PMID- 16322327
OWN - NLM
STAT- MEDLINE
DCOM- 20060310
LR  - 20081121
IS  - 1351-0088 (Print)
IS  - 1351-0088 (Linking)
VI  - 12
IP  - 4
DP  - 2005 Dec
TI  - High-mobility group A2 gene expression is frequently induced in non-functioning 
      pituitary adenomas (NFPAs), even in the absence of chromosome 12 polysomy.
PG  - 867-74
AB  - The high-mobility group A2 (HMGA2) gene has a critical role in benign tumors 
      where it is frequently rearranged, and in malignant tumors, where it is 
      overexpressed in the absence of structural modification of the HMGA2 locus. By 
      previous fluorescence in situ hybridization (FISH) and reverse transcriptase PCR 
      analyses on human prolactin-secreting pituitary adenomas we detected 
      rearrangement of the HMGA2 gene and amplification of its native region associated 
      with activated expression. These data indicated a role for the HMGA2 gene in the 
      development of human pituitary prolactinomas, since they are consistent with the 
      appearance of prolactin/growth hormone adenomas in transgenic mice overexpressing 
      the HMGA2 gene. To assess a more general role for HMGA2 in pituitary oncogenesis, 
      we investigated HMGA2 amplification and expression in a panel of non-functioning 
      pituitary adenomas (NFPAs) which account for 25% of all pituitary adenomas. We 
      provide evidence that out of 18 NFPA tumors tested, 12 expressed HMGA2, but, 
      different from prolactinomas, only in two cases the upregulation of the gene 
      could be associated with amplification and/or rearrangement of the HMGA2 locus. 
      Increased dosage of chromosome 12 was found in the expressing and non-expressing 
      NFPAs, confirming that this sole event is insufficient to drive up activation of 
      the HMGA2 gene. A role for chromosome 12 polysomy to promote structural 
      instability of HMGA2 is confirmed, but the mechanism via trisomy is less 
      prevalent in the frequently diploid NFPAs than in the usually hyperdiploid 
      prolactinomas. Micro-rearrangements of HMGA2 gene not detectable by FISH analysis 
      and/or sequence alterations could contribute to upregulation of HMGA2 gene in 
      pituitary adenomas of the NFPA subtype. However, it cannot be excluded that the 
      HMGA2 overexpression may be due, in some NFPA patients, to the same, still mainly 
      unknown, mechanisms responsible for HMGA2 overexpression in malignant neoplasias.
FAU - Pierantoni, Giovanna Maria
AU  - Pierantoni GM
AD  - Dipartimento di Biologia e Patologia Cellulare e Molecolare, Facolta di Medicina 
      e Chirurgia, Universita degli Studi di Napoli Federico II, Italy.
FAU - Finelli, Palma
AU  - Finelli P
FAU - Valtorta, Emanuele
AU  - Valtorta E
FAU - Giardino, Daniela
AU  - Giardino D
FAU - Rodeschini, Ornella
AU  - Rodeschini O
FAU - Esposito, Francesco
AU  - Esposito F
FAU - Losa, Marco
AU  - Losa M
FAU - Fusco, Alfredo
AU  - Fusco A
FAU - Larizza, Lidia
AU  - Larizza L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Endocr Relat Cancer
JT  - Endocrine-related cancer
JID - 9436481
RN  - 0 (HMGA2 Protein)
SB  - IM
MH  - Adenoma/chemistry/*genetics
MH  - Aneuploidy
MH  - Chromosomes, Human, Pair 12/*genetics
MH  - *Gene Amplification
MH  - Gene Expression
MH  - Gene Expression Regulation, Neoplastic
MH  - Gene Rearrangement
MH  - HMGA2 Protein/analysis/*genetics
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Pituitary Neoplasms/chemistry/*genetics
MH  - Transcriptional Activation
EDAT- 2005/12/03 09:00
MHDA- 2006/03/11 09:00
CRDT- 2005/12/03 09:00
PHST- 2005/12/03 09:00 [pubmed]
PHST- 2006/03/11 09:00 [medline]
PHST- 2005/12/03 09:00 [entrez]
AID - 12/4/867 [pii]
AID - 10.1677/erc.1.01049 [doi]
PST - ppublish
SO  - Endocr Relat Cancer. 2005 Dec;12(4):867-74. doi: 10.1677/erc.1.01049.