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Our observations exclude MLK-3 as the MEN1 gene. Paper-1050290.
We can now exclude PLCB3 from candidacy as the MEN1 gene. Paper-866128.
These studies exclude FKBP2 as a candidate gene for MEN1. Paper-196581.
Mutations of the MEN1 and Mody (2/3) genes were ruled out. Paper-12335343.
This gene locus, INT2, was found to be closely linked to the MEN1 gene. Paper-6461443.
Consequently, the HNP36 gene was studied as a candidate for the MEN1 gene. Paper-1116669.
A germline mutation was found in the APC gene but not in the MEN1 gene. Paper-9349635.
Exclusion of FAU as the multiple endocrine neoplasia type 1 ( MEN1) gene. Paper-7587788.
Thus, our results indicate that ZFM1 is excluded as a candidate gene for MEN1. Paper-1014640.
We conclude that FAU is not likely to be the MEN1 tumour suppressor gene. Paper-7587788.
These data suggest that ZFM1 might be a candidate for mutations that cause MEN1. Paper-124515.
These results indicate that menin is required for TGF-beta action in the parathyroid. Paper-10378122.
A carrier of both MEN1 and BRCA2 mutations: case report and review of the literature. Paper-12619703.
Interaction of MLL amino terminal sequences with menin is required for transformation. Paper-13366393.
Functional interaction between tumor suppressor menin and activator of S-phase kinase. Paper-10611402.
Type B1 thymoma in multiple endocrine neoplasia type 1 ( MEN-1) syndrome. Paper-9086006.
As an additional menin target, analysis of the p18 ( CDKN2C) gene was included. Paper-13396843.
Cdx4 and menin co-regulate hoxa9 expression in hematopoietic cells. Paper-12363288.
Menin links estrogen receptor activation to histone H3K4 trimethylation. Paper-11843832.
We found detectable bFGF ranging from 0.24-1.28 ng/mL in 21 of 50 subjects with MEN1. Paper-7587406.
Menin associates with FANCD2, a protein involved in repair of DNA damage. Paper-9772362.
Over expressing active CHK1 (1-365) increased chromatin- bound menin, similar to UV. Paper-12003043.
Myasthenia gravis and thymoma in multiple endocrine neoplasia ( MEN-1) syndrome. Paper-6506446.
Fine mapping of the MLK-3 gene within 11q13 and its exclusion as the MEN1 susceptibility gene. Paper-1050290.
Phosphorylated p65 levels negatively correlated with menin expression (r(2) = 0.42, P = 0.05). Paper-11009152.
Menin interacts with IQGAP1 to enhance intercellular adhesion of beta-cells. Paper-13622826.
The expression profile of p16, APC and MENIN was investigated by immunohistochemistry. Paper-13162565.
We conclude that the altered MEN1 gene function is of importance in the development of FIHP. Paper-9221315.
In the tumor DNA, we found the loss of one allele with PYGM, the closest probe to the MEN-1 locus. Paper-95777.
In vitro and in vivo activity of analogues of the kinin B2 receptor antagonist MEN1 1270. Paper-9569137.
Menin critically links MLL proteins with LEDGF on cancer-associated target genes. Paper-12868921.
The MEN1 gene product interacts with glial fibrillary acidic protein ( GFAP) in the brain. Paper-9827142.
The commonest tumors secrete PTH or gastrin in MEN1, and calcitonin or catecholamines in MEN2. Paper-9104004.
MEN1 status was assessed clinically and by polymerase chain reaction-based mutational analysis. Paper-10793398.
Chromogranin A expression in hepatocellular carcinoma in a patient with germline MEN1 gene mutation. Paper-2111694.
Menin regulates the function of hematopoietic stem cells and lymphoid progenitors. Paper-13623161.
Indeed, MEN1 is altered in about 25% of nonfamilial PETs, although no mutations have been found in VHL. Paper-8942844.
The assessment of calcium, gastrin, and prolactin is sufficient for biochemical screening in MEN-1. Paper-13762367.
Expression of HIF-1alpha and CA9 was not found in islets of controls and in MEN1 microadenomas. Paper-13734457.
The phospholipase C beta 3 gene located in the MEN1 region shows loss of expression in endocrine tumours. Paper-8186041.
Knockdown of menin reduces both activated TFF1 ( pS2) transcription and H3K4 trimethylation. Paper-11843832.
Linkage was clearly excluded between FIHP and the MEN1 and MEN2A loci as well as to the PTH gene. Paper-7591668.
Menin represses JunD- activated transcription by a histone deacetylase-dependent mechanism. Paper-8277138.
These responses to TGF-beta were lost when menin was specifically inactivated by antisense oligonucleotides. Paper-10378122.
Menin localizes to chromatin through an ATR- CHK1 mediated pathway after UV-induced DNA damage. Paper-12003043.
Contrastingly, inhibition of menin expression with Men1 siRNA decreases TCF reporter gene activity. Paper-13508090.
Menin interacts with histone H3 methyltransferases such as MLL (mixed lineage leukemia) protein. Paper-13507205.
Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription. Paper-1754758.
The majority of pituitary adenomas associated with MEN 1 secrete prolactin or growth hormone. Paper-7969338.
Inactivation of menin, a Smad3-interacting protein, blocks transforming growth factor type beta signaling. Paper-8672367.
The FAU gene properties, together with its chromosomal localisation on 11q13, make it a candidate gene for MEN1. Paper-7587788.
Competitive PCR was performed with the housekeeping gene PGK-1 to quantitate menin gene expression. Paper-1571287.
Menin suppresses osteoblast differentiation by antagonizing the AP-1 factor, JunD. Paper-10800451.
We previously reported a basic fibroblast growth factor (bFGF)-like substance in the plasma of subjects with MEN1. Paper-7587406.
Menin, a product of the MEN1 tumor suppressor gene, is also a component of the 1-MDa MLL complex. Paper-10326736.
These results make it very unlikely that the NF-kappa B3 gene is the gene responsible for the development of MEN 1. Paper-1044424.
We observed a previously undescribed multicentric glucagon- producing tumor disease that is not related to MEN1. Paper-13566449.
Seven of 8 MEN1 subjects with untreated pituitary tumors had detectable plasma bFGF-like immunoreactivity. Paper-7587406.
Our data indicate that menin is involved in the activation of S-phase arrest in response to ionizing radiation. Paper-12206281.
Moreover, TGF-beta did not affect the proliferation and PTH production of parathyroid cells from a Men1 patient. Paper-10378122.
Together, these results suggest that menin plays a critical role in repair of DNA damage in concert with FANCD2. Paper-9772362.
We found by immunohistochemistry that somatostatin receptor-positive cells (SSTR2A) express menin. Paper-13029000.
Hepatocellular carcinoma ( HCC) was found in a patient with multiple endocrine neoplasia type 1 ( MEN 1). Paper-2111694.
This tumor represents a novel, non-endocrine MEN1-phenotype, compatible with a role of MEN1- GFAP in glial oncogenesis. Paper-9827142.
Cells express several neuroendocrine markers such as CGRP, MAP-2, Ash1, CgrA, Scg2. Paper-10842250.
Parathyroid gastrin and parathormone- producing tumour in the Zollinger-Ellison syndrome of MEN 1 origin. Paper-7005452.
In vitro studies have shown menin binding to JunD, Pem, Smad3, NF-kappaB, nm23H1, and RPA2 proteins. Paper-11448161.
Oncogenic mutant forms of MLL retain an ability to interact with menin but not other identified complex components. Paper-10326736.
Constitutively active CHK1 (1-365) transfection increased chromatin- bound menin, mimicking UV irradiation. Paper-12003043.
Basic fibroblast growth factor ( BFGF) is elevated in many patients with MEN 1 and may play a pathogenetic role. Paper-8300351.
Patients with MEN 1 (n = 43) were monitored (mean, 6.3 years) with annual biochemical and radiologic adrenal evaluation. Paper-422505.
We conclude that pituitary tumor is a possible source of high circulating bFGF immunoreactivity in MEN1 plasma. Paper-7587406.
The expressions of RPL10 and NEUROD1 were prominent in the MEN1 human and heterozygous mouse exocrine pancreas. Paper-13681365.
Effect of treatment with depot somatostatin analogue octreotide on primary hyperparathyroidism in MEN1 patients. Paper-13074908.
Transcripts that map to the MEN1 interval PYGM-D11S449 include SGC35223, IB1256, AA147620, ZFM1, FAU, and CAPN1. Paper-1116680.
Three different regions of loss, one near MEN1, the second near D11S913, and the third near INT2 locus were observed. Paper-9529413.
Familial adenomatous polyposis associated with sporadic MEN 1 and thyroid carcinoma related to APC mutation. Paper-9698893.
Mapping studies of the gene encoding mu-calpain ( CAPN1) located CAPN1 to 11q13 and in the vicinity of the MEN1 locus. Paper-554893.
The data suggest menin localization to chromatin after UV irradiation is the result of an ATR- CHK1 dependent pathway. Paper-12003043.
RESULTS: Tumors and MEN1 nontumorous endocrine cells showed a prominent cytoplasmatic NEUROG3 and NEUROD1 expression. Paper-13681365.
A heterozygous deletion of 1 bp of the MEN1 gene in exon 10 (1785delA) was found in affected members of family 1. Paper-9205209.
Northern blot analysis of 13 SCLC cell lines showed the MEN1 transcript to be present and of normal size. Paper-2199253.
Menin associates with a trithorax family histone methyltransferase complex and with the hoxc8 locus. Paper-10204885.
Allelic deletion of the MEN1 gene in duodenal gastrin and somatostatin cell neoplasms and their precursor lesions. Paper-13191569.
Identification of plasminogen activator inhibitor-2 as a gastrin-regulated gene: Role of Rho GTPase and menin. Paper-9505601.
