Molecular genetics of pituitary tumours

Abstract

The last several years have seen a significant increase in our understanding of the molecular and biochemical changes associated with pituitary tumour initiation and progression. The combined data, from several groups, now allow a tentative map to be drawn showing that reduction to hemizygosity at several chromosomal loci (10q, 11q13 and 13q) is associated with the transition to the invasive phenotype, while loss on chromosome 9p and methylation of the tumour suppressor gene p16 appear to occur early in pituitary tumorigenesis. Changes in the expression/status of several genes and/or proteins including p53, the cAMP response element-binding factor (CREB), growth hormone-releasing hormone (GHRH), nm23, p16 and p27 have also been identified along this multi-step pathway. Prospective studies will determine whether these markers are truly predictive of subsequent tumour behaviour and can be used to aid clinical management in a manner not possible when current histological criteria are used.