Clonality of pituitary tumours: More complicated than initially envisaged?

The application of allelotype microsatellite polymorphisms and X chromosome inactivation analysis in samples from women allow assessment of clonality, Early studies showed that sporadic human pituitary tumors are benign adeno mas of monoclonal origin, This implies that they arise from de novo somatic mutation(s) within a single pituitary cell, However, the evidence obtained from a number of studies indicate that morphology cannot predict clonality , clonality within a given tumour may be multiple or single, multiple tumou rs arising on the background of hyperplasia may be of identical or differin g clonality, and multiple "sporadic" tumours within a gland may be of diffe ring clonal origin, Thus, while the early available evidence indicated that pituitary tumours appear largely monoclonal, it is simplistic to assume th at this is inevitable and that these cannot be multiclonal in origin. These observations would be entirely compatible with an initiating stimulus resu lting in hyperplasia of specific cell types in the pituitary, which itself gives rise to several distinct clones with variable potential to develop in to tumours, Such stimuli might include hypothalamic trophic factors, intrap ituitary growth factors, or pituitary specific oncogenes.