title: The molecular pathogenesis of corticotroph tumours.
abstract: BACKGROUND
  The pathogenesis of tumour formation in the anterior pituitary including adrenocorticotropic hormone (ACTH)-secreting tumours has been intensively studied, but the causative mechanisms involved in pituitary cell transformation and tumourigenesis remain unclear.
  
  
  METHODS
  We searched PubMed on any paper related with molecular pathology of pituitary corticotroph adenomas and have included to this review all relevant references published up to June 2011.
  
  
  RESULTS
  Current studies increased our knowledge on the genetic basis of McCune-Albright syndrome (MAS), multiple endocrine neoplasia type 1 (MEN1), Carney complex (CNC), pituitary adenoma predisposition syndromes and tuberous sclerosis, but they have performed little to elucidate the causes of sporadic pituitary tumours including Cushing disease.
  
  
  CONCLUSIONS
  The aim of this review was to focus on the most recently published advances in the molecular pathology of corticotroph adenomas, which are presented in the context of changes seen in all types of pituitary adenomas, as well as in terms of corticotrophin-releasing hormone/ACTH/cortisol-specific pathways.
  
  
  CONCLUSIONS
  We would expect that over the next 5 years, more detailed analysis of inter-cellular communication pathways between pituitary cells, including the cadherins and integrins, and their interactions with other signalling pathways such as the β-catenin cascade will help elucidate what exactly goes awry in the formation of a benign corticotroph adenoma. This should in turn predict novel forms of pharmacological tumour control.
authors.affiliation: Department of Endocrinology, Kings College Hospital, Denmark Hill, London, UK.
authors.forename: Dorota
authors.initials: D
authors.lastname: Dworakowska
authors.forename: Ashley B
authors.initials: AB
authors.lastname: Grossman
mesh_terms: D049913:ACTH-Secreting Pituitary Adenoma / Q000209:etiology* / Q000378:metabolism; D000236:Adenoma / Q000209:etiology* / Q000378:metabolism; D052680:Corticotrophs / Q000378:metabolism*; D006801:Humans; D047748:Pituitary ACTH Hypersecretion / Q000209:etiology* / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology