title: Prevalence of double pituitary adenomas in a surgical series: Clinical, histological and genetic features.
abstract: BACKGROUND
  The term double pituitary adenomas (DPA) is usually referred to those rare lesions showing two distinct cellular components. Genetic background may sustain the proliferation of more than one cell at the same time but no information is available on the presence of aip mutations in these patients.
  
  
  OBJECTIVE
  We report the prevalence and the endocrinological, neuroradiological, histopathological and genetic features of DPA detected in a large surgical series. The contribution of pituitary transcription factor immunostains in DPA was also evaluated.
  
  
  METHODS
  One-hundred-forty-four patients undergoing surgery for tumors of the sellar region were evaluated. Histopathology, immunohistochemistry and the mutational analysis for the entire coding region of the AIP and MEN1 genes were performed.
  
  
  RESULTS
  One-hundred-seventeen patients out of 144 had a pituitary adenoma. DPA was found in 3 (2.6%) out of 117 patients with pituitary adenoma. Immunohistochemistry and transcription factors analysis demonstrated two not yet described histotype associations in DPA. The coexistence of somatotroph-lactotroph and silent mammosomatotroph histotype in 1 case and the coexistence of sparsely granulated lactotroph and null cell adenomas in the remaining two cases were first identified. Sequencing data for the coding region of the aip and the menin gene resulted in wild type sequences in all patients with DPA.
  
  
  CONCLUSIONS
  The prevalence of DPA observed in our unselected surgical series is not negligible (2.6%). Furthermore, the evaluation of the treatment outcome would suggest that the clinical management of DPAs requires a careful diagnostic approach and follow- up.
authors: Fondazione Salvatore Maugeri IRCCS, Istituto Superiore Prevenzione e Sicurezza Lavoro, University of Pavia, Italy.
authors: F
authors: F
authors: Magri
authors: C
authors: C
authors: Villa
authors: D
authors: D
authors: Locatelli
authors: P
authors: P
authors: Scagnelli
authors: M S
authors: MS
authors: Lagonigro
authors: P
authors: P
authors: Morbini
authors: M
authors: M
authors: Castellano
authors: E
authors: E
authors: Gabellieri
authors: M
authors: M
authors: Rotondi
authors: E
authors: E
authors: Solcia
authors: A F
authors: AF
authors: Daly
authors: L
authors: L
authors: Chiovato
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000236:Adenoma / Q000453:epidemiology* / Q000235:genetics / Q000601:surgery; D000328:Adult; D002352:Carrier Proteins / Q000096:biosynthesis / Q000235:genetics; D004252:DNA Mutational Analysis; D004273:DNA, Neoplasm / Q000235:genetics; D051528:Guanylate Kinases; D006801:Humans; D007150:Immunohistochemistry; D052682:Lactotrophs / Q000473:pathology; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D010911:Pituitary Neoplasms / Q000453:epidemiology* / Q000235:genetics / Q000601:surgery; D015175:Prolactinoma / Q000235:genetics / Q000473:pathology / Q000601:surgery; D011518:Proto-Oncogene Proteins / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014157:Transcription Factors / Q000235:genetics; D016896:Treatment Outcome
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D002352:Carrier Proteins; D004273:DNA, Neoplasm; C105373:MEN1 protein, human; D011518:Proto-Oncogene Proteins; D014157:Transcription Factors; D051528:Guanylate Kinases; C485777:MAGI2 protein, human