PMID- 12239610
OWN - NLM
STAT- MEDLINE
DCOM- 20030225
LR  - 20091119
IS  - 1019-6439 (Print)
IS  - 1019-6439 (Linking)
VI  - 21
IP  - 4
DP  - 2002 Oct
TI  - Distinct target regions for chromosome 1p deletions in parathyroid adenomas and 
      carcinomas.
PG  - 727-35
AB  - Primary hyperparathyroidism is a common endocrine disease with a multifaceted 
      genetic background, the elucidation of which has only begun. Among others, loss 
      of the short arm of chromosome 1 and somatic inactivation of the multiple 
      endocrine neoplasia type 1 gene (MEN1) in 11q13 represent significant alterations 
      in the tumorigenesis. In the present study deletions of 1p were characterized and 
      the findings were evaluated in relation to the loci of MEN1 and histone 
      deacetylase 1 gene (HDAC1), a menin interacting partner in 1p, as well as to the 
      clinical characteristics. Overall 1p LOH was detected in 18 of the 42 tumors 
      analyzed (43%), and from the deletion patterns a main target interval of 40 cM 
      was identified within 1p band 32.3-36.2. The mapping of HDAC1 centromeric of the 
      main interval, and the lack of altered mRNA expression in tumors with LOH, 
      suggest that HDAC1 is not the main target for 1p deletions in parathyroid tumors. 
      Twenty-five of the 42 tumors (60%) showed alteration of either 1p, of the MEN1 
      locus, or both. Tumors with LOH at 11q13 had a significantly higher weight than 
      tumors with 1p LOH. In conclusion, LOH in primary sporadic parathyroid adenomas 
      occur frequently on the distal part of chromosome 1p and are thus clearly 
      different from parathyroid carcinomas where the deletions are more proximally 
      located. The findings support that the short arm of chromosome 1 harbors at least 
      two different tumor suppressor genes involved in parathyroid tumorigenesis, the 
      exact identification of which may provide a molecular basis for differential 
      diagnosis of benign and malignant disease in the future.
FAU - Valimaki, S
AU  - Valimaki S
AD  - Department of Molecular Medicine, Endocrine Tumor Unit, CMM L8:01, Karolinska 
      Hospital, SE-171 76 Stockholm, Sweden. stiina.valimaki@cmm.ki.se
FAU - Forsberg, L
AU  - Forsberg L
FAU - Farnebo, L-O
AU  - Farnebo LO
FAU - Larsson, C
AU  - Larsson C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Greece
TA  - Int J Oncol
JT  - International journal of oncology
JID - 9306042
RN  - 0 (RNA, Messenger)
RN  - EC 3.5.1.98 (HDAC1 protein, human)
RN  - EC 3.5.1.98 (Histone Deacetylase 1)
RN  - EC 3.5.1.98 (Histone Deacetylases)
SB  - IM
MH  - Adenoma/*genetics
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Carcinoma/*genetics
MH  - *Chromosome Deletion
MH  - *Chromosomes, Human, Pair 1
MH  - Female
MH  - Histone Deacetylase 1
MH  - Histone Deacetylases/genetics
MH  - Humans
MH  - In Situ Hybridization
MH  - In Situ Hybridization, Fluorescence
MH  - Loss of Heterozygosity
MH  - Male
MH  - Middle Aged
MH  - Models, Genetic
MH  - Nucleic Acid Hybridization
MH  - Parathyroid Neoplasms/*genetics
MH  - RNA, Messenger/metabolism
MH  - Radiation Hybrid Mapping
EDAT- 2002/09/20 10:00
MHDA- 2003/02/26 04:00
CRDT- 2002/09/20 10:00
PHST- 2002/09/20 10:00 [pubmed]
PHST- 2003/02/26 04:00 [medline]
PHST- 2002/09/20 10:00 [entrez]
PST - ppublish
SO  - Int J Oncol. 2002 Oct;21(4):727-35.