In contrast, RAR-beta2 expression is intact in MEFs devoid of menin, a component of MLL1 and MLL2 H3K4MT complexes. Paper-12277296.
Thirteen patients with MEN1 (4.6%) showed 41 insulinomas and 133 tumors expressing islet hormones other than insulin. Paper-13632986.
Endogenous menin is colocalized with GFAP and vimentin in glioma cells as determined by confocal microscopy. Paper-9531129.
Establishment of human fibroma cell lines from a MEN1 patient by introduction of either hTERT or SV40 early region. Paper-10803342.
OBJECTIVE: The aim of the study was to investigate cases of MEN1 or related states for germline mutations in all CDKI genes. Paper-13756785.
The deletion was approximately 68kbp flanked by a 3-base pair repeat and included the whole MEN1, MAP4K2 and KAPPA-200 genes. Paper-10270421.
Here we report that menin functions as a transcriptional repressor through interaction with the transcription factor JunD. Paper-8277138.
Multiple endocrine neoplasia type 1 ( MEN1), a human familial tumor syndrome, results from mutations in the Men1 gene. Paper-13122901.
Both wild-type MLL and MLL fusion proteins interact with the tumor suppressor menin and with the Hoxa9 locus in vivo. Paper-13366393.
During the course of cloning SIPA-1, the MEN1 gene was identified, thus excluding human SIPA-1 as a candidate for this disease. Paper-1526085.
Mutations of the p53 gene were found in two lines (SNU-80 and SNU-373), but no mutations in the RET or MEN1 genes were observed. Paper-12432722.
The expression increased as cells entered into S phase, indicating cell cycle-associated transcriptional regulation of the MEN1 gene. Paper-8388258.
Ten transcripts were identified by cDNA selection of a focused 300-kb genomic region telomeric to the MEN1 consensus region. Paper-1116680.
Exclusion of the nuclear factor-kappa B3 ( REL A) gene as candidate for the multiple endocrine neoplasia type 1 ( MEN 1) gene. Paper-1044424.
One exception is the developmentally programmed transcription factor, HLXB9, which is overexpressed in islets in the absence of menin. Paper-12027314.
Menin can interact directly with the vitamin D receptor ( VDR) and enhance the transcriptional activity of VDR. Paper-14029332.
Rapid Mutation Screening for HRPT2 and MEN1 Mutations Associated with Familial and Sporadic Primary Hyperparathyroidism. Paper-12289513.
RESULTS: Fourteen patients (5%) without evidence of MEN1 showed 53 macrotumors and 285 microtumors expressing exclusively insulin. Paper-13632986.
The menin- RPA2 interaction was confirmed in a conventional yeast two-hybrid system and by direct interaction between purified proteins. Paper-9684472.
In summary, we report a case of FIHP associated with a new intronic heterozygous germline mutation (IVS9 + 1 G>A) of MEN1 gene. Paper-10514117.
Menin represses p65-mediated transcriptional activation on NF-kappaB sites in a dose-dependent and specific manner. Paper-8854893.
CONCLUSIONS: Our results support the previous finding that germline CDKN1B/p27(Kip1) mutations predispose to a human MEN1-like condition. Paper-13377929.
Multiple endocrine neoplasia type 1 ( MEN1) is tightly linked to the muscle-type glycogen phosphorylase ( PYGM) gene in 11q13. Paper-1209161.
Studies of known TSG at these loci, including the menin gene and RB1, would suggest a limited role, if any, in pituitary tumors. Paper-8373499.
Results of this study suggest that a candidate tumor-suppressor gene, not the MEN1 gene, maps between D11S4907 and GSTP1 in NPC. Paper-9416098.
We studied the MEN1 gene in a kindred where three patients (the proposita and two of her sons) were affected with hyperparathyroidism. Paper-1731030.
It is unclear whether FIHP corresponds to a different genetic entity or a variant of MEN1 (or hyperparathyroidism-jaw tumor syndrome). Paper-10514117.
CONCLUSIONS: FIHP is a genetically heterogeneous disease with a subset linked to MEN1, most likely representing a variant of MEN1. Paper-2147993.
Inactivation of the RIZ1 gene may cause parathyroid tumorigenesis via a mechanism in which genetic alteration of the MEN1 gene is redundant. Paper-10065442.
Genetic interaction studies showed that neither overexpression nor loss of MEN1 modified the ICL sensitivity of FANCD2 mutants. Paper-12747225.
We report here a sibship with three premenopausal breast cancers and hyperparathyroidism, and no detectable BRCA or MEN1 gene mutations. Paper-13076081.
The MEN1 gene encodes a putative growth-suppressor protein, menin, binding JunD, a transcriptional factor belonging to the AP-1 complex. Paper-8425724.
Clinical and biochemical characteristics of HPT were apparently unrelated to the presence or absence of LOH and the MEN1 gene mutations. Paper-1529508.
Together, these results define a novel menin- IQGAP1 pathway that controls cell migration and cell-cell adhesion in endocrine cells. Paper-13622826.
MAIN OUTCOME MEASURES: We analyzed germline CDKN1B/p27(Kip1) mutations in individuals with pituitary adenoma and MEN1-like features. Paper-13377929.
Isolated familial somatotropinomas (IFS) rarely occurs in the absence of multiple endocrine neoplasia type I ( MEN1) or the Carney complex. Paper-9624915.
Four of the marker systems are on the centromeric side of MEN1, and four on the telomeric side, based on meiotic crossovers. Paper-56681.
CONCLUSION: These results suggest a functional link among Cdx4, menin and histone modifications in Hoxa9 regulation in hematopoietic cells. Paper-12363288.
The NF-kappaB proteins p50, p52 and p65 were found to interact specifically and directly with menin in vitro and in vivo. Paper-8854893.
Its protein product, called menin, has been shown to associate with the AP1 transcription factor JunD and to repress JunD-mediated transcription. Paper-9531129.
In contrast, there was greater expression of VMAT 1 in VHL than MEN 2 tumours, while expression of VMAT 2 did not differ significantly. Paper-11146407.
Four small families with a family history of hyperparathyroidism without clear- cut MEN-1 features were screened for a MEN1 mutation. Paper-9169001.
BACKGROUND: Transcription factor Cdx4 and transcriptional coregulator menin are essential for Hoxa9 expression and normal hematopoiesis. Paper-12363288.
In cancer cell lines and in normal cells, the siRNA-based inhibition of MEN1 does not lead to the up-regulation of hTERT mRNA expression. Paper-12933722.
Mutations in the MEN1 gene were sought using polymerase chain reaction analysis on paraffin embedded tissue from two members of one of the families. Paper-8843469.
Using a yeast two-hybrid screen with menin as the bait, we have identified the transcription factor JunD as a direct menin-interacting partner. Paper-1754758.
The identification of compounds that could restore H3K4me3 on menin target genes would provide new therapeutic strategies for MEN1 patients. Paper-13838782.
In these cells, overexpression of menin significantly enhances TCF gene assay reporter activity in response to beta-catenin activation. Paper-13508090.
We have now extended our mutation analysis to 34 more unrelated FMEN1 probands and to two related states, sporadic MEN1 and familial hyperparathyroidism. Paper-1113987.
In SCLC, loss of heterozygosity ( LOH) at the MEN1 gene on chromosome band 11q13 was detected in one primary tumor and two cell lines. Paper-2199253.
Thus, LEDGF critically associates with MLL and menin at the nexus of transcriptional pathways that are recurrently targeted in diverse diseases. Paper-12868921.
OBJECTIVE: Our objective was to characterize the clinical and genealogical features of non- MEN1/ CNC familial isolated pituitary adenomas (FIPA). Paper-12216292.
This region of RPA2 contains a weak single-stranded DNA-binding domain, but menin had no detectable effect on RPA-DNA binding in vitro. Paper-9684472.
Moreover, Men1 ablation in cells reduces acetylation of histones H3 and H4 at the 5'-UTR of the caspase 8 locus bound by menin in vivo. Paper-12527902.
These data indicate that menin through binding to NMHC II-A could participate in cell division and in other processes that involve NMHC II-A. Paper-10010042.
Of these MEN 1 patients, we used 28 individuals, diagnosed with HP at our hospitals, to study the clinical aspects of MEN 1- associated HP. Paper-8597806.
Here we demonstrate that menin interacts with a putative tumor metastasis suppressor nm23H1/nucleoside diphosphate (NDP) kinase A in mammalian cells. Paper-9171840.
Conclusion: Our results suggest that mutations in the CDKN1B and AIP genes are relatively uncommon in MEN1 mutation-negative MEN1 syndrome patients. Paper-13532979.
CONCLUSION: We conclude that CDK4 and c-Myc is generally expressed in benign and malignant PETs, and regardless of MEN1 mutational status. Paper-12486047.
METHODS: DNA sequences analyses were performed of the MEN1 gene and codons Arg201 and Gln227 of the GNAS1 gene, using leucocyte and endocrine tissue DNA. Paper-13230397.
Messenger RNA levels of VDR target genes CYP24 and KLK6 were significantly lower in MEN1 parathyroid adenomas compared to normal tissue. Paper-14029332.
Isolation and characterization of a novel gene encoding nuclear protein at a locus ( D11S636) tightly linked to multiple endocrine neoplasia type 1 ( MEN1). Paper-124515.
We show that Menin inhibits ERK-dependent phosphorylation and activation of both JunD and the Ets-domain transcription factor Elk-1. Paper-9550828.
Menin, the multiple endocrine neoplasia type 1 gene product, exhibits GTP-hydrolyzing activity in the presence of the tumor metastasis suppressor nm23. Paper-9171840.
A putative human zinc-finger gene ( ZFPL1) on 11q13, highly conserved in the mouse and expressed in exocrine pancreas. The European Consortium on MEN 1. Paper-1561918.
