scholarly journals Germline Mutation of the Multiple Endocrine Neoplasia Type 1(MEN1) Gene in a Family with Primary Hyperparathyroidism.

1998 ◽  
Vol 45 (6) ◽  
pp. 719-723 ◽  
Author(s):  
HIDEMI OHYE ◽  
MAKOTO SATO ◽  
SHUJI MATSUBARA ◽  
AKIRA MIYAUCHI ◽  
HITOMI IMACHI ◽  
...  
Keyword(s):  
Primary Hyperparathyroidism ◽  
Germline Mutation ◽  
Multiple Endocrine Neoplasia ◽  
Multiple Endocrine Neoplasia Type ◽  
Men1 Gene ◽  
Endocrine Neoplasia ◽  
Endocrine Neoplasia Type

scholarly journals A Novel Germline Mutation of Multiple Endocrine Neoplasia Type 1 (MEN1) Gene in a Japanese MEN1 Patient and Her Daughter.

1999 ◽  
Vol 46 (2) ◽  
pp. 325-329 ◽  
Author(s):  
HIDEMI OHYE ◽  
MAKOTO SATO ◽  
SHUJI MATSUBARA ◽  
AKIRA MIYAUCHI ◽  
KEIKO KISHI-IMAI ◽  
...  
Keyword(s):  
Germline Mutation ◽  
Multiple Endocrine Neoplasia ◽  
Multiple Endocrine Neoplasia Type ◽  
Men1 Gene ◽  
Endocrine Neoplasia ◽  
Endocrine Neoplasia Type

scholarly journals No Evidence of Germline Mutation or Somatic Deletion of the MEN1 Gene in a Case of Familial Multiple Endocrine Neoplasia Type 1(MEN1).

1999 ◽  
Vol 46 (6) ◽  
pp. 811-816 ◽  
Author(s):  
HIROYOSHI NAMIHIRA ◽  
MAKOTO SATO ◽  
SHUJI MATSUBARA ◽  
HIDEMI OHYE ◽  
MMR BHUIYAN ◽  
...  
Keyword(s):  
Germline Mutation ◽  
Multiple Endocrine Neoplasia ◽  
Multiple Endocrine Neoplasia Type ◽  
Men1 Gene ◽  
Endocrine Neoplasia ◽  
Endocrine Neoplasia Type

scholarly journals Role of miR-24 in Multiple Endocrine Neoplasia Type 1: A Potential Target for Molecular Therapy

2021 ◽  
Vol 22 (14) ◽  
pp. 7352
Author(s):  
Francesca Marini ◽  
Maria Luisa Brandi
Keyword(s):  
Multiple Endocrine Neoplasia ◽  
Multiple Endocrine Neoplasia Type ◽  
Current Knowledge ◽  
Neuroendocrine Cells ◽  
Molecular Therapy ◽  
Multiple Cancer ◽  
Men1 Gene ◽  
Endocrine Neoplasia ◽  
Endocrine Neoplasia Type

Multiple endocrine neoplasia type 1 (MEN1) is a rare autosomal dominant inherited multiple cancer syndrome of neuroendocrine tissues. Tumors are caused by an inherited germinal heterozygote inactivating mutation of the MEN1 tumor suppressor gene, followed by a somatic loss of heterozygosity (LOH) of the MEN1 gene in target neuroendocrine cells, mainly at parathyroids, pancreas islets, and anterior pituitary. Over 1,500 different germline and somatic mutations of the MEN1 gene have been identified, but the syndrome is completely missing a direct genotype-phenotype correlation, thus supporting the hypothesis that exogenous and endogenous factors, other than MEN1 specific mutation, are involved in MEN1 tumorigenesis and definition of individual clinical phenotype. Epigenetic factors, such as microRNAs (miRNAs), are strongly suspected to have a role in MEN1 tumor initiation and development. Recently, a direct autoregulatory network between miR-24, MEN1 mRNA, and menin was demonstrated in parathyroids and endocrine pancreas, showing a miR-24-induced silencing of menin expression that could have a key role in initiation of tumors in MEN1-target neuroendocrine cells. Here, we review the current knowledge on the post-transcriptional regulation of MEN1 and menin expression by miR-24, and its possible direct role in MEN1 syndrome, describing the possibility and the potential approaches to target and silence this miRNA, to permit the correct expression of the wild type menin, and thereby prevent the development of cancers in the target tissues.

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