title: Common genetic changes in hereditary and sporadic pituitary adenomas detected by comparative genomic hybridization.
abstract: Twenty-four pituitary adenomas, both the sporadic type (n = 18) and the type arising in association with either multiple endocrine neoplasia, type 1 (MEN1; n = 2), or Carney complex (CNC, n = 4) were analyzed by comparative genomic hybridization. Twenty-one (88%) tumors displayed chromosomal alterations. The number of chromosomal aberrations in each tumor varied from 2 to greater than 10. Several recurrent chromosomal abnormalities were identified in this study. The most frequently detected losses of chromosomal material involved 1p (14 of 24, 58%), 11p (11 of 24, 46%), 17 (10 of 24, 42%), 16p (9 of 24, 38%), 4 (8 of 24, 33%), 10p (6 of 24, 25%), 12 (6 of 24, 25%), 20 (6 of 24, 25%), 22q (6 of 24, 25%), 13q (5 of 24, 21%), and 9p (4 of 24, 17%). Copy number increases were detected on 4q (7 of 24, 29%), 17 (8 of 24, 33%), 19 (7 of 24, 29%), 1p (6 of 24, 25%), 5 (6 of 24, 25%), 20 (6 of 24, 25%), 6q (5 of 24, 21%), 13q21-qter (5 of 24, 21%), and 16p (5 of 24, 21%). Chromosome 11 loss, which involved 11p in all cases, was the most significant finding and was common to tumors arising sporadically and in association with MEN1 and CNC. In addition, the majority of the tumors (18 of 24, 75% overall and 86% of all tumors with chromosomal abnormalities) showed involvement of chromosome 1. Tumors had either loss (14 of 24, 58%) or gain (6 of 24, 25%) in the 1p32-1pter region. Finally, changes on chromosome 17, either loss or gain, occurred in 71% (17) of all 24 patients. In summary, all the tumors with chromosomal rearrangements (21 of 24, 88%), whether sporadic pituitary adenomas or those associated with MEN1 or CNC, had alteration(s) of 1p32, 11p, or 17.
authors.affiliation: Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
authors.forename: Svetlana D
authors.initials: SD
authors.lastname: Pack
authors.forename: Liu-Xiu
authors.initials: LX
authors.lastname: Qin
authors.forename: Evgenia
authors.initials: E
authors.lastname: Pak
authors.forename: Yun
authors.initials: Y
authors.lastname: Wang
authors.forename: David O
authors.initials: DO
authors.lastname: Ault
authors.forename: Poonam
authors.initials: P
authors.lastname: Mannan
authors.forename: Sivakumar
authors.initials: S
authors.lastname: Jaikumar
authors.forename: Constantine A
authors.initials: CA
authors.lastname: Stratakis
authors.forename: Edward H
authors.initials: EH
authors.lastname: Oldfield
authors.forename: Zhengping
authors.initials: Z
authors.lastname: Zhuang
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Weil
mesh_terms: D000236:Adenoma / Q000235:genetics* / Q000601:surgery; D000293:Adolescent; D000328:Adult; D002675:Child, Preschool; D002872:Chromosome Deletion; D002874:Chromosome Mapping; D004273:DNA, Neoplasm / Q000235:genetics; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009693:Nucleic Acid Hybridization / Q000235:genetics; D010911:Pituitary Neoplasms / Q000235:genetics* / Q000601:surgery
chemical_list: D004273:DNA, Neoplasm