Glucagonoma risk factors: Difference between revisions
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==Overview== | ==Overview== | ||
The most common risk factor in the development of glucagonoma is positive family history of [[multiple endocrine neoplasia type 1]] | The most common risk factor in the development of glucagonoma is a positive family history of [[multiple endocrine neoplasia type 1|multiple endocrine neoplasia type1]] which is characterized by the presence of [[Pituitary adenoma|pituitary adenomas]], [[Islet cell tumor|islet cell tumors]] of the [[pancreas]], and [[hyperparathyroidism]]. | ||
==Risk Factors== | ==Risk Factors== | ||
The most common risk factor in the development of glucagonoma is positive family history of [[multiple endocrine neoplasia type 1]].<ref name="pmid22970401">{{cite journal| author=Afsharfard A, Atqiaee K, Lotfollahzadeh S, Alborzi M, Derakhshanfar A| title=Necrolytic migratory erythema as the first manifestation of glucagonoma. | journal=Case Rep Surg | year= 2012 | volume= 2012 | issue= | pages= 974210 | pmid=22970401 | doi=10.1155/2012/974210 | pmc=PMC3434377 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22970401 }} </ref><ref name=causes>Glucagonoma. U.S. National Library of Medicine. https://www.nlm.nih.gov/medlineplus/ency/article/000326.htm</ref> | * The most common risk factor in the development of glucagonoma is a positive family history of [[multiple endocrine neoplasia type 1]].<ref name="pmid22970401">{{cite journal| author=Afsharfard A, Atqiaee K, Lotfollahzadeh S, Alborzi M, Derakhshanfar A| title=Necrolytic migratory erythema as the first manifestation of glucagonoma. | journal=Case Rep Surg | year= 2012 | volume= 2012 | issue= | pages= 974210 | pmid=22970401 | doi=10.1155/2012/974210 | pmc=PMC3434377 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22970401 }} </ref><ref name="causes">Glucagonoma. U.S. National Library of Medicine. https://www.nlm.nih.gov/medlineplus/ency/article/000326.htm</ref> | ||
* It is an autosomal dominant syndrome that is usually caused by mutations in the [[MEN1 syndrome|''MEN1'' gene]]. | |||
* It is characterized by the development of the following tumors:<sup>[[Multiple endocrine neoplasia type 1 pathophysiology#cite note-wikipedia-1|[1]]]</sup> | |||
* [[Pituitary adenoma|Pituitary adenomas]] | |||
* [[Islet cell tumor|Islet cell tumors]] of the [[pancreas]] (commonly [[gastrinoma]] and glucagonoma) | |||
* [[Parathyroid]] [[hyperplasia]] with resulting [[hyperparathyroidism]] | |||
* The [[gene]] [[locus]] causing [[multiple endocrine neoplasia type 1]] has been localized to [[chromosome]] 11q13 by studies of [[loss of heterozygosity]] on [[multiple endocrine neoplasia type 1]]-associated [[Tumor|tumors]] and by linkage analysis in [[multiple endocrine neoplasia type 1]] families.<sup>[[Multiple endocrine neoplasia type 1 pathophysiology#cite note-pmid17014705-2|[2]]][[Multiple endocrine neoplasia type 1 pathophysiology#cite note-pmid2894610-3|[3]]][[Multiple endocrine neoplasia type 1 pathophysiology#cite note-pmid2568587-4|[4]]][[Multiple endocrine neoplasia type 1 pathophysiology#cite note-pmid2568586-5|[5]]][[Multiple endocrine neoplasia type 1 pathophysiology#cite note-pmid1968641-6|[6]]]</sup>''MEN1'', spans about 10 Kb and consists of ten exons encoding a 610 [[amino acid]] nuclear protein, named menin.<sup>[[Multiple endocrine neoplasia type 1 pathophysiology#cite note-pmid17014705-2|[2]]]</sup> | |||
* ''MEN1'' [[gene]] is a putative [[tumor suppressor gene]] and causes type 1 multiple endocrine neoplasia by Knudson's "two hits" model for [[tumor]] development.<sup>[[Multiple endocrine neoplasia type 1 pathophysiology#cite note-pmid7902574-7|[7]]]</sup> | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Parminder Dhingra, M.D. [2] Mohammed Abdelwahed M.D[3]
Overview
The most common risk factor in the development of glucagonoma is a positive family history of multiple endocrine neoplasia type1 which is characterized by the presence of pituitary adenomas, islet cell tumors of the pancreas, and hyperparathyroidism.
Risk Factors
- The most common risk factor in the development of glucagonoma is a positive family history of multiple endocrine neoplasia type 1.[1][2]
- It is an autosomal dominant syndrome that is usually caused by mutations in the MEN1 gene.
- It is characterized by the development of the following tumors:[1]
- Pituitary adenomas
- Islet cell tumors of the pancreas (commonly gastrinoma and glucagonoma)
- Parathyroid hyperplasia with resulting hyperparathyroidism
- The gene locus causing multiple endocrine neoplasia type 1 has been localized to chromosome 11q13 by studies of loss of heterozygosity on multiple endocrine neoplasia type 1-associated tumors and by linkage analysis in multiple endocrine neoplasia type 1 families.[2][3][4][5][6]MEN1, spans about 10 Kb and consists of ten exons encoding a 610 amino acid nuclear protein, named menin.[2]
- MEN1 gene is a putative tumor suppressor gene and causes type 1 multiple endocrine neoplasia by Knudson's "two hits" model for tumor development.[7]
References
- ↑ Afsharfard A, Atqiaee K, Lotfollahzadeh S, Alborzi M, Derakhshanfar A (2012). "Necrolytic migratory erythema as the first manifestation of glucagonoma". Case Rep Surg. 2012: 974210. doi:10.1155/2012/974210. PMC 3434377. PMID 22970401.
- ↑ Glucagonoma. U.S. National Library of Medicine. https://www.nlm.nih.gov/medlineplus/ency/article/000326.htm