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Our aim is to improve the prognosis of children with cancer by identifying the most effective drugs for those with the specific genetic mutations that cause their disease. This proposal focuses on the function of the retinoblastoma tumor suppressor (Rb) in a subgroup of pediatric solid tumors, defined by a characteristic subset of genetic changes that are hyper-mutated compared to the remaining cancers. It is unclear why some cancer cells undergo mutagenic reprogramming to become very unstable, accumulating mutations and chromosomal rearrangements while remaining cancer cells without these genetic alterations remain relatively stable. We propose that these unstable cancer cells represent a unique subset of cells that become transformed due to specific mutations or defects in the Rb tumor suppressor, which initiates mutagenic reprogramming of the cells. These cells are hyper-mutated because they suffer a dominant DNA mismatch repair (MMR) deficiency. Recently we have identified a subset of pediatric sarcomas, osteosarcomas (OS) and chondrosarcomas (CS), that are hyper-mutated, MMR-deficient, and have characteristic mutations in Rb. The following steps are necessary to identify effective drugs for these tumors: 1) to improve our understanding of the function of Rb in the regulation of the cell cycle and genomic stability in cancer cells, 2) to determine the cell type specificity and oncogenic role of these Rb mutations, 3) to develop an in vivo model of OS and CS, and 4) to identify effective drugs for the Rb mutant tumors. To achieve the first goal, we will examine the role of Rb in cell cycle regulation in cell lines with these mutations. In order to determine the oncogenic role of these mutations, we will characterize the properties of these cell lines and determine whether a cell can escape from Rb regulation by cooperating with activated Ras or Myc. The last two goals will be approached by crossing mice with these tumors with mice expressing activated Ras or Myc. These genetic and molecular studies will provide clues to the mechanism of oncogenesis in the Rb mutant tumors and the mechanisms by which Rb regulates the cell cycle in normal cells. More importantly, these studies will provide the rationale for targeted therapy against Rb mutant tumors. Since many human cancers have a poor outcome, identification of effective drugs is an important goal of pediatric cancer research. We hope that these studies will result in new therapies and improve the survival of children with these pediatric cancers. Show HN:

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