Multiple endocrine neoplasia type 1 historical perspective: Difference between revisions
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* In 1982, McCarthy identified 2 different causes of [[Zollinger-Ellison syndrome]], [[malignant]] type and the one linked with multiple endocrine neoplasia type 1. | * In 1982, McCarthy identified 2 different causes of [[Zollinger-Ellison syndrome]], [[malignant]] type and the one linked with multiple endocrine neoplasia type 1. | ||
* In 1983, Hershon identified family members from Pacific Northwest with [[prolactinoma]]s but with no [[pancreatic tumor]]s. | * In 1983, Hershon identified family members from Pacific Northwest with [[prolactinoma]]s but with no [[pancreatic tumor]]s. | ||
* In 1985, Bear referred the disorders reported from Burin as multiple endocrine neoplasia type 1 Burin | * In 1985, Bear referred the disorders reported from Burin as multiple endocrine neoplasia type 1 Burin. | ||
* In 1986 Brandi suggested the [[humoral]] cause of primary [[hyperparathyroidism]] in familial multiple endocrine neoplasia type 1. | * In 1986 Brandi suggested the [[humoral]] cause of primary [[hyperparathyroidism]] in familial multiple endocrine neoplasia type 1. | ||
* In 1986 Schimke suggested a 2 step model of [[pathogenesis]] which include [[germline mutation]] followed by somatic [[mutation]] later. | * In 1986 Schimke suggested a 2 step model of [[pathogenesis]] which include [[germline mutation]] followed by somatic [[mutation]] later. | ||
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* In 1998 the multiple endocrine neoplasia type 1 [[gene]] was [[cloned]].<ref name="Guru1998">Guru SC, Manickam P, Crabtree JS, Olufemi SE, Agarwal SK, Debelenko LV. Identification and characterization of the multiple endocrine neoplasia type 1 (MEN1) gene. ''J Intern Med'' 243(6) 433-9</ref> | * In 1998 the multiple endocrine neoplasia type 1 [[gene]] was [[cloned]].<ref name="Guru1998">Guru SC, Manickam P, Crabtree JS, Olufemi SE, Agarwal SK, Debelenko LV. Identification and characterization of the multiple endocrine neoplasia type 1 (MEN1) gene. ''J Intern Med'' 243(6) 433-9</ref> | ||
* In 1999, Yu identified that gastrinoma growth is the single most important factor in deciding the long term survival of patients with [[Zollinger-Ellison syndrome]]. | * In 1999, Yu identified that gastrinoma growth is the single most important factor in deciding the long term survival of patients with [[Zollinger-Ellison syndrome]]. | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
[[Category:Hereditary cancers]] | [[Category:Hereditary cancers]] | ||
Revision as of 10:58, 11 September 2015
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [3]
Overview
Multiple endocrine neoplasia type 1 was first described by Dr. Erdheim, a German physician, in 1903 by reporting a case of an acromegalic patient with pituitary adenoma and three enlarged parathyroid glands.
Historical Perspective
- In 1903 Erdheim described the case of an acromegalic patient with pituitary adenoma and three enlarged parathyroid glands.
- In 1953 Underdahl reported case series of patients with a syndrome of pituitary, parathyroid, and pancreatic islet adenomas.
- In 1954 Wermer noted that this syndrome was transmitted as a dominant trait.
- In 1962, Williams and Celestin described bronchial carcinoid as a feature of Multiple endocrine neoplasia type 1.
- In 1963, Jacobs and Underwood presented case of hypoglycemia and islet cell adenomas in 3 members of the family, with father having hyperparathyroidism and broncial carcinoma and son and daughter with idiopathic epilepsy.
- In 1966, Guida identified pituitary adenoma and duodenal carcinoid in patients with multiple endocrine neoplasia type 1 syndrome.
- In 1967, Johnson presented a multiple endocrine neoplasia type 1 case devoid of peptic ulcer.
- In 1968 Steiner introduced the term "multiple endocrine neoplasia" (MEN) to describe disorders featuring combinations of endocrine tumors and proposed the terms 'Wermer syndrome' for MEN 1 and 'Sipple syndrome' for MEN 2.
- In 1972, Vance suggested the importance of primary genetic lesion in endocrine adnomatosis in developing neoplasia and hyperfunctioning of islet of langerhans.[1]
- In 1980, Farid identified 4 family members in Burin, Newfoundland with hyperparathyroidism and prolactinoma but with no pancreatic tumors. 2 of them had carcinoid in thymus and lung.
- In 1981, Stacpoole identified 3 men with pancreatic tumor.
- In 1982, McCarthy identified 2 different causes of Zollinger-Ellison syndrome, malignant type and the one linked with multiple endocrine neoplasia type 1.
- In 1983, Hershon identified family members from Pacific Northwest with prolactinomas but with no pancreatic tumors.
- In 1985, Bear referred the disorders reported from Burin as multiple endocrine neoplasia type 1 Burin.
- In 1986 Brandi suggested the humoral cause of primary hyperparathyroidism in familial multiple endocrine neoplasia type 1.
- In 1986 Schimke suggested a 2 step model of pathogenesis which include germline mutation followed by somatic mutation later.
- In 1986, Bahn identified 25 year old monozygotic twins with one having primary hyperparathyroidism, Zollinger-Ellison syndrome, cushing disease, and hyperprolactinemia and the other have primary hyperparathyroidism and hyperprolactinemia.
- In 1986, Maton identified that cushing's syndrome is more common with Zollinger-Ellison syndrome.
- In 1988 the multiple endocrine neoplasia type 1 locus was assigned to chromosome 11 (11q13).
- In 1993, Gaitan, described mother and daughter with cushing's disease due to ACTH secreting tumor.
- In 1994, Petty et al, identified that gene involved in Pacific Northwest studies and Burin studies linked to 11q chromosome.
- In 1998 the multiple endocrine neoplasia type 1 gene was cloned.[2]
- In 1999, Yu identified that gastrinoma growth is the single most important factor in deciding the long term survival of patients with Zollinger-Ellison syndrome.