Here, we show that MLL sequences between amino acids 5 and 44 are required for interaction with menin and for the transformation of hematopoietic progenitors. Paper-13366393.
The Gs alpha subunit, GHRH receptor, and MEN1 genes were intact, and tumor tissue abundantly expressed pituitary tumor transforming gene ( PTTG). Paper-8385699.
Chromatin immunoprecipitation experiments reveal that binding of menin to the Hoxc8 locus is not affected by phosphorylation on Ser(543) or Ser(583). Paper-12279319.
Multiple endocrine neoplasia type 1 ( MEN1) associates primary hyperparathyroidism, lesions of the endocrine pancreas and pituitary adenomas. Paper-38794.
We have identified a germ-line nonsense mutation in the human CDKN1B gene in a MEN1 mutation-negative patient presenting with pituitary and parathyroid tumors. Paper-12277335.
Moreover menin was seen to colocalize with this myosin isoform in the cleavage furrow of dividing cells by indirect immunofluoresence. Paper-10010042.
CONTEXT: Familial pituitary adenomas occur rarely in the absence of multiple endocrine neoplasia type 1 ( MEN1) and Carney complex ( CNC). Paper-12216292.
A rat strain with multiple endocrine tumours, a phenotypic overlap of both MEN1 and MEN2, has been reported to have a homozygous germline p27 ( CDKN1B) mutation. Paper-13532979.
Although subtle mutations in menin NLSs do not affect menin association with chromatin, they abolish menin binding to the IGFBP-2 promoter in vivo. Paper-12038814.
In contrast to the supF results, both MEN1 and FANCD2 mutants were hypermutable using a different assay based on the lats tumor suppressor gene. Paper-12747225.
CONCLUSIONS: Expression of p15, p18 and p27 was not generally related to the MEN1 gene mutational status of the investigated 18 PETs. Paper-12694143.
Aberrant expression of menin target genes in tumours in MEN1 patients suggests that loss of writing of the H3K4me3 mark contributes to MEN1 tumourigenesis. Paper-13838782.
Alanine scanning mutagenesis of residues 30-55 revealed two different amino acids, P41 and P44, of mouse JunD that were critical for interaction with menin. Paper-8629372.
Ablation of menin abrogates Cdx4 access to the chromatin target and significantly reduces both active and repressive histone H3 modifications in the Hoxa9 locus. Paper-12363288.
The hereditary forms are associated with multiple endocrine neoplasia type 1 ( MEN-1), von Hippel-Lindau syndrome, neurofibromatosis, and tuberous sclerosis. Paper-10445116.
Thus, this study identifies a new, critical player in leukemias caused by MLL fusion proteins and defines the biochemical function of menin in the MLL complex. Paper-12868916.
Our localization of the human protooncogene SEA between PYGM and INT2, two markers that flank MEN-1, suggests SEA as a potential candidate for the MEN-1 locus. Paper-47139.
Mammalian menin protein is associated with chromatin modifying complexes and has been shown to bind a number of nuclear proteins, including the transcription factor JunD. Paper-12242313.
Surgery may be undertaken in ZES- MEN-1 patients with focal lesions visualized by radiology or PTP in order to minimize the risk of malignant development in a gross tumor. Paper-6955400.
We found that Drosophila larval tissue and mouse embryonic fibroblasts mutant for the MEN1 homologue were deficient for a DNA damage- activated S-phase checkpoint. Paper-12206281.
One of these cDNAs encodes ZFM1, a protein previously identified at the locus linked to multiple endocrine neoplasia type 1 ( MEN1) and as presplicing factor SF1. Paper-1372157.
This study describes the development and validation of rapid scanning for mutations in two tumor suppressor genes linked to familial hyperparathyroidism- MEN1 and HRPT2. Paper-12289513.
Menin, a nuclear protein encoded by the tumor suppressor gene MEN1, interacts with the AP-1 transcription factor JunD and inhibits its transcriptional activity. Paper-9550828.
The MEN1 gene encodes menin, a nuclear protein interacting with JunD/ AP1, Smad3, NFkappaB, and other proteins involved in transcription and cell growth regulation. Paper-9507940.
However, menin does not specifically associate with telomeres in somatic cells, as indicated by lack of co-localization with the known telomeric protein TRF2. Paper-9567346.
This strategy has resulted in the isolation and identification of nonmuscle myosin type II-A heavy chain ( NMHC II-A) as a menin interacting protein. Paper-10010042.
Transforming growth factor beta (TGFbeta) reduced cyclin D1 levels in the majority of tumors, this effect being not influenced by CaSR activation and menin expression levels. Paper-13384688.
CONCLUSIONS: Homogeneous and heterogeneous expression of prolactinomas, somatotropinomas, NS, and Cushing's disease can occur within families in the absence of MEN1/ CNC. Paper-12216292.
METHODS: Seven FIHP families were ascertained and venous blood samples obtained from 35 members (17 affected and 18 unaffected) for DNA sequence analysis of the MEN1 gene. Paper-9692557.
CONCLUSION: Rare germline mutation in any among four ( p15, p18, p21, and p27) of the seven CDKIs is a probable cause of MEN1 or of some related states. Paper-13756785.
LOH analysis was performed by fluorescence in situ hybridisation (FISH), using probes containing the MEN1 gene locus and the centromere 11 ( C11) region. Paper-13191569.
No significant differences of CDK4 expression were observed between the groups of benign and malignant PETs or between tumors with or without MEN1 gene mutations. Paper-12486047.
A novel genetic mutation involving a CGG to CGT alteration in codon 219 of the MEN1 gene was discovered; to our knowledge, this particular variation has not been reported previously. Paper-11549654.
CONCLUSIONS: A gene array showed PAI-2 to be a novel gastrin-regulated gene, stimulated in part through CREB and AP-1 and inhibited by the tumor suppressor menin. Paper-9505601.
CONCLUSIONS: Subtotal and total PTx result in durable control of MEN1- associated hyperparathyroidism and have longer recurrence-free intervals compared with lesser resection. Paper-10065434.
We have pursued studies to facilitate identification of the MEN1 gene by narrowing this critical region to a 900-kb interval between the VRF and D11S1783 loci through melotic mapping. Paper-1207871.
In the present study, we extend the analysis of human NE lung tumors to include 9 primary SCLCs, 36 SCLC cell lines, and 13 primary LCNECs for MEN1 gene inactivation. Paper-2199253.
Early diagnosis of pancreatic endocrine tumours in MEN-1 is enhanced by the use of a standardized meal stimulation test with measurements of serum PP and gastrin response. Paper-1509246.
Moreover, TGF-beta does not affect the proliferation and PTH production of parathyroid cells from multiple endocrine neoplasia type 1 ( MEN1) patients. Paper-10767346.
Additionally, LOH in 1 or both small-cell carcinomas was detected at 3p, 4q31.2-qter, 8p21-24, 11q13 ( MEN-1 locus), 11q23.3, 11q24.1-25, 16q24.1 ( H-cadherin locus), and 17q25. Paper-8853272.
We show that phaeochromocytomas from MEN 2 patients express substantially more CGA than tumours from VHL patients at both the mRNA (3-fold greater) and protein (20-fold) level. Paper-12641805.
The findings support variable calcium insensitivity of [Ca2+]i and PTH release in hyperparathyroidism of MEN 1, apparently coupled to heterogeneously reduced CAS expression. Paper-424235.
The objective of this study was to evaluate the possible contribution of CDKN1B and AIP germline mutations in a cohort of MEN1 mutation-negative MEN1 syndrome patients. Paper-13532979.
These findings indicate that MEN1 gene mutations contributed to tumorigenesis of the right upper parathyroid gland in this case of phosphate- induced tertiary hyperparathyroidism. Paper-9091933.
The MEN1 locus is tightly linked to the marker PYGM on chromosome 11q13, and linkage analysis has placed the MEN1 gene within a 2-Mb interval flanked by D11S1883 and D11S449. Paper-1116681.
Global expression profiling of sex cord stromal tumors from Men1 heterozygous mice identifies altered TGF-beta signaling, decreased Gata6 and increased Csf1r expression. Paper-13555718.
The lats assay showed that FANCD2 mutants had a high frequency of large deletions, which the supF assay was not able to detect, while large deletions were rare in MEN1 mutants. Paper-12747225.
While urolithiasis was a cardinal clinical manifestation of MEN-1, there was otherwise considerable phenotypic polymorphism, even among patients bearing the same MEN1 gene mutation. Paper-11055794.
Primary hyperparathyroidism is usually expressed at an early age and is highly penetrated in MEN type 1 ( MEN1), suggesting that some FHP may be a variant type or early stage of MEN1. Paper-1944627.
These studies link the menin tumor suppressor protein with the MLL histone methyltransferase machinery, with implications for Hox gene expression in development and leukemia pathogenesis. Paper-10326736.
The nearest proximal and distal markers that show recombination with the disease are D11S822 and GSTP1, respectively, thereby narrowing the candidate region for MEN1 by 50% on the distal side. Paper-379840.
The East African Indian and Beijing spoligotypes were concordant with SCG-1 and SCG-2, respectively; X and Central Asian spoligotypes were also associated with one SCG or subgroup combination. Paper-10817092.
Familial acromegaly may occur as an isolated pituitary disorder or as a feature of hereditary syndromes, such as multiple endocrine neoplasia type 1 ( MEN1) or the Carney complex. Paper-8676519.
Further analysis of radiation-reduced hybrid DNAs and chromosome 11-specific YAC clones established that the HNP36 gene is within 80 kb of D11S913, a marker tightly linked to the MEN1 gene. Paper-1116669.
The hypergastrinemic patients ( MEN-1, pernicious anemia) had elevated plasma Gamide but unaltered CTFP demonstrating differential secretion of these 2 progastrin-derived peptides. Paper-12313994.
