PMID- 11576946
OWN - NLM
STAT- MEDLINE
DCOM- 20011204
LR  - 20190815
IS  - 1523-6838 (Electronic)
IS  - 0272-6386 (Linking)
VI  - 38
IP  - 4 Suppl 1
DP  - 2001 Oct
TI  - Putative parathyroid tumor suppressor on 1p: independent molecular mechanisms of 
      tumorigenesis from 11q allelic loss.
PG  - S165-7
AB  - Multiple endocrine neoplasia type 1 (MEN1) gene was identified to be a tumor 
      suppressor that encodes menin, playing an important role in the development of 
      MEN1-associated tumors. Somatic MEN1 gene mutations also were detected in 
      sporadic non-MEN1 endocrine tumors. Frequent loss of chromosomal arm 1p has been 
      reported in parathyroid adenomas, suggesting the existence of putative 
      tumor-suppressor genes on 1p. In this study, we performed allelotyping of 
      chromosomes 1p and 11q on 60 sporadic parathyroid adenomas. Thirteen of 48 (27%) 
      informative tumors had allelic loss on 1p, and 18 of 50 (36%) had allelic loss on 
      11q. Ten of 18 tumors with 11q allelic loss successfully completed the sequence 
      of the MEN1 gene coding region and splice junctions, and 3 of 10 (30%) tumors had 
      no somatic mutation, indicating that other putative tumor-suppressor genes on 11q 
      may contribute to their tumorigenesis. Frequency of allelic losses on 1p was 
      significantly higher in tumors without 11q allelic losses (7 of 11 informative 
      tumors [64%]) than in tumors with 11q allelic losses (3 of 17 informative tumors 
      [18%]) by chi-square test (P = 0.0131; chi-square = 6.152). These observations 
      suggested that putative tumor-suppressor genes locate on 1p, and pathways of 
      their tumorigenesis are independent from inactivation of tumor-suppressor genes 
      on 11q.
FAU - Imanishi, Y
AU  - Imanishi Y
AD  - Center for Molecular Medicine, University of Connecticut Health Center, 
      Farmington, CT, USA. imanishi@med.osaka-cu.ac.jp
FAU - Tahara, H
AU  - Tahara H
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Am J Kidney Dis
JT  - American journal of kidney diseases : the official journal of the National Kidney 
      Foundation
JID - 8110075
RN  - 0 (MEN1 protein, human)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Proto-Oncogene Proteins)
SB  - IM
MH  - Adenoma/complications/*genetics
MH  - Chromosome Breakage
MH  - Chromosomes, Human, Pair 1/*genetics
MH  - Chromosomes, Human, Pair 11/*genetics
MH  - Frameshift Mutation
MH  - Genes, Tumor Suppressor/physiology
MH  - Humans
MH  - Hyperparathyroidism/etiology
MH  - *Mutation
MH  - Mutation, Missense
MH  - Neoplasm Proteins/*genetics
MH  - Parathyroid Neoplasms/complications/*genetics
MH  - *Proto-Oncogene Proteins
EDAT- 2001/09/29 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/09/29 10:00
PHST- 2001/09/29 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/09/29 10:00 [entrez]
AID - S0272-6386(01)05325-2 [pii]
AID - 10.1053/ajkd.2001.27430 [doi]
PST - ppublish
SO  - Am J Kidney Dis. 2001 Oct;38(4 Suppl 1):S165-7. doi: 10.1053/ajkd.2001.27430.