The main objective of this program is to make fundamental contributions to an understanding of the molecular mechanisms responsible for cancer by investigating fundamental genetic processes involved in the control of cell growth and the maintenance of genomic stability. The projects that make up the Program collectively address a number of general issues relevant to this objective. These include the mechanisms of control of the cell cycle, control of cell growth by tumor suppressor genes, the mechanisms of DNA transposition and chromosomal rearrangement, the regulation of chromosome segregation, the role of telomerase in normal growth and tumorigenesis, and the relationship between tissue stem cells and """"""""tumor stem cells"""""""". In addition to these mechanistic aspects, a goal is to develop important new tools for dissecting tumorigenesis. These range from technologies for disrupting gene function systematically to developing comprehensive candidate gene lists for potential tumor suppressors, to the development and exploitation of novel mouse models for the dissecting the contributions of genomic instability and dysregulation of stem cells to the genesis of cancer.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Research Program Projects (P01)
Project #
Application #
Study Section
Subcommittee G - Education (NCI)
Program Officer
Read-Connole, Elizabeth Lee
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
Johns Hopkins University
Schools of Medicine
United States
Zip Code
Janes, K; Symons-Liguori, A M; Jacobson, K A et al. (2016) Identification of A3 adenosine receptor agonists as novel non-narcotic analgesics. Br J Pharmacol 173:1253-67
Oh, Sekyung; Kato, Masaki; Zhang, Chi et al. (2015) A Comparison of Ci/Gli Activity as Regulated by Sufu in Drosophila and Mammalian Hedgehog Response. PLoS One 10:e0135804
Price, Jessica C; Pollock, Lana M; Rudd, Meghan L et al. (2014) Sequencing of candidate chromosome instability genes in endometrial cancers reveals somatic mutations in ESCO1, CHTF18, and MRE11A. PLoS One 8:e63313
Newman, Robert H; Hu, Jianfei; Rho, Hee-Sool et al. (2013) Construction of human activity-based phosphorylation networks. Mol Syst Biol 9:655
O'Donnell, Kathryn A; An, Wenfeng; Schrum, Christina T et al. (2013) Controlled insertional mutagenesis using a LINE-1 (ORFeus) gene-trap mouse model. Proc Natl Acad Sci U S A 110:E2706-13
Rybanska-Spaeder, Ivana; Reynolds, Taylor L; Chou, Jeremy et al. (2013) 53BP1 is limiting for NHEJ repair in ATM-deficient model systems that are subjected to oncogenic stress or radiation. Mol Cancer Res 11:1223-34
Gnanakkan, Veena P; Jaffe, Andrew E; Dai, Lixin et al. (2013) TE-array--a high throughput tool to study transposon transcription. BMC Genomics 14:869
Le Gallo, Matthieu; O'Hara, Andrea J; Rudd, Meghan L et al. (2012) Exome sequencing of serous endometrial tumors identifies recurrent somatic mutations in chromatin-remodeling and ubiquitin ligase complex genes. Nat Genet 44:1310-5
O'Donnell, Kathryn A; Keng, Vincent W; York, Brian et al. (2012) A Sleeping Beauty mutagenesis screen reveals a tumor suppressor role for Ncoa2/Src-2 in liver cancer. Proc Natl Acad Sci U S A 109:E1377-86
Burns, Kathleen H; Boeke, Jef D (2012) Human transposon tectonics. Cell 149:740-52

Showing the most recent 10 out of 246 publications