We show that menin physically interacts with proteins involved in the canonical Wnt signaling pathway, including beta-catenin, TCF3 ( TCFL1), and weakly with TCF4 ( TCFL2). Paper-13508090.
Although we have a limited number of patients in our cohort, our data is consistent with others in the literature suggesting that CDKN1B and AIP mutations are extremely rare in MEN1 syndrome. Paper-13532979.
In conclusion, menin is a key regulator of gene networks that are activated in fibrogenesis associated with hepatocellular carcinoma through the modulation of TGF-beta response. Paper-12289199.
HYPOTHESIS: Primary hyperparathyroidism in Keeshonden is genetically transmitted and is caused by a mutation in 1 of 4 genes implicated in human FIHP: MEN1, CASR, HRPT2, or RET. Paper-13140201.
Menin overexpression increases expression of the Wnt/ beta-catenin downstream target gene Axin2, which is associated with increased H3K4 trimethylation of the Axin2 gene promoter. Paper-13508090.
Promoter hypermethylation of RIZ1 was detected in 36% of the parathyroid tumors and was related to LOH at the RIZ1 locus (P=.01), and absence of somatic mutation of the MEN1 gene (P=.044). Paper-10065442.
Here, we have compared the relative mRNA expression level and CpG methylation status of p18, p27 and p15 in 18 pancreatic endocrine tumours (PETs) with or without MEN1 gene mutations. Paper-12694143.
These beta-lactamases are divided in two groups: TEM and SHV derivatives and non-TEM and non-SHV extended-spectrum beta-lactamases (CTX-M1, CTX-M2, MEN-1, PER-1, PER-2, TOHO-1, and VEB-1). Paper-1619134.
Whether it is a separate entity or a variant of multiple endocrine neoplasia type 1 ( MEN1 at 11q13) or hyperparathyroidism-jaw tumor ( HPT-JT or HRPT2 at 1q21-32) syndrome is not known. Paper-1462387.
This finding was consistent with the extensive overlap in the nuclear localization patterns of endogenous menin, RPA2, and RPA1 observed by immunofluorescence. Paper-9684472.
RESULTS: Patients with MEN-1 and hypergastrinaemia tended to have a higher plasma PAM activity than MEN-1 subjects with normal circulating G-NH2 indicating a cosecretion of hormone and PAM. Paper-7589011.
We showed a biochemical interaction between human menin and CHES1 and showed that the COOH terminus of menin, which is frequently mutated in MEN1 patients, is necessary for this interaction. Paper-12206281.
This chapter reviews the molecular biology of neuroendocrine tumors, including the roles of MENIN, TSC2, NF-1, vHL, p53, bcl-2, bax, VEGF, IGF, PDGF, EGFR, and mTOR. Paper-12469242.
The locus for MEN1 is tightly linked to the marker PYGM on chromosome 11q13, and linkage analysis places the MEN1 gene within a 2-Mb interval flanked by the markers D11S1883 and D11S449. Paper-1140183.
In addition, a monohormonal type of pancreatic microadenomatosis was identified that consisted of either insulinomas or glucagon- producing tumors and was not associated with MEN1 or VHL. Paper-12003990.
The analysis entailed the search for allelic loss ( LOH) or imbalances of polymorphic microsatellite markers at the corresponding chromosomal loci of the genes MEN-1 (11q13), p53 (17p13). Paper-8885490.
SNUOT- RB1 and SNUOT-RB4 gained chromosomal copy numbers commonly in chromosome 11, especially in locus 11q13, which is responsible for cancer-related genes such as CCND1, MEN1, and FGF3. Paper-12949236.
No MEN1 germline mutation was found in five probands with familial hyperparathyroidism, suggesting that familial hyperparathyroidism often is caused by mutation in another gene or gene(s). Paper-1113987.
Combined linkage analysis in MEN 1 families and deletion mapping in MEN 1-related tumors suggest the MEN 1 gene is located centromeric to D11S807 and telomeric to PYGM. Paper-7218598.
Thus, aberrant gene expression in MEN1 tumours is not caused by lower global H3K4me3, but rather by specific effects on genes that are regulated by menin-interacting proteins, such as VDR. Paper-14029332.
Here we show that menin specifically interacts with FANCD2, a protein encoded by a gene involved in DNA repair and mutated in patients with an inherited cancer-prone syndrome, Fanconi anemia. Paper-9772362.
CONCLUSIONS: Allelic deletion of the MEN1 gene may reflect a pivotal event in the development of multifocal gastrin and somatostatin cell neoplasms in the duodenum of patients with MEN1. Paper-13191569.
However, it remains unclear how menin up-regulates caspase 8 expression and whether menin- mediated caspase 8 expression plays a role in repressing MEN1 development. Paper-12527902.
Our data also suggest that TSGs located in areas where no LOH was detected ( PTEN, MEN1, Cyclin D1, BRCA2 and RFC3) are not involved or do not have an important role in tumour progression. Paper-8884490.
Evaluation of CDKN2C/ p18, CDKN1B/ p27 and CDKN2B/ p15 mRNA expression, and CpG methylation status in sporadic and MEN1-associated pancreatic endocrine tumours. Paper-12694143.
Menin binds to the N terminus of the chromatin-remodeling histone methyltransferase MLL and is essential for the transforming activity of at least several oncogenic MLL fusion proteins. Paper-12868916.
Assessment of p27 ( cyclin-dependent kinase inhibitor 1B) and AIP ( aryl hydrocarbon receptor-interacting protein) genes in MEN1 syndrome patients without any detectable MEN1 gene mutations. Paper-13532979.
The observation of distinct deletion patterns in small synchronous tumours supports the concept that each gastrin- producing tumour in an individual MEN1 patient arises from an independent cell clone. Paper-13191569.
Menin was recently shown to interact with several components of a trithorax family histone methyltransferase complex including ASH2, Rbbp5, WDR5, and the leukemia proto-oncoprotein MLL. Paper-12027314.
DESIGN AND METHODS: Plasma CgA levels were measured using a commercial enzyme-linked immunosorbent assay in 61 patients with sporadic GEP NET and in 25 with MEN 1 including 16 with GEP NET. Paper-9684596.
None of the four patient with MEN 2A syndrome had persistent or recurrent disease, but hypoparathyroidism developed in one patient; hypoparathyroidism developed in three patients with MEN 1 syndrome. Paper-7217599.
Alternatively the differences in expression in CGA and other secretory constituents may reflect downregulation of the entire regulated secretory pathway in VHL compared to MEN 2 tumours. Paper-12641805.
We further show that relative to increases in plasma catecholamines, patients with phaeochromocytomas associated with MEN 2 have higher plasma concentrations of CGA than those with tumours in VHL syndrome. Paper-12641805.
Combined mutations of p27(-/-) and Men1(+/-), in contrast, did not exhibit noticeable synergistic stimulation of Rb kinase activity, cell proliferation, and tumor growth. Paper-12445887.
These findings suggest an alternative process of tumorigenesis in VHL- and MEN 2- associated pheochromocytomas and implicate Epo as a clinical biomarker to differentiate these tumors. Paper-11290025.
OBJECTIVE: Multiple endocrine neoplasia type 1 ( MEN1) is characterized by a triad of neoplasia affecting the parathyroid glands, enteropancreatic endocrine tissue and the anterior pituitary gland. Paper-9911274.
The locus for MEN1 is tightly linked to the marker PYGM on chromosome 11q13, and linkage analysis has previously placed the MEN1 gene within a 2-Mb interval flanked by markers D11S1883 and D11S449. Paper-1248934.
This is achieved by menin interacting physically and functionally with bone morphogenetic protein (BMP)-2 regulated Smads, such as Smad1 and Smad5, and the key osteoblast regulator, Runx2. Paper-10767346.
The allelic loss of loci for unknown oncosuppressor genes are currently under investigation, while an exceedingly limited role for menin gene and RB1 has been demonstrated for sporadic pituitary tumors. Paper-9148110.
Multiple endocrine neoplasia type 1 syndrome ( MEN1, MIM 131100), an autosomal dominant disease, is characterized by parathyroid hyperplasia, pancreatic endocrine tumors, and pituitary adenomas. Paper-1481340.
NPY levels in phaeochromocytomas from VHL patients were lower (P<0.0001) than in those from MEN 2 patients for both mRNA (84-fold difference) and the peptide (99-fold difference). Paper-13212380.
But papillary thyroid cancer was never regarded as its component before in Korea. Herein we present a 39-year-old woman who manifested typical features of MEN1 with a coincidental papillary thyroid carcinoma. Paper-12854288.
They arise sporadically or occur secondary to inherited cancer syndromes, such as multiple endocrine neoplasia type II ( MEN2), von Hippel-Lindau disease ( VHL), or neurofibromatosis type I ( NF1). Paper-10601936.
Southern blot analysis with constitutional DNA from probands of 14 independent MEN 1 families and DNA from four MEN 1 tumor specimens did not reveal any structural abnormality of the NF-kappa B3 gene. Paper-1044424.
Although menin and MLL fusion proteins cooperate to activate Homeobox (Hox) gene expression during transformation, little is known about the normal hematopoietic functions of menin. Paper-13623161.
We now show that the pathogenesis of MEN1- associated parathyroid lesions involves unmasking of a recessive mutation at the disease locus and that sporadic primary hyperparathyroidism shares the same mechanisms. Paper-6501592.
We conclude that the pathogenesis of GH- secreting adenomas in MEN-1 is influenced by secondary factors acting in synergy with the well-documented primary MEN-1 gene defect on chromosome 11q13. Paper-555682.
In a large kindred with familial isolated familial HP, MEN1 germ line mutation 249 del4 and LOH was associated with the HP phenotype and a predisposition to non-endocrine malignancies. Paper-8360902.
Site-specific probes for chromosome 11q13 including PYGM, D11S146, and INT2 were used in 7 sporadic PRL- secreting adenomas to detect deletions of the MEN-1 locus on chromosome 11. Paper-94420.
Pancreatic endocrine tumors (PETs) occur in association with multiple endocrine neoplasia type 1 ( MEN1) and von Hippel-Lindau ( VHL) syndromes caused by germline alterations in MEN1 and VHL, respectively. Paper-8942844.
In this study, 46 cases of cystic parathyroid adenomas previously investigated for HRPT2 mutations were characterized with regard to MEN1 gene mutations, cyclin D1 expression and parafibromin expression. Paper-12019402.
Multiple endocrine neoplasia I ( MEN1) maps to this region of copy number gain in aggressive prostate tumors and was shown to be the only gene at this locus at increased expression in prostate cancer. Paper-13542482.
The patient underwent genetic testing for Cowden syndrome ( PTEN gene), Carney complex ( PRKAR1A gene), and multiple endocrine neoplasia syndrome type 1 ( MEN1 gene); no deleterious mutations were identified. Paper-13181317.
RECENT FINDINGS: The molecular and clinical genetics of familial GEP NETs have been further elucidated by the characterization of the tumor suppressor genes, MEN1, VHL, NF-1, TSC1, and TSC2. Paper-13565065.
Mapping of the gene encoding the B56 beta subunit of protein phosphatase 2A ( PPP2R5B) to a 0.5-Mb region of chromosome 11q13 and its exclusion as a candidate gene for multiple endocrine neoplasia type 1 ( MEN1). Paper-1148133.
The product of the multiple endocrine neoplasia type 1 ( MEN1) tumor suppressor gene, menin, is an integral component of MLL1/ MLL2 histone methyltransferase complexes specific for Lys4 of histone H3 (H3K4). Paper-11843832.
Ten pheochromocytomas ( VHL patients n = 5, MEN 2 patients n = 5) were examined for the presence or absence of Epo and Epo-R using Western blot, immunohistochemistry, and RT-PCR analyses. Paper-11290025.
The present data extend prior reports of the absence of mutation in MEN1, GHRH-R, and GNAS1 and describe the first family with isolated acromegaly in which germline mutation in GNAI2 has been searched. Paper-8676519.
One such mutation has been reported in a GH- producing tumour from a patient with multiple endocrine neoplasia type 1 ( MEN 1) although mutations have not been reported in other tumours associated with MEN 1. Paper-273809.
Pituitary adenomas occur in a familial setting in multiple endocrine neoplasia type 1 ( MEN1) and Carney's complex ( CNC), which occur due to mutations in the genes MEN1 and PRKAR1A respectively. Paper-12505223.
We mapped the MenX locus to the distal part of rat chromosome 4, excluding the homologs of the genes responsible for the MEN syndromes (RET and MEN1) and syndromes with an endocrine tumor component ( VHL and NF1). Paper-12277335.
These observations suggest that menin inhibits hPRL promoter activity and cell proliferation, raising the possibility that menin might play an important role in the tumorigenesis of prolactinoma. Paper-9648321.
MEN1 disease started with primary hyperparathyroidism followed by Cushing disease, the detection of tumors of the pituitary, adrenal cortex, and the pancreas and also an elevated serum gastrin level. Paper-12865074.
1. In this study, we report the physical localisation of the 13-kDa FK506 and rapamycin binding protein gene ( FKBP2) to the cosmid marker D11S750, which is located inside the MEN1 region of non-recombination. Paper-196581.
No MEN1 germ-line mutations were found in 7/54 (13%) MEN1 families, in 2/11 (18%) isolated MEN1 cases, in 13/19 (68. 5%) MEN1-related cases, and in a kindred with familial isolated hyperparathyroidism. Paper-1660195.
Neither mutation hot spot nor phenotype-genotype correlation has been established in MEN1 although some missense mutations may be specifically associated with a phenotype of familial isolated hyperparathyroidism. Paper-13499816.
Taken together, our data suggest that Menin uncouples ERK and JNK activation from phosphorylation of their nuclear targets Elk-1, JunD and c-Jun, hence inhibiting accumulation of active Fos/Jun heterodimers. Paper-9550828.
Previous studies of VHL- associated and MEN 2-associated pheochromocytomas suggest morphological, biochemical, and clinical differences exist among the tumors, but the process by which they develop remains unclear. Paper-11290025.
Loss of heterozygosity on 11q13 was detected in 1 mixed GH/ PRL adenoma, and the somatic 22-bp deletion of the multiple endocrine neoplasia type 1 ( MEN1) gene encoding menin was detected in this tumor. Paper-1529455.
Consistent with an essential role for menin in regulating beta-cell adhesion in vivo, accumulations of beta-catenin and E-cadherin are reduced at cell junctions in the islets from Men1-excised mice. Paper-13622826.
Duplex polymerase chain reaction ( PCR) was standardised in order to quantify the expression of the menin gene using intron-spanning primers across exons 9 and 10 in relation to the 'house-keeping' gene GAPDH. Paper-1843850.
Loss of heterozygosity studies in MEN 1 and sporadic tumors suggest that the MEN1 gene encodes a tumor suppressor and have helped to narrow the location of the gene to a 600-kb interval between PYGM and D11S449. Paper-1140183.
Coexpression of Epo and Epo-R was found in all five VHL-associated pheochromocytomas; in contrast, expression of Epo-R, but not Epo, was documented in all five MEN 2-associated pheochromocytomas. Paper-11290025.
Here, we demonstrate an oncogenic role for MEN1 in prostate cancer using a variety of independent assays.Prostate Cancer and Prostatic Diseases advance online publication, 9 September 2008; doi:10.1038/pcan.2008.45. Paper-13542482.
The case of a 33-year-old-woman with Multiple Endocrine Neoplasia Type 1 ( MEN1) syndrome and acromegaly due to ectopic growth hormone-releasing hormone ( GHRH) secretion by a thymic carcinoid tumour is reported. Paper-9504380.
Conversely, a subset of menin mutations in multiple endocrine neoplasia type 1 patients abrogate interaction with LEDGF while preserving MLL interaction but nevertheless compromise MLL/ menin-dependent functions. Paper-12868921.
By examination of allele losses in MEN1-associated lesions, we could define deletions of chromosome 11 and map the MEN1 locus to a small region within chromosome band 11q13, telomeric to the PYGM locus. Paper-6501592.
The MEN1 locus has been previously localised to chromosome 11q13, and a <300 kb gene-rich region flanked centromerically by PYGM and telomerically by D11S1783 defined by combined meiotic and tumour deletion mapping studies. Paper-1113988.
SCLIP siRNA also decreased the level of secretion of endogenous CHGA and SCG2, as well as transfected human growth hormone, while SCG10 siRNA decreased the level of regulated secretion of endogenous CHGB. Paper-12861455.
A case of Zollinger-Ellison syndrome of multiple endocrine neoplasia type 1 ( MEN 1) origin with hyperparathyroidism and with a rise in serum gastrin due to an unusual parathyroid " gastrinoma" has been investigated. Paper-7005452.
The genetic defect responsible for MEN-1 in three families was recently mapped to the long arm of chromosome II by linkage between the MEN-1 locus and the gene for skeletal muscle glycogen phosphorylase ( PYGM) at 11q13. Paper-6359662.
Linkage between MEN1 and 6 of the 7 loci was established, and the highest peak lod scores [Z(theta)] were observed with PYGM and D11S97 at Z(theta) = 13.71, theta = 0.047 and Z(theta) = 13.76, theta = 0.076 respectively. Paper-7588608.
This was achieved by investigating 17 cosmids for microsatellite polymorphisms, which defined two novel polymorphisms at the VRF and A0138 loci, and utilizing these to characterize recombinants in MEN1 families. Paper-1207871.
RT-PCR assays have revealed that overexpression of menin inhibits hTERT mRNA expression in some cell types, although this inhibition does not lead to a significant down-regulation of telomerase activity. Paper-12933722.
OBJECTIVE: To investigate a family with an unusual combination of multiple endocrine neoplasia ( MEN1) and the McCune-Albright syndrome for MEN1 mutations and activating GNAS1 mutations at codons Arg201 and Gln227. Paper-13230397.
Triple immunofluorescence labeling studies with antibodies against menin, BrdU, and GFAP show that menin and GFAP colocalize in glioma cells at the S-G2 phase of the cell cycle, as measured by BrdU incorporation. Paper-9531129.
Phosphorylation-defective mutants of either or both of these residues retain the associated histone methyltransferase activity of menin, as well as binding to the trithorax complex members Ash2L, Rbbp5, and MLL2 and to RNA polymerase II. Paper-12279319.
CGA has several functions, some of which may be involved in the distinct phenotypic differences of phaeochromocytomas in patients with von Hippel-Lindau ( VHL) syndrome compared to multiple endocrine neoplasia type 2 ( MEN 2). Paper-12641805.
Our experience with the meal stimulation test indicates that an elevated basal or exaggerated serum PP and/or gastrin response is an earlier sign of pancreatic involvement in the MEN 1 trait than is abdominal computerized tomography. Paper-5777451.
We suggest that careful growth records be kept for children at risk of developing inherited MEN1 and, in the event of a decelerating growth rate, further diagnostic evaluation be undertaken with regards to ACTH-secreting pituitary tumours. Paper-10926229.
Cells overexpressing menin had normal telomerase activity, and tumors with homozygous MEN1 mutations showed no aberrations in telomere length, indicating that menin does not directly regulate telomerase activity. Paper-9567346.
Menin was co-immunoprecipitated with Smad1/5 in ST2 and MC3T3-E1 cells, and inactivation of menin antagonized BMP-2-induced transcriptional activity of Smad1/5 in ST2 cells, but not MC3T3-E1 cells. Paper-10561295.
