MECHANISMS FOR PITUITARY TUMORIGENESIS

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Although pituitary tumors are common monoclonal neoplasms, they rarely metastasize outside the pituitary fossa, but cause considerable morbidity and mortality. Many molecular events underlying pituitary tumorigenesis have been elucidated in recent years, but no clear tumor marker has emerged which assists clinical decisions regarding appropriate therapy. We have recently described a novel estrogen-regulated activating oncogene, Pituitary Tumor Transforming Gene (PTTG), which is potently transforming in vitro and in vivo, regulates basic fibroblast growth factor (bFGF) secretion and inhibits chromatid separation. In experimental animal pituitary tumor models, increased PTTG expression occurs early in cell transformation (normal ? hyperplastic cell) and PTTG overexpression was observed in 99% of pituitary tumors. PTTG presents an attractive target for designing subcellular pituitary tumor therapy and increased understanding of its role and that of other genetic events in pituitary tumorigenesis may provide novel approaches to pituitary tumor management.