PMID- 8881452
OWN - NLM
STAT- MEDLINE
DCOM- 19961218
LR  - 20190813
IS  - 0300-0664 (Print)
IS  - 0300-0664 (Linking)
VI  - 45
IP  - 2
DP  - 1996 Aug
TI  - Loss of heterozygosity studies at the retinoblastoma and breast cancer 
      susceptibility (BRCA2) loci in pituitary, parathyroid, pancreatic and carcinoid 
      tumours.
PG  - 195-200
AB  - OBJECTIVE: Allelic deletion of the retinoblastoma (Rb) gene on chromosome 13 has 
      been reported in both pituitary and parathyroid tumours. We have investigated the 
      roles of the Rb and the hereditary breast cancer susceptibility gene (BRCA2), 
      which lie within 25 cM of each other on chromosome 13q12-14, in the multi-step 
      aetiology of endocrine tumours. PATIENTS AND MEASUREMENTS: Seventy-seven 
      endocrine tumours (43 anterior pituitary, 22 parathyroid, 7 carcinoid, and 5 
      pancreatic islet cell tumours) with paired leucocytes have been examined for loss 
      of heterozygosity (LOH) at the Rb and BRCA2 loci by using specific 
      oligonucleotide primers for the PCR amplification of microsatellite polymorphisms 
      at three intragenic Rb markers, Rb1.20, Rbi4 and D13S153, and D13S260 which is 
      linked to the BRCA2 locus. RESULTS: Seventy-five of the 77 tumour-leucocyte pairs 
      were informative and LOH was detected in 1 of 16 non-functioning pituitary 
      tumours, 1 of 8 prolactinomas, 3 of 19 parathyroid adenomas and 1 of 1 
      parathyroid carcinoma. All the 3 parathyroid adenomas with LOH were associated 
      with aggressive clinical and histopathological features. Allele loss was not 
      detected in any of the 16 somatotrophinomas, 2 corticotrophinomas, 1 
      gonadotrophinoma, 7 carcinoid tumours (6 bronchial, 1 metastatic intestinal) or 5 
      pancreatic islet cell tumours that were informative. CONCLUSIONS: These results 
      demonstrate that allelic deletions of the 13q12-14 region occur in some pituitary 
      adenomas and 16% of parathyroid adenomas. The extensive loss, which involves both 
      the Rb gene and the BRCA2 locus, suggests that tumour suppressor genes in this 
      region other than Rb or BRCA2 may be involved in the development and progression 
      of some endocrine tumours.
FAU - Pearce, S H
AU  - Pearce SH
AD  - MRC Molecular Endocrinology Group, Royal Postgraduate Medical School, London, UK.
FAU - Trump, D
AU  - Trump D
FAU - Wooding, C
AU  - Wooding C
FAU - Sheppard, M N
AU  - Sheppard MN
FAU - Clayton, R N
AU  - Clayton RN
FAU - Thakker, R V
AU  - Thakker RV
LA  - eng
PT  - Journal Article
PL  - England
TA  - Clin Endocrinol (Oxf)
JT  - Clinical endocrinology
JID - 0346653
RN  - 0 (BRCA2 Protein)
RN  - 0 (DNA Primers)
RN  - 0 (Genetic Markers)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - BRCA2 Protein
MH  - Carcinoid Tumor/genetics
MH  - *Chromosomes, Human, Pair 13
MH  - DNA Primers/genetics
MH  - Endocrine Gland Neoplasms/*genetics
MH  - *Gene Deletion
MH  - *Genes, Retinoblastoma
MH  - Genetic Markers
MH  - Humans
MH  - Microsatellite Repeats
MH  - Neoplasm Proteins/*genetics
MH  - Pancreatic Neoplasms/genetics
MH  - Parathyroid Neoplasms/genetics
MH  - Pituitary Gland, Anterior
MH  - Pituitary Neoplasms/genetics
MH  - Polymerase Chain Reaction
MH  - Transcription Factors/*genetics
EDAT- 1996/08/01 00:00
MHDA- 1996/08/01 00:01
CRDT- 1996/08/01 00:00
PHST- 1996/08/01 00:00 [pubmed]
PHST- 1996/08/01 00:01 [medline]
PHST- 1996/08/01 00:00 [entrez]
AID - 10.1046/j.1365-2265.1996.d01-1561.x [doi]
PST - ppublish
SO  - Clin Endocrinol (Oxf). 1996 Aug;45(2):195-200. doi: 
      10.1046/j.1365-2265.1996.d01-1561.x.