ArticleJournal of medical genetics1997
Localisation of a gene causing endocrine neoplasia to a 4 cM region on chromosome 1p35-p36.
Article in Journal of medical genetics, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 65 citations in OpenAlex.
- Detection of genetic alterations in gastric cancer patients from Saudi Arabia using comparative genomic hybridization (CGH).PloS one · 2018Article
- Genetic characterization of large parathyroid adenomas.Endocrine-related cancer · 2012Article
- Histone deacetylase inhibitors upregulate Rap1GAP and inhibit Rap activity in thyroid tumor cells.Endocrine-related cancer · 2011Article
- Downregulation of Rap1GAP in human tumor cells alters cell/matrix and cell/cell adhesion.Molecular and cellular biology · 2010Article
- Loss of Rap1GAP in papillary thyroid cancer.The Journal of clinical endocrinology and metabolism · 2009Article
- Downregulation of Rap1GAP contributes to Ras transformation.Molecular and cellular biology · 2007Article
- Article
- Independent genetic events associated with the development of multiple parathyroid tumors in patients with primary hyperparathyroidism.The American journal of pathology · 2002Article
- Isolation and characterization of the TERE1 gene, a gene down-regulated in transitional cell carcinoma of the bladder.Oncogene · 2001Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of some endocrine tumours, such as medullary thyroid carcinomas, phaeochromocytomas, anterior pituitary adenomas, and parathyroid adenomas involve a putative tumour suppressor gene located on chromosome 1p32-pter, a region that represents 111 cM. In order to refine the location of this gene, 93 endocrine tumours (39 parathyroid adenomas, 40 anterior pituitary adenomas, seven pancreatic islet cell adenomas, and seven carcinoids) were investigated for loss of tumour heterozygosity (LOH) using the seven polymorphic loci 1pter-D1S228-D1S507-D1S234-D1S476-D1S22 0-D1S207-D1S206-1cen. LOH was detected in 27% of the parathyroid tumours and in 7.5% of the pituitary tumours, but in none of the pancreatic islet cell or carcinoid tumours. In addition, seven of the 10 parathyroid tumours that showed LOH of chromosome 1p facilitated a more precise mapping of this putative tumour suppressor gene; five tumours involved a loss only of the telomeric locus D1S228, whereas two other tumours showed LOH at the centromeric loci D1S507, D1S234, D1S476, and D1S220, but not D1S228. Thus, our results have mapped this tumour suppressor gene implicated in endocrine tumours to a 4 cM region flanked by D1S228 and D1S507 on chromosome 1p35-p36.
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