PMID- 9187127
OWN - NLM
STAT- MEDLINE
DCOM- 19970710
LR  - 20051117
IS  - 0008-5472 (Print)
IS  - 0008-5472 (Linking)
VI  - 57
IP  - 11
DP  - 1997 Jun 1
TI  - Allelic deletions on chromosome 11q13 in multiple endocrine neoplasia type 
      1-associated and sporadic gastrinomas and pancreatic endocrine tumors.
PG  - 2238-43
AB  - Endocrine tumors (ETs) of pancreas and duodenum occur sporadically and as a part 
      of multiple endocrine neoplasia type 1 (MEN1). The MEN1 tumor suppressor gene has 
      been localized to chromosome 11q13 by linkage analysis but has not yet isolated. 
      Previous allelic deletion studies in enteropancreatic ETs suggested MEN1 gene 
      involvement in tumorigenesis of familial pancreatic ETs (nongastrinomas) and 
      sporadic gastrinomas. However, only a few MEN1-associated duodenal gastrinomas 
      and sporadic pancreatic nongastrinomas have been investigated. We used tissue 
      microdissection to analyze 95 archival pancreatic and duodenal ETs and metastases 
      from 50 patients for loss of heterozygosity (LOH) on 11q13 with 10 polymorphic 
      markers spanning the area of the putative MEN1 gene. Chromosome 11q13 LOH was 
      detected in 23 of 27 (85%) MEN1-associated pancreatic ETs (nongastrinomas), 14 of 
      34 (41%) MEN1-associated gastrinomas, 3 of 16 (19%) sporadic insulinomas, and 8 
      of 18 (44%) sporadic gastrinomas. Analysis of LOH on 11q13 showed different 
      deletion patterns in ETs from different MEN1 patients and in multiple tumors from 
      individual MEN1 patients. The present results suggest that the MEN1 gene plays a 
      role in all four tumor types. The lower rate of 11q13 LOH in MEN1-associated and 
      sporadic gastrinomas and sporadic insulinomas as compared to MEN1 nongastrinomas 
      may reflect alternative genetic pathways for the development of these tumors or 
      mechanisms of the MEN1 gene inactivation that do not involve large deletions. The 
      isolation of the MEN1 gene is necessary to further define its role in 
      pathogenesis of pancreatic and duodenal ETs.
FAU - Debelenko, L V
AU  - Debelenko LV
AD  - Laboratory of Pathology, National Cancer Institute, NIH, Bethesda, Maryland 
      20892, USA.
FAU - Zhuang, Z
AU  - Zhuang Z
FAU - Emmert-Buck, M R
AU  - Emmert-Buck MR
FAU - Chandrasekharappa, S C
AU  - Chandrasekharappa SC
FAU - Manickam, P
AU  - Manickam P
FAU - Guru, S C
AU  - Guru SC
FAU - Marx, S J
AU  - Marx SJ
FAU - Skarulis, M C
AU  - Skarulis MC
FAU - Spiegel, A M
AU  - Spiegel AM
FAU - Collins, F S
AU  - Collins FS
FAU - Jensen, R T
AU  - Jensen RT
FAU - Liotta, L A
AU  - Liotta LA
FAU - Lubensky, I A
AU  - Lubensky IA
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Cancer Res
JT  - Cancer research
JID - 2984705R
RN  - 0 (MEN1 protein, human)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Proto-Oncogene Proteins)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Alleles
MH  - *Chromosome Deletion
MH  - *Chromosomes, Human, Pair 11/genetics
MH  - Dosage Compensation, Genetic
MH  - Duodenal Neoplasms/*genetics
MH  - Female
MH  - Gastrinoma/*genetics
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Multiple Endocrine Neoplasia/*genetics
MH  - Neoplasm Proteins/*genetics
MH  - Pancreatic Neoplasms/*genetics
MH  - *Proto-Oncogene Proteins
MH  - Sequence Analysis, DNA
EDAT- 1997/06/01 00:00
MHDA- 1997/06/01 00:01
CRDT- 1997/06/01 00:00
PHST- 1997/06/01 00:00 [pubmed]
PHST- 1997/06/01 00:01 [medline]
PHST- 1997/06/01 00:00 [entrez]
PST - ppublish
SO  - Cancer Res. 1997 Jun 1;57(11):2238-43.