CONCLUSIONS: Based on the occurrence of complications in our experience, TPTX followed by autograft and guided by intraoperative PTH monitoring represents a better surgical option in MEN1- HPT compared with other surgical approaches. Paper-13435119.
RESULTS: Adrenaline-producing phaeochromocytomas in MEN 2 patients expressed more noradrenaline transporter mRNA and protein than noradrenaline- producing tumours in VHL patients. Paper-11146407.
METHODS: Menin gene expression, along with glyceraldehyde phosphate dehydrogenase ( GAPDH) gene expression, has been studied in a group of normal pituitaries and in 23 pituitary tumours not associated with the MEN 1 syndrome. Paper-1843850.
BACKGROUND: Glucagon-producing tumors are either solitary neoplasms of the pancreas, occasionally associated with a glucagonoma syndrome, or multiple neoplasms associated with multiple endocrine neoplasia type 1 ( MEN1). Paper-13566449.
Pancreatic involvement in young MEN-1 patients is most consistently demonstrated by analysing serum insulin, proinsulin, PP as well as plasma glucagon chromogranin A levels, which have exhibited sensitivities of 56, 67, 37 and 60%, respectively. Paper-1509246.
Moreover, menin interacts with activator of S-phase kinase (ASK), a component of the Cdc7/ASK kinase complex that is crucial for cell proliferation, but does not appear to alter Cdc7 kinase activity in in vitro kinase assays. Paper-10611402.
CONCLUSION: We report an unusual case of clearly high circulating immunoreactive FSH due to a functioning FSH- secreting gonadotroph adenoma in a man with the MEN 1 syndrome. Paper-12977923.
The ability to direct multi-lineage mesenchymal stem sell ( MSC) potential towards an osteogenic phenotype by stimulation with Menin and Shh are important, as are the modulatory roles of Notch-1 and PPARgamma. Paper-10369178.
A subset of families are likely to be genetic variants of other familial tumour syndromes in which PHPT is the main feature, for example multiple endocrine neoplasia type 1 ( MEN 1) and the hyperparathyroidism-jaw tumour syndrome ( HPT-JT). Paper-9221315.
In the present study deletions of 1p were characterized and the findings were evaluated in relation to the loci of MEN1 and histone deacetylase 1 gene ( HDAC1), a menin interacting partner in 1p, as well as to the clinical characteristics. Paper-9316078.
In order to establish further the location of MEN1, we have utilized the seven polymorphic DNA probes: D11S288, D11S149, PGA, PYGM, D11S97, D11S146 and INT2, in linkage studies of 339 members (116 affected) from 27 MEN1 families. Paper-7588608.
PLCB3 plays an important role in signal transduction and, moreover, shows loss of expression in some endocrine tumors, in accordance with a putative tumor suppressor gene function, and thus appears to be an excellent candidate for MEN1. Paper-866128.
The strikingly different mutation spectra of MEN1 and FANCD2 mutants together with lack of evidence for genetic interaction between these genes indicate MEN1 plays an essential role in ICL repair distinct from the Fanconi anemia genes. Paper-12747225.
Together, our results indicate that menin enhances the caspase 8 expression by binding the caspase 8 locus, and suggest that menin suppresses MEN1 tumorigenesis, at least in part, by up-regulating caspase 8 expression. Paper-12527902.
Since the initial testing, the family has been confirmed to be a MEN-1 family as the mother has developed abdominal pain and an elevated serum pancreatic polypeptide and the younger brother an anterior pituitary tumor and recurrent HPT. Paper-9169001.
Screening of the MEN 1 gene and genetic analysis of the hot spot regions of the GNAS 1 (codons 201 and 227) and GNAI 2 (codons 179 and 205) genes did not show any mutations in the constitutional DNA or the adrenal tissue DNA of the index patient. Paper-9630904.
Promoter methylation was not detected for p18 and p27. p15 expression was undetectable in 8/18 (44%) of the PETs, and no general relations to tumour syndrome, malignancy or MEN1 gene mutations were evident. Paper-12694143.
CONCLUSIONS: Our results provide further support for FIHP being a distinct allelic variant of MEN1, and an analysis of the 16 mutations reported to date indicate that FIHP is associated with a higher frequency of missense MEN1 mutations. Paper-9692557.
The meiotic mapping studies indicated that the most likely location of the MEN1 gene was in the interval flanked by PYGM and D11S97, and the results of mitotic mapping suggested a possible location of the MEN1 gene telomeric to SEA. Paper-554893.
To detect possible point mutations, or other small structural aberrations, direct sequencing of PLC beta 3 cDNAs from two affected persons from two different MEN 1 families was performed, but no MEN 1-specific abnormalities were revealed. Paper-866129.
We further demonstrate that both Cdx4 and menin bind to the same regulatory region at the Hoxa9 locus in vivo, and co-activate the reporter gene driven by the Hoxa9 cis-elements that contain Cdx4 binding sites. Paper-12363288.
In symptomatic individuals carrying MEN1 germ line mutations, annual clinical and biochemical (calcium, PTH, gastrin, prolactin) follow-up as well as routine pancreatic and pituitary imaging may be complemented as individually needed. Paper-8510746.
In contrast, mono- or oligo-clonal parathyroid neoplasia underlays most other HPT variants: multiple endocrine neoplasia type 1 ( MEN1), multiple endocrine neoplasia type 2A ( MEN2A), and hyperparathyroidism-jaw tumor syndrome ( HPT-JT). Paper-9637266.
In the course of constructing a conting, we have identified the location of the gene encoding the B56 beta subunit of protein phosphatase 2A ( PP2A), which is involved in cell signal transduction pathways and thus represents a candidate gene for MEN1. Paper-1148133.
This review presents the newest information on the clinical and molecular genetics of the MENs ( MEN 1, MEN 2, and Carney complex), including recommendations for genetic screening, and discusses briefly the related syndromes PJS, CD and VHLD. Paper-8986953.
The data (1) underline the need for early investigation for acromegaly in patients with CNC; (2) provide a molecular hypothesis for its clinical progression; and (3) suggest a model for MAS- and, perhaps, MEN 1-related GH-producing tumor formation. Paper-8628740.
Primary hyperparathyroidism may occur as part of hereditary syndromes, including multiple endocrine neoplasia types 1 and 2A ( MEN1 and MEN2A), hyperparathyroidism-jaw tumor syndrome, and the familial isolated hyperparathyroidism ( FIHP). Paper-10514117.
When pancreatic involvement in MEN-1 is biochemically diagnosed efforts should be made to localize the lesions by computed tomography, angiography and, in some patients, also transhepatic portal vein catheterization and venous sampling ( PTP). Paper-6955400.
Cyclin D1 is an oncogene that encodes a key regulator of the cell cycle, while MEN1 is a tumor suppressor gene that has also been implicated in familial multiple endocrine neoplasia type 1 ( MEN1), in which primary HPT is common. Paper-9282241.
In the present study, we describe two unrelated Italian kindreds with FIHP, in which the clinical, histopathological and genetic analyses of the MEN1 gene and HPRT2 locus at 1q21-32 suggest that both might be a variant of MEN1 and HPT-JT syndromes. Paper-9205209.
The two main types of hereditary pancreatic neuroendocrine tumours are found in multiple endocrine neoplasia type 1 ( MEN-1) and von Hippel-Lindau disease ( VHL), but also in the rarer disorders of neurofibromatosis type 1 and tuberous sclerosis. Paper-10503679.
Polymerase chain reaction-single-stranded DNA conformation polymorphism analysis and sequencing demonstrated a somatic mutation in the MEN1 gene in only one of the 40 tumors, a prolactinoma, which had a 1-bp deletion in the coding sequence of exon 2. Paper-1936421.
The forkhead transcription factor CHES1 ( FOXN3) was identified as an interacting protein by a genetic screen, and overexpression of CHES1 restored both cell cycle arrest and viability of MEN1 mutant flies after ionizing radiation exposure. Paper-12206281.
CHES1 is a component of a transcriptional repressor complex, that includes mSin3a, histone deacetylase (HDAC) 1, and HDAC2, and it interacts with menin in an S-phase checkpoint pathway related to DNA damage response. Paper-12206281.
Phosphorylation of Rb protein at both CDK2 and CDK4/ CDK6 sites were significantly increased in normal bronchial epithelia and tumor cells derived from p18(-/-);Men1(+/-) mice compared to those from single p18(-/-) or Men1(+/-) mice. Paper-13168553.
We show that menin is a transcriptional coactivator of the nuclear receptors for estrogen and vitamin D. Activation of the endogenous estrogen-responsive TFF1 ( pS2) gene results in promoter recruitment of menin and in elevated trimethylation of H3K4. Paper-11843832.
We analyzed 21 intramedullary spinal, 14 ventricular, 11 filum terminale and 6 intracerebral ependymomas for mutations in the MEN1 gene, which is located at 11q13, and mutations in the NF2 gene, which is located at 22q12, as well as for LOH on 11q and 22q. Paper-8710950.
Patients: Eighteen sporadic and three familial cases of MEN1 mutation-negative MEN1 syndrome were studied (18 pituitary adenomas, 12 hyperparathyroidism, 10 neuroendocrine tumours including 2 ACTH-secreting lesions and one adrenal nodular hyperplasia). Paper-13532979.
Menin- mediated repression is relieved by the histone deacetylase inhibitor trichostatin A, indicating that deacetylation of histones is an essential component of this repression mechanism, as has recently been demonstrated for the retinoblastoma protein. Paper-8277138.
In this study we examined the expression of menin in parathyroid tumors from primary hyperparathyroidism (PHP), secondary hyperparathyroidism (SHP), and MEN1 and thyroid tumors including Basedow's disease, thyroid cancer, and adrenocortical tumors. Paper-8410281.
