Multiple endocrine neoplasia type 1 historical perspective: Difference between revisions
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{{CMG}}; {{AE}} {{Ammu}} | {{CMG}}; {{AE}} {{Ammu}} | ||
==Overview== | ==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 a pituitary adenoma and three enlarged parathyroid | 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 a [[pituitary adenoma]] and three enlarged [[parathyroid gland]]s. | ||
==Historical Perspective== | ==Historical Perspective== | ||
* In 1903 Erdheim described the case of an acromegalic patient with a pituitary adenoma and three enlarged parathyroid | * In 1903 Erdheim described the case of an acromegalic patient with a [[pituitary adenoma]] and three enlarged [[parathyroid gland]]s. | ||
* In 1953 Underdahl ''et al.'' reported a case series of patients with a syndrome of pituitary, parathyroid, and pancreatic islet | * In 1953 Underdahl ''et al.'' reported a case series of patients with a syndrome of [[pituitary]], [[parathyroid]], and [[pancreatic islet adenoma]]s. | ||
* In 1954 Wermer noted that this syndrome was transmitted as a dominant trait. | * In 1954 Wermer noted that this syndrome was transmitted as a [[dominant]] trait. | ||
* 1968 Steiner ''et al.'' introduced the term "multiple endocrine neoplasia" (MEN) to describe disorders featuring combinations of endocrine | * 1968 Steiner ''et al.'' introduced the term "multiple endocrine neoplasia" (MEN) to describe disorders featuring combinations of [[endocrine tumor]]s and proposed the terms 'Wermer syndrome' for MEN 1 and 'Sipple syndrome' for [[MEN 2]]. | ||
* In 1972, Vance et al, suggested the importance of primary genetic lesion in endocrine adnomatosis in developing neoplasia and hyperfunctioning of islet of | * In 1972, Vance et al, suggested the importance of primary genetic lesion in endocrine adnomatosis in developing [[neoplasia]] and hyperfunctioning of [[islet of langerhan]]s.<ref>[http://omim.org/entry/131100] MULTIPLE ENDOCRINE NEOPLASIA, TYPE I; MEN1</ref> | ||
* In 1986 Brandi et al, suggested the humoral cause of primary hyperparathyroidism in familial MEN type 1. | * In 1986 Brandi et al, suggested the humoral cause of primary [[hyperparathyroidism]] in familial MEN 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. | ||
* 1988 the MEN1 locus was assigned to | * 1988 the MEN1 [[locus]] was assigned to [[chromosome]] 11 (11q13). | ||
* 1993 | * 1993 [[mutation]]s in the [[RET]] [[oncogene]] were shown to be the cause of MEN 2A by Lois Mulligan, working in the laboratory of Dr Bruce Ponder in Cambridge.<ref>Germ-line mutations of the RET proto-oncogene in multiple endocrine neoplasia type 2A. | ||
Mulligan LM, Kwok JB, Healey CS, Elsdon MJ, Eng C, Gardner E, Love DR, Mole SE, Moore JK, Papi L, et al. ''Nature'' 1993 Jun 3;363(6428) 458-60 PMID 8099202</ref> | Mulligan LM, Kwok JB, Healey CS, Elsdon MJ, Eng C, Gardner E, Love DR, Mole SE, Moore JK, Papi L, et al. ''Nature'' 1993 Jun 3;363(6428) 458-60 PMID 8099202</ref> | ||
* 1998 the MEN1 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> | * 1998 the MEN1 [[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> | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
[[Category:Hereditary cancers]] | |||
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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 a pituitary adenoma and three enlarged parathyroid glands.
Historical Perspective
- In 1903 Erdheim described the case of an acromegalic patient with a pituitary adenoma and three enlarged parathyroid glands.
- In 1953 Underdahl et al. reported a 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.
- 1968 Steiner et al. 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 et al, suggested the importance of primary genetic lesion in endocrine adnomatosis in developing neoplasia and hyperfunctioning of islet of langerhans.[1]
- In 1986 Brandi et al, suggested the humoral cause of primary hyperparathyroidism in familial MEN type 1.
- In 1986 Schimke suggested a 2 step model of pathogenesis which include germline mutation followed by somatic mutation later.
- 1988 the MEN1 locus was assigned to chromosome 11 (11q13).
- 1993 mutations in the RET oncogene were shown to be the cause of MEN 2A by Lois Mulligan, working in the laboratory of Dr Bruce Ponder in Cambridge.[2]
References
- ↑ [1] MULTIPLE ENDOCRINE NEOPLASIA, TYPE I; MEN1
- ↑ Germ-line mutations of the RET proto-oncogene in multiple endocrine neoplasia type 2A. Mulligan LM, Kwok JB, Healey CS, Elsdon MJ, Eng C, Gardner E, Love DR, Mole SE, Moore JK, Papi L, et al. Nature 1993 Jun 3;363(6428) 458-60 PMID 8099202
- ↑ 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