The last several years have seen a significant increase in our underst
anding of the molecular and biochemical changes associated with pituit
ary 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 as
sociated 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 respon
se element-binding factor (CREB), growth hormone-releasing hormone (GH
RH), nm23, p16 and p27 have also been identified along this multi-step
path way. Prospective studies will determine whether these markers ar
e truly predictive of subsequent tumour behaviour and can be used to a
id clinical management in a manner not possible when current histologi
cal criteria are used.