GEP NETs occur either sporadically or as part of endocrine tumor susceptibility syndromes such as multiple endocrine neoplasia type 1 ( MEN1), von Hippel Lindau ( VHL) syndrome, neurofibromatosis ( NF-1), and possibly tuberous sclerosis ( TSC). Paper-13565065.
Cells mutant for multiple endocrine neoplasia type I ( MEN1) or any of the Fanconi anemia ( FA) genes are hypersensitive to the killing effects of crosslinking agents, but the precise roles of these genes in the response to interstrand crosslinks (ICLs) are unknown. Paper-12747225.
METHODS: Comparative genomic hybridization (CGH), loss of heterozygosity ( LOH) and multiple endocrine neoplasia type 1 gene ( MEN1) mutation analysis were used to analyze twelve parathyroid tumors from nine patients with lithium- associated HPT. Paper-9206289.
Prostate cancer is the second leading cause of cancer-related deaths in menin the United States. Genistein is a prominent isoflavonoid found in soy products and has been proposed to be responsible for lowering the rate of prostate cancer in Asians. Paper-9270254.
An N-terminal deletion mutant of Menin that cannot inhibit JunD phosphorylation by JNK, can still repress JunD phosphorylation by ERK2, suggesting that Menin interferes with ERK and JNK pathways through two distinct inhibitory mechanisms. Paper-9550828.
A combination of methods was used to assess clonality, including MEN1 gene mutation analysis, loss of heterozygosity analysis of the MEN1 locus, and analysis of X-chromosome inactivation at the human androgen receptor locus (human androgen receptor analysis). Paper-2081558.
Since overexpression of the catalytic subunit of human telomerase ( hTERT) is known to minimally alter the cellular phenotype, we focused on the establishment of cell lines derived from human fibroma from a MEN1 patient by ectopic expression of hTERT. Paper-10803342.
Hereditary predisposition to lipomas is observed in familial multiple lipomatosis ( OMIM 151900) and benign cervical lipomatosis ( OMIM 151800) and can also be associated with mutations in the MEN1 and PTEN genes ( OMIM 131100 and 153480, respectively). Paper-8948405.
We have assessed the specificity of 10 different siRNAs corresponding to the MEN1 gene by examining the expression of two additional genes, TP53 ( p53) and CDKN1A ( p21), which are considered functionally unrelated to menin but are sensitive markers of cell state. Paper-10349713.
Menin interacts with Smad3, and antisense menin suppresses transforming growth factor type beta- induced and Smad3-induced transcriptional activity by inhibiting Smad3/4-DNA binding at specific transcriptional regulatory sites. Paper-8672367.
In osteoblasts the interaction of menin and the transforming growth factor-beta/ Smad3 pathway negatively regulates the BMP-2/ Smad1/5- and Runx2-induced transcriptional activities leading to inhibition of late-stage differentiation. Paper-10561295.
The following percentages of participants felt that, if a specific germline mutation is present in a definitely affected family member, DNA diagnosis should be performed in the offspring of this patient before the age of 10: 78% for MEN-1, 93% for MEN-2, and 71% for VHL. Paper-1509264.
Background: In patients with multiple endocrine neoplasia type 1 ( MEN1), expression of somatostatin receptor ( SST) in parathyroid adenomas and effectiveness of therapy with somatostatin analogues on primary hyperparathyroidism (PHP) have been scarcely investigated. Paper-13074908.
To determine if MEN1 and the FA genes function cooperatively in the same repair process or in distinct repair processes, we exploited Drosophila genetics to compare the mutation frequency and spectra of MEN1 and FANCD2 mutants and to perform genetic interaction studies. Paper-12747225.
Herein, we characterized a newly identified kindred with isolated acromegaly and searched for germline mutation in genes that have been associated with endocrine tumors [i.e. MEN1, Gs alpha ( GNAS1), and Gi2 alpha ( GNAI2)], as well as the GHRH receptor ( GHRH-R) gene. Paper-8676519.
Forty-two patients with primary hyperparathyroidism ( HPT) of multiple endocrine neoplasia type 1 ( MEN-1) were evaluated a mean of 8.9 years after subtotal parathyroid resection (SPX, n = 34) or total parathyroidectomy with autotransplantation to the forearm ( TPX, n = 23). Paper-7216475.
Here, we show that point mutations in three individual NLSs, NLS1, NLS2, and a novel accessory NLS, NLSa, do not block nuclear translocation, but compromise the ability of menin to repress expression of the endogenous insulin-like growth factor binding protein-2 ( IGFBP-2) gene. Paper-12038814.
Taken together, most missense and in-frame MEN1 genomic alterations affect one or all domains of menin interacting with JunD [codons 1-40; 139-242; 323-428], Smad3 [distal to codon 478], and NFkappaB [codons 276-479], three major effectors in transcription and cell growth regulation. Paper-9507940.
These data suggest that RET gene mutation may not be involved in the development of sporadic parathyroid tumors and hyperplasia secondary to uremia and that MEN1 gene mutation may not be or is rarely associated with development of parathyroid hyperplasia in MEN2A patients. Paper-8597763.
Direct sequencing of cDNAs from two affected subjects from 2 different MEN 1 families, as well as nucleotide sequence analysis of exon/ intron boundaries in these patients, did not reveal MEN 1-specific point mutations or other small structural aberrations in the NF-kappa B3 gene. Paper-1044424.
Here we have investigated the roles of transforming growth factor (TGF)-beta and menin, the product of the multiple endocrine neoplasia type 1 ( Men1) gene, in the proliferation and PTH production of parathyroid cells from either patients with secondary hyperparathyroidism or Men1. Paper-10378122.
METHODS: Fifty patients with MEN 1 with hyperparathyroidism were followed up 2 to 27 years after subtotal (SPX; n = 35) or total parathyroidectomy with forearm autografiing ( TPX; n = 15), including 24 who underwent 28 reoperations because of persistent or recurrent hyperparathyroidism. Paper-1676704.
Menin- RPA2 binding was inhibited by a number of menin missense mutations found in individuals with multiple endocrine neoplasia type 1, and the interacting regions were mapped to the N-terminal portion of menin and amino acids 43 to 171 of RPA2. Paper-9684472.
In the duodenum and the pancreas, the MEN1- associated germline mutation of the menin gene obviously causes hyperplasia of the gastrin and somatostatin cells ( duodenum) and the glucagon cells ( pancreas), resulting in multifocal development of tumors. Paper-12630141.
Upregulated genes (n = 39) included both known genes associated with extracellular matrix remodeling, cell communication, metabolism, and post-transcriptional regulation gene (e.g., ZFP36L1), as well as the tumor suppressor gene menin ( multiple endocrine neoplasia type 1; MEN1). Paper-12289199.
Menin and Smad3 were co-immunoprecipitated, and combined menin and Smad3 overexpression antagonized, whereas menin and the dominant-negative Smad3DeltaC together enhanced BMP-2-induced transcriptional activity of Smad1/5 and Runx2. Paper-10561295.
BACKGROUND AND OBJECTIVES: Familial hyperparathyroidism may occur as familial isolated hyperparathyroidism ( FIHP) or as part of an inherited syndrome, in particular multiple endocrine neoplasia types 1 and 2A ( MEN1, MEN2A) and hyperparathyroidism-jaw tumour ( HPT-JT) syndrome. Paper-1909700.
Collectively, these data suggest that menin has an essential role in Wnt/ beta-catenin signaling through a mechanism that eventually affects histone trimethylation of the downstream target gene Axin2, and activation of Wnt/ beta-catenin signaling inhibits islet tumor cell proliferation. Paper-13508090.
The assay employs immobilized affinity-purified N-terminal-specific anti- bFGF antibodies (antigen capture) and high affinity binding to radioiodinated heparin. bFGF-like immunoreactivity was undetectable (< 0.2 ng/mL) in normal subjects and in most unaffected relatives of MEN1 subjects. Paper-7587406.
In the pituitary and pancreatic islets, phosphorylation of the retinoblastoma ( Rb) protein at both CDK2 and CDK4/6 sites was increased in p18(-/-) and Men1(+/-) cells and was further increased in p18(-/-); Men1(+/-) cells. Paper-12445887.
This manuscript reviews genetic aspects of hereditary GH-secreting tumors, data from animal models resulting from the inactivation of the MEN1 and PRKAR1A tumor suppressor genes and available in vitro data regarding possible functions of menin, the product of the MEN1 gene. Paper-12277843.
In support of previous findings in islet tumors, we found down-regulation of the cell-cycle regulator, p18, in both the pancreatic islet and pituitary adenomas, suggesting that reduced p18 levels may be important for Men1-related tumorigenesis in multiple tissues. Paper-13314596.
For this study, we analyzed a series of menin proteins with single amino acid alterations and found that all of the MEN1-causing missense mutations tested led to greatly diminished levels of the affected proteins in comparison with wild-type and benign polymorphic menin protein levels. Paper-10344141.
Phaeochromocytoma is a neural-crest-derived tumour that may be a feature of several familial cancer syndromes including von Hippel-Lindau ( VHL) disease, multiple endocrine neoplasia type 2 ( MEN 2), neurofibromatosis type 1 ( NF1) and germline succinate dehydrogenase subunit (SDHB and SDHD) mutations. Paper-10755996.
These data indicate that loss of heterozygosity in these affected family members appears independent of MEN-1 gene changes and suggest that a novel (tissue-specific?) tumor suppressor gene(s) linked to the PYGM marker and expressed in the pituitary is essential for regulation of somatotrope proliferation. Paper-1704488.
In the largest reported family of patients with multiple endocrine neoplasia type 1 ( MEN 1), hyperparathyroidism was expressed at first screening in 33 patients by elevation of ionized calcium (IC) (30 cases) or parathyroid hormone (three cases) without elevation of albumin-corrected total calcium (ACTC). Paper-7218603.
