Multiple endocrine neoplasia type 1: New clinical and basic findings

Debra H. Schussheim, Monica C. Skarulis, Sunita K. Agarwal, William F. Simonds, A. Lee Burns, Allen M. Spiegel, Stephen J. Marx

Research output: Contribution to journalArticle

145 Citations (Scopus)

Abstract

Multiple endocrine neoplasia type 1 (MEN1) provides a prime example of how a rare disease can advance our understanding of basic cell biology, neoplasia and common endocrine tumors. MEN1 is expressed mainly as parathyroid, enteropancreatic neuroendocrine, anterior pituitary and foregut carcinoid tumors. It is an autosomal dominant disease caused by mutation of the MEN1 gene. Since its identification, the MEN1 gene has been implicated in many common endocrine and non-endocrine tumors. This is a brief overview of recent scientific advances relating to MEN1, including newly recognized clinical features that are now better characterized by genetic analysis, insights into the function of the MEN1-encoded protein menin, and refined recommendations for mutation testing and tumor screening, which highlight our increasing understanding of this complex syndrome.

Original languageEnglish (US)
Pages (from-to)173-178
Number of pages6
JournalTrends in Endocrinology and Metabolism
Volume12
Issue number4
StatePublished - 2001
Externally publishedYes

Fingerprint

Multiple Endocrine Neoplasia Type 1
Neoplasms
Mutation
Carcinoid Tumor
Rare Diseases
Genes
Cell Biology
Proteins

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Schussheim, D. H., Skarulis, M. C., Agarwal, S. K., Simonds, W. F., Burns, A. L., Spiegel, A. M., & Marx, S. J. (2001). Multiple endocrine neoplasia type 1: New clinical and basic findings. Trends in Endocrinology and Metabolism, 12(4), 173-178.

Multiple endocrine neoplasia type 1 : New clinical and basic findings. / Schussheim, Debra H.; Skarulis, Monica C.; Agarwal, Sunita K.; Simonds, William F.; Burns, A. Lee; Spiegel, Allen M.; Marx, Stephen J.

In: Trends in Endocrinology and Metabolism, Vol. 12, No. 4, 2001, p. 173-178.

Research output: Contribution to journalArticle

Schussheim, DH, Skarulis, MC, Agarwal, SK, Simonds, WF, Burns, AL, Spiegel, AM & Marx, SJ 2001, 'Multiple endocrine neoplasia type 1: New clinical and basic findings', Trends in Endocrinology and Metabolism, vol. 12, no. 4, pp. 173-178.
Schussheim DH, Skarulis MC, Agarwal SK, Simonds WF, Burns AL, Spiegel AM et al. Multiple endocrine neoplasia type 1: New clinical and basic findings. Trends in Endocrinology and Metabolism. 2001;12(4):173-178.
Schussheim, Debra H. ; Skarulis, Monica C. ; Agarwal, Sunita K. ; Simonds, William F. ; Burns, A. Lee ; Spiegel, Allen M. ; Marx, Stephen J. / Multiple endocrine neoplasia type 1 : New clinical and basic findings. In: Trends in Endocrinology and Metabolism. 2001 ; Vol. 12, No. 4. pp. 173-178.
@article{4c180145e2b049c2a679e6776c5207d8,
title = "Multiple endocrine neoplasia type 1: New clinical and basic findings",
abstract = "Multiple endocrine neoplasia type 1 (MEN1) provides a prime example of how a rare disease can advance our understanding of basic cell biology, neoplasia and common endocrine tumors. MEN1 is expressed mainly as parathyroid, enteropancreatic neuroendocrine, anterior pituitary and foregut carcinoid tumors. It is an autosomal dominant disease caused by mutation of the MEN1 gene. Since its identification, the MEN1 gene has been implicated in many common endocrine and non-endocrine tumors. This is a brief overview of recent scientific advances relating to MEN1, including newly recognized clinical features that are now better characterized by genetic analysis, insights into the function of the MEN1-encoded protein menin, and refined recommendations for mutation testing and tumor screening, which highlight our increasing understanding of this complex syndrome.",
author = "Schussheim, {Debra H.} and Skarulis, {Monica C.} and Agarwal, {Sunita K.} and Simonds, {William F.} and Burns, {A. Lee} and Spiegel, {Allen M.} and Marx, {Stephen J.}",
year = "2001",
language = "English (US)",
volume = "12",
pages = "173--178",
journal = "Trends in Endocrinology and Metabolism",
issn = "1043-2760",
publisher = "Elsevier Inc.",
number = "4",

}

TY - JOUR

T1 - Multiple endocrine neoplasia type 1

T2 - New clinical and basic findings

AU - Schussheim, Debra H.

AU - Skarulis, Monica C.

AU - Agarwal, Sunita K.

AU - Simonds, William F.

AU - Burns, A. Lee

AU - Spiegel, Allen M.

AU - Marx, Stephen J.

PY - 2001

Y1 - 2001

N2 - Multiple endocrine neoplasia type 1 (MEN1) provides a prime example of how a rare disease can advance our understanding of basic cell biology, neoplasia and common endocrine tumors. MEN1 is expressed mainly as parathyroid, enteropancreatic neuroendocrine, anterior pituitary and foregut carcinoid tumors. It is an autosomal dominant disease caused by mutation of the MEN1 gene. Since its identification, the MEN1 gene has been implicated in many common endocrine and non-endocrine tumors. This is a brief overview of recent scientific advances relating to MEN1, including newly recognized clinical features that are now better characterized by genetic analysis, insights into the function of the MEN1-encoded protein menin, and refined recommendations for mutation testing and tumor screening, which highlight our increasing understanding of this complex syndrome.

AB - Multiple endocrine neoplasia type 1 (MEN1) provides a prime example of how a rare disease can advance our understanding of basic cell biology, neoplasia and common endocrine tumors. MEN1 is expressed mainly as parathyroid, enteropancreatic neuroendocrine, anterior pituitary and foregut carcinoid tumors. It is an autosomal dominant disease caused by mutation of the MEN1 gene. Since its identification, the MEN1 gene has been implicated in many common endocrine and non-endocrine tumors. This is a brief overview of recent scientific advances relating to MEN1, including newly recognized clinical features that are now better characterized by genetic analysis, insights into the function of the MEN1-encoded protein menin, and refined recommendations for mutation testing and tumor screening, which highlight our increasing understanding of this complex syndrome.

UR - http://www.scopus.com/inward/record.url?scp=0035347317&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035347317&partnerID=8YFLogxK

M3 - Article

C2 - 11295574

AN - SCOPUS:0035347317

VL - 12

SP - 173

EP - 178

JO - Trends in Endocrinology and Metabolism

JF - Trends in Endocrinology and Metabolism

SN - 1043-2760

IS - 4

ER -