In this present work, the authors discuss some recent advances in the
pathogenesis of pituitary tumours. The model of transgenic mices sugge
st that chronic hormonal stimulation and some growth factors could sus
tain pituitary tumour development. However, these data are not suitabl
e for human pituitary adenomas. The evidence that most pituitary adeno
mas are monoclonal in origin has prompted a search for somatic mutatio
ns. The mutated Gs alpha are found in only 30-40% of somatotroph adeno
mas and the ras mutations seem to be associated with the malignant tra
nsformation. In some prolactinomas resistant to the bromocriptine trea
tment, quantitative and qualitative alterations of the dopamine recept
or D2, have been described. Mutations of protein kinase C have been id
entified in some invasive pituitary tumours. Molecular abnormalities h
ave been reported in some cases (allele loss at the 11q13 locus, retin
oblastoma gene mutation, aberrant expression of hst gene, Pit-1 overex
pression) but none by itself can explain the tumour formation. The pit
uitary tumorigenesis is certainly a multistep process with the interve
ntion of multiple promoting factors.