PPP1A, which has been postulated as a MEN-1 candidate tumor suppressor gene, and GST3, a gene transcriptionally active in many human cancers, both map distal to the bcl-1 translocation cluster and the region containing MEN-1, and therefore are unlikely to be directly involved in bcl-1 or MEN-1. Paper-47139.
Pheochromocytoma is a neuroendocrine tumor associated with a variety of genetic disorders, which include von Hippel-Lindau disease ( VHL), multiple endocrine neoplasia type 2 ( MEN 2), neurofibromatosis type 1, hereditary paraganglioma, and succinate dehydrogenase gene-related tumors. Paper-11290025.
We have characterized a panel of seven rodent-human somatic cell hybrids which contain fragments of human chromosome 11 with breakpoints in the pericentromeric region by using eight DNA sequences (D11S149, PGA, PYGM, D11S97, INT2, D11S37, D11S533, and D11S147) to define the region containing MEN1. Paper-80375.
Expression of Epo appears to be a result of VHL gene deficiency, possibly through activation of the hypoxia inducible factor-1 pathway, whereas Epo-R is an embryonal marker whose sustained expression in both VHL- and MEN 2-associated pheochromocytomas reflects an arrest or defect in development. Paper-11290025.
Frequent genetic alterations of loss and gain of gene copy number included gain of GSTP1 and multiple endocrine neoplasia type 1 ( MEN1), and loss of malignant fibrous histiocytoma amplified sequence 1 ( MFHAS1) and IGSF4 in over 50% of the squamous cell carcinoma of the vulva cell lines. Paper-13551054.
Northern studies have revealed that FKBP2 is expressed in those tissues predisposed to hyperplasia in MEN1; however, single-strand conformation polymorphism analysis and direct sequencing of DNAs from affected members of MEN1 kindreds and sporadic tumour DNAs have been performed and no mutations have been found. Paper-196581.
A question confronting clinicians is whether they should screen patients with apparently sporadic pheochromocytomas for unsuspected germline mutations of some or all of the seven genes known to cause hereditary paraganglioma or pheochromocytoma ( NF1, VHL, RET, MEN1, SDHD, SDHC, and SDHB). Paper-12081116.
These results suggest that the MEN-1 gene, which plays the role of a tumor suppressor gene in parathyroid tissue, has been localized telomeric to PYGM and centromeric INT2 loci on chromosome 11q13 and that the MEN-1 gene can be a tumor suppressor gene for sporadic parathyroid adenomas. Paper-715521.
In a previous study, we demonstrated that the Men1 gene is mainly expressed in the proliferative crypt compartment of the small intestine and that a reduction of menin expression in the crypt-like IEC-17 cell line induces an increase in proliferation rate concomitant with an increase in cyclin D1 expression. Paper-12898066.
In addition, genetic mouse model studies have indicated that cyclins and cyclin-dependent kinases that determine cell cycle progression are involved in beta cell replication, and more recently, menin in association with cyclin-dependent kinase inhibitors has been demonstrated to be important in beta cell growth. Paper-13552038.
Familial isolated hyperparathyroidism ( FIHP) can result occasionally from the incomplete expression of a syndromic form of familial hyperparathyroidism ( HPT), specifically multiple endocrine neoplasia type 1 ( MEN1), familial hypocalciuric hypercalcemia, or the hyperparathyroidism-jaw tumor syndrome ( HPT-JT). Paper-10392874.
Clonalities were determined using the X-chromosome-linked human androgen receptor ( HUMARA) gene and the phosphoglycerate kinase ( PGK) gene, and multiple endocrine neoplasia type 1 ( MEN1) gene abnormality was analyzed by studying loss of heterozygosity ( LOH) in 11q13 and somatic mutations in the MEN1 gene. Paper-2026907.
However, the 70-kDa subunit ( RPA1) was coprecipitated from HeLa cell extracts along with RPA2 by menin-specific antibodies, suggesting that menin binds to the RPA heterotrimer or a novel RPA1- RPA2-containing complex in vivo. Paper-9684472.
To determine if genes involved in MEN syndromes might play a role in this particular triad, we investigated the presence of somatic or germline mutations in the RET proto-oncogene and menin gene by non isotopic polymerase chain reaction single stranded conformation polymorphism (PCR-SSCP) and heteroduplex gel electro-phoresis. Paper-12318479.
These ordered polymorphic markers will be of help in studying the genes responsible for several diseases that have been localized to this region, including genes responsible for multiple endocrine neoplasia type I ( MEN1), ataxia telangiectasia (AT), tuberous sclerosis ( TSC), and some forms of asthma and rhinitis. Paper-13382.
Interest has focused on Smad3 as a candidate endocrine tumor suppressor gene because 1) it is localized to 15q and 2) it encodes a TGF beta signaling molecule that has been identified as a binding partner of the multiple endocrine neoplasm type 1 gene product menin, itself involved in enteropancreatic and parathyroid neoplasia. Paper-9527560.
We propose that sex cord tumor susceptibility in Men1(+/-) mice involves deregulated cell proliferation due to dysregulation of multiple cell growth regulating genes including: reduced Cdkn2c transcription, loss of TGF-beta pathway tumor suppressor function (e.g., Gata6) and transcriptional activation of Csf1r. Paper-13555718.
Menin has no effect on the known activities of nm23; that is, nucleoside diphosphate kinase, protein kinase, or GTPase-activating protein for Ras-related GTPase Rad. However, we found that menin hydrolyzes GTP to GDP efficiently in the presence of nm23, whereas nm23 or menin alone shows little or no detectable GTPase activity. Paper-9171840.
As far as the possible loss of anti-oncogenes in pituitary tumors is concerned, gene alterations have not been found in the p53 nor in the retinoblastoma gene, while loss of chromosome 11q13 sequences, which contain the deduced location of the yet uncloned MEN-1 gene, has been reported in a subset of GH-secreting adenomas. Paper-8002522.
The cyclin-dependent kinase inhibitor p27 ( CDKN1B) is a downstream target of menin and has been recently shown to be responsible for the multiple endocrine neoplasia-like syndrome in rats, where affected animals develop multiple tumors and hyperplasia in endocrine tissues, including the pancreatic islets of Langerhans. Paper-13396843.
Whether these tumors derive from preexisting endocrine microadenomatosis as in multiple endocrine neoplasia type 1 ( MEN1) is yet unknown. pVHL regulates hypoxia-inducible factor (HIF) that causes transcription activity of target genes like carbonic anhydrase 9 ( CA9), vascular endothelial growth factor ( VEGF), and cyclin D1. Paper-13734457.
In order to shed further light on the MEN-1 syndrome an investigation in vitro was made of parathyroid hormone ( PTH) release of dispersed parathyroid cell from 11 patients with parathyroid hyperplasia associated with MEN-1, 10 patients with single parathyroid adenomas, and 10 preparations of normal bovine parathyroid glands. Paper-5776649.
The idea that multiple endocrine neoplasia type 1 ( MEN-1) tumours in the pancreas originate from multipotent stem cells is supported by our demonstration that CD44 is expressed in exocrine cells, in gastrin-producing endocrine cells only and in some non-functioning islet cell tumours; there are no gastrin-producing cells in the adult pancreas. Paper-806905.
PARATHYROID: In cultured parathyroid cells from uremic hemodialysis patients, in which the menin signaling pathways are probably still intact, menin inactivation achieved by menin antisense oligonucleotides leads to loss of TGF-beta inhibition of parathyroid cell proliferation and parathyroid hormone ( PTH) secretion. Paper-10767346.
Menin, the product of the MEN1 ( multiple endocrine neoplasia type 1) tumor suppressor gene, is involved in activation of gene transcription as part of an MLL1 (mixed-lineage leukemia 1)/MLL2 (KMT2A/B)-containing protein complex which harbors methyltransferase activity for lysine 4 of histone H3 (H3K4). Paper-13955954.
OBJECTIVE: Menin, encoded by the multiple endocrine neoplasia type 1 ( MEN1) gene at 11q13, enhances transcription of the cyclin-dependent kinase inhibitors (CDIs), CDKN2C ( p18) and CDKN1B (p27) in mouse pancreatic islets, and inactivation of menin reduced CDKN2B ( p15) expression in this mouse model. Paper-12694143.
We have evaluated all the measures now available for treating patients with sporadic gastrinomas or gastrinomas associated with Multiple Endocrine Neoplasia Type 1, ( MEN 1) including medical therapy such as antisecretory drugs and somatostatin analogs ( SST), chemotherapy and chemoembolization, and surgical procedures. Paper-11457852.
These synonyms are used for gene MEN1 (multiple endocrine neoplasia I): SCG2, Menin, MEAI.
These accession numbers are used for gene MEN1: Q7Z5Y5 (UNIPROT__AC), AAH02544 (NCBI_GENBANK__AC), AAC51229 (NCBI_GENBANK__AC), A5HBC6 (UNIPROT__AC).
MEN1 is a homologue of Mnn1 (Menin 1) from Drosophila melanogaster.
MEN1 is a homologue of MEN1 (multiple endocrine neoplasia I) from Bos taurus.
MEN1 is a homologue of MEN1 (multiple endocrine neoplasia I) from Pan troglodytes.
MEN1 is a homologue of MEN1 (multiple endocrine neoplasia I) from Canis lupus familiaris.
MEN1 is a homologue of Men1 (multiple endocrine neoplasia 1) from Mus musculus.
MEN1 is a homologue of Men1 (multiple endocrine neoplasia 1) from Rattus norvegicus.
MEN1 is a homologue of men1 (multiple endocrine neoplasia type 1) from Danio rerio.
MEN1 is a homologue of AgaP_AGAP008130 (AGAP008130-PA) from Anopheles gambiae str. PEST.
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