PMID- 19407509
OWN - NLM
STAT- MEDLINE
DCOM- 20090723
LR  - 20211020
IS  - 1423-0046 (Electronic)
IS  - 0301-0163 (Print)
IS  - 0301-0163 (Linking)
VI  - 71 Suppl 2
IP  - Suppl 2
DP  - 2009 Apr
TI  - The MEN1 gene and pituitary tumours.
PG  - 131-8
LID - 10.1159/000192450 [doi]
AB  - Sporadic multiple endocrine neoplasia type 1 (MEN1) is defined as the occurrence 
      of tumours in two of three main endocrine tissue types: parathyroid, pituitary 
      and pancreaticoduodenal. A prolactinoma variant or Burin variant of MEN1 was 
      found to occur in three large kindreds, with more prolactinomas and fewer 
      gastrinomas than typical MEN1. MEN1 tumours differ from common tumours by showing 
      features from the MEN1 gene (e.g. larger pituitary tumours). They also show 
      various expressions of tumour multiplicity; however, pituitary tumour in MEN1 is 
      usually solitary. Diagnosis in MEN1 carriers during childhood is not directed at 
      cancers but at benign morbid tumours. Morbid prolactinoma occurred at the age of 
      5 years in one MEN1 individual; hence, this is the earliest age at which to 
      recommend tumour surveillance in carriers. The MEN1 gene shows biallelic 
      inactivation in 30% of some types of common variety endocrine tumours (e.g. 
      parathyroid adenoma, gastrinoma, insulinoma and bronchial carcinoid), but in only 
      1-5% of common pituitary tumours. Heterozygous knockout of MEN1 in mice provides 
      a robust model of MEN1 and has been found to support further research on 
      anti-angiogenesis therapy for pituitary tumours. The rarity of MEN1 mutations in 
      some MEN1-like states aids the identification of other mutated genes, such as 
      AIP, HRPT2 and p27(Kip1). We present recent clinical and basic findings about the 
      MEN1 gene, particularly concerning hereditary vs. common variety pituitary 
      tumours.
CI  - Copyright 2009 S. Karger AG, Basel.
FAU - Agarwal, Sunita K
AU  - Agarwal SK
AD  - Metabolic Diseases Branch, National Institute of Diabetes and Digestive and 
      Kidney Diseases, National Institutes of Health, Bethesda, Md., USA.
FAU - Ozawa, Atsushi
AU  - Ozawa A
FAU - Mateo, Carmen M
AU  - Mateo CM
FAU - Marx, Stephen J
AU  - Marx SJ
LA  - eng
GR  - ZIA DK075035-01/ImNIH/Intramural NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Intramural
PT  - Review
DEP - 20090429
PL  - Switzerland
TA  - Horm Res
JT  - Hormone research
JID - 0366126
RN  - 0 (CDC73 protein, human)
RN  - 0 (CDKN1B protein, human)
RN  - 0 (Cdkn1b protein, mouse)
RN  - 0 (HRPT2 protein, mouse)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (MEN1 protein, human)
RN  - 0 (Men1 protein, mouse)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 0 (aryl hydrocarbon receptor-interacting protein)
RN  - 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27)
SB  - IM
MH  - Animals
MH  - Cyclin-Dependent Kinase Inhibitor p27/genetics/metabolism
MH  - Gene Knockout Techniques
MH  - Humans
MH  - Intracellular Signaling Peptides and Proteins/genetics/metabolism
MH  - Mice
MH  - Multiple Endocrine Neoplasia Type 1/genetics/*metabolism
MH  - Mutation
MH  - Prolactinoma/genetics/*metabolism
MH  - Proto-Oncogene Proteins/genetics/*metabolism
MH  - Tumor Suppressor Proteins/genetics/metabolism
PMC - PMC6413329
MID - NIHMS1011553
COIS- Disclosure Statement The authors have no conflicts of interest to disclose.
EDAT- 2009/05/07 09:00
MHDA- 2009/07/25 09:00
PMCR- 2019/03/12
CRDT- 2009/05/02 09:00
PHST- 2009/05/02 09:00 [entrez]
PHST- 2009/05/07 09:00 [pubmed]
PHST- 2009/07/25 09:00 [medline]
PHST- 2019/03/12 00:00 [pmc-release]
AID - 000192450 [pii]
AID - 10.1159/000192450 [doi]
PST - ppublish
SO  - Horm Res. 2009 Apr;71 Suppl 2(Suppl 2):131-8. doi: 10.1159/000192450. Epub 2009 
      Apr 29.