PMID- 15704128
OWN - NLM
STAT- MEDLINE
DCOM- 20050524
LR  - 20050321
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 43
IP  - 1
DP  - 2005 May
TI  - Common genetic changes in hereditary and sporadic pituitary adenomas detected by 
      comparative genomic hybridization.
PG  - 72-82
AB  - 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.
CI  - Copyright 2005 Wiley-Liss, Inc.
FAU - Pack, Svetlana D
AU  - Pack SD
AD  - Laboratory of Immunopathology, National Institute of Allergy and Infectious 
      Diseases, National Institutes of Health, Bethesda, Maryland, USA.
FAU - Qin, Liu-Xiu
AU  - Qin LX
FAU - Pak, Evgenia
AU  - Pak E
FAU - Wang, Yun
AU  - Wang Y
FAU - Ault, David O
AU  - Ault DO
FAU - Mannan, Poonam
AU  - Mannan P
FAU - Jaikumar, Sivakumar
AU  - Jaikumar S
FAU - Stratakis, Constantine A
AU  - Stratakis CA
FAU - Oldfield, Edward H
AU  - Oldfield EH
FAU - Zhuang, Zhengping
AU  - Zhuang Z
FAU - Weil, Robert J
AU  - Weil RJ
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
RN  - 0 (DNA, Neoplasm)
SB  - IM
MH  - Adenoma/*genetics/surgery
MH  - Adolescent
MH  - Adult
MH  - Child, Preschool
MH  - Chromosome Deletion
MH  - Chromosome Mapping
MH  - DNA, Neoplasm/genetics
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Nucleic Acid Hybridization/genetics
MH  - Pituitary Neoplasms/*genetics/surgery
EDAT- 2005/02/11 09:00
MHDA- 2005/05/25 09:00
CRDT- 2005/02/11 09:00
PHST- 2005/02/11 09:00 [pubmed]
PHST- 2005/05/25 09:00 [medline]
PHST- 2005/02/11 09:00 [entrez]
AID - 10.1002/gcc.20162 [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2005 May;43(1):72-82. doi: 10.1002/gcc.20162.