Absence of mutations in the p53 tumor suppressor gene in non-invasive Cushing adenomas

A lot of evidence supports the existence of a monoclonal origin for pituita ry tumors, and several genetic alterations have already been confirmed as n ecessary or sufficient for unrestrained cellular growth and pituitary funct ion. The p53 gene, a known tumor-suppressor gene (TSG), encodes a protein t hat exerts antiproliferative effects such as cell-growth arrest and apoptos is in response to several types of stimuli. In fact, several human cancers are believed to be caused by p53 mutations. In the case of pituitary tumors , p53 protein accumulation has been described in ACTH-secreting pituitary a denomas. Since increased amounts of the p53 protein are often related to mu tations of its gene, we decided to explore the existence of p53 mutations i n the tumor tissues of 9 patients bearing non-invasive corticotropinomas, e xcised by the transphenoidal route. We screened mutations in exons 5 to 8 o f the p53 gene by the PCR-SSCP analysis. We were not able to find any mutat ion in the exons investigated: Our results are in close accordance with tho se obtained previously for other types of pituitary tumors.