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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The decision to exit from mitosis is a fateful one, and Amon and colleagues have shown that it involves both an early and a late component. The FEAR network initiates the exit machinery, while the previously described MEN pathway maintains it.
Mol Cell 2002 Feb
PMID:The FEAR factor. 1186 93

Although relatively rare, endocrine tumors of the digestive tract and pancreas have been widely investigated and represent a complex tumor entity. The two major categories of well-differentiated and poorly differentiated tumors show important phenotypic and clinical differences. In well-differentiated tumors the multiple endocrine neoplasia syndrome of Type 1 (MEN1) gene is frequently abnormal, though a complex multiple gene involvement is postulated for different tumor types. Poorly differentiated carcinomas show frequent p53 gene hyperexpression/defects, characterizing severe cell abnormality and possibly accounting for the malignancy of such carcinomas.
Expert Rev Mol Diagn 2001 Sep
PMID:Endocrine tumors of the digestive tract and pancreas: histogenesis, diagnosis and molecular basis. 1190 38

Pheochromocytoma cell lines derived from neurofibromatosis knockout mice express high levels of the receptor tyrosine kinase Ret, which is involved in the pathogenesis of human pheochromocytomas in hereditary multiple endocrine neoplasia syndrome type 2 (MEN2). Mouse pheochromocytoma (MPC) cells respond to the Ret-activating ligand GDNF by exhibiting Ret phosphorylation, neurite outgrowth, decreased proliferation, and altered expression of catecholamine biosynthetic enzymes. GDNF exerts similar effects on human pheochromocytoma cells in primary cultures. Ret is minimally expressed by normal mouse chromaffin cells, from which pheochromocytomas are derived. Its expression at high levels by MPC cells suggests possible relationships between two previously unrelated tumor syndromes, neurofibromatosis, and MEN2. The responsiveness of these cells to GDNF suggests that they may be a valuable new model for neurobiology.
Mol Cell Neurosci 2002 Jul
PMID:High-level expression of receptor tyrosine kinase Ret and responsiveness to Ret-activating ligands in pheochromocytoma cell lines from neurofibromatosis knockout mice. 1213 16

Parental imprinting regulates processes as diverse as mammalian development and seed size in crop plants. In Arabidopsis, the DNA glycosylase DEMETER regulates early seed development, through activation of the maternal copy of the imprinted MEDEA Polycomb gene. Paternal silencing of MEA appears to be a default condition.
Mol Cell 2002 Jul
PMID:DEMETER, Goddess of the harvest, activates maternal MEDEA to produce the perfect seed. 1215 Aug 99

Phaeochromocytomas are neoplasias of neural crest origin arising from the adrenal medulla. Extra-adrenal phaeochromocytomas occur and may be referred to as paragangliomas, although this term is also used to describe vascular head and neck tumours, which most commonly develop at the carotid bifurcation. Historically, genetic factors have been implicated in up to 10% of phaeochromocytoma cases, but recent data suggest that germline mutations may be detected in approximately 25% of unselected cases. The most frequent causes of phaeochromocytoma susceptibility are von Hippel-Lindau disease (VHL), multiple endocrine neoplasia type 2 (MEN 2), the newly delineated phaeochromocytoma-paraganglioma syndrome and, less commonly, neurofibromatosis type 1. Germline mutations in three of the succinate dehydrogenase (SDH, mitochondrial complex II) subunits (SDHