science foundation of the Program Project has allowed members to identify vulnerabilities in cancer and develop novel and highly specific therapeutic strategies. This Program continues to take a multi-pronged approach grounded in basic cancer research to identify and disrupt the molecular dependencies underlying cancer. Within this Program, there are five highly integrated Projects (Chromosome Inheritance; Regulation of Pre- mRNA Splicing in Tumorigenesis; Long Non-Coding RNAs and Cancer; Transcriptional Coactivators and Enhancers In Human Cancer; Tumor Suppressor and Tumor Maintenance Genes) and four innovative Cores that are using cutting edge technologies to study the molecular mechanisms of cancer biology. To achieve the Program's goals, these studies will exploit novel animal models of human cancers, pioneering functional genomics technologies, therapeutic antisense oligonucleotide strategies against otherwise undruggable targets, and cutting-edge methods in biochemistry, cell biology and molecular biology. The researchers will interrogate the basis of many of the most devastating types of tumors, including leukemias, breast, pancreatic, and highly aggressive liver cancers. All of this work is supported by four Cores that provide access to technologies, services, and expertise that all combine to enhance productivity and promote interactions. The interactive and collaborative nature of this Program guides each of these Projects beyond their singular potential. Research in all five Projects touches on overlapping themes and benefits from the expertise of the other Program members. Together, this Program is making significant progress towards its goal of identifying novel therapeutic targets that will substantially impact cancer treatment.
- OVERALL Despite decades of research, cancer claims more than half a million lives in the US each year. Using innovative approaches and cutting edge technology, this Program Project aims to understand how basic cellular processes are altered as normal cells become cancerous. The insights gained through this research are likely to reveal highly specific, new vulnerabilities in cancer cells that will be the basis of innovative drug development in the fight against cancer.
|On, Kin Fan; Jaremko, Matt; Stillman, Bruce et al. (2018) A structural view of the initiators for chromosome replication. Curr Opin Struct Biol 53:131-139|
|Knott, Simon R V; Wagenblast, Elvin; Khan, Showkhin et al. (2018) Asparagine bioavailability governs metastasis in a model of breast cancer. Nature 554:378-381|
|Shamay, Yosi; Shah, Janki; I??k, Mehtap et al. (2018) Quantitative self-assembly prediction yields targeted nanomedicines. Nat Mater 17:361-368|
|Tramentozzi, Elisa; Ferraro, Paola; Hossain, Manzar et al. (2018) The dNTP triphosphohydrolase activity of SAMHD1 persists during S-phase when the enzyme is phosphorylated at T592. Cell Cycle 17:1102-1114|
|Arun, Gayatri; Diermeier, Sarah D; Spector, David L (2018) Therapeutic Targeting of Long Non-Coding RNAs in Cancer. Trends Mol Med 24:257-277|
|Tarumoto, Yusuke; Lu, Bin; Somerville, Tim D D et al. (2018) LKB1, Salt-Inducible Kinases, and MEF2C Are Linked Dependencies in Acute Myeloid Leukemia. Mol Cell 69:1017-1027.e6|
|Xu, Yali; Milazzo, Joseph P; Somerville, Tim D D et al. (2018) A TFIID-SAGA Perturbation that Targets MYB and Suppresses Acute Myeloid Leukemia. Cancer Cell 33:13-28.e8|
|Huang, Yu-Han; Klingbeil, Olaf; He, Xue-Yan et al. (2018) POU2F3 is a master regulator of a tuft cell-like variant of small cell lung cancer. Genes Dev 32:915-928|
|Livshits, Geulah; Alonso-Curbelo, Direna; Morris 4th, John P et al. (2018) Arid1a restrains Kras-dependent changes in acinar cell identity. Elife 7:|
|Tiriac, Hervé; Belleau, Pascal; Engle, Dannielle D et al. (2018) Organoid Profiling Identifies Common Responders to Chemotherapy in Pancreatic Cancer. Cancer Discov 8:1112-1129|
Showing the most recent 10 out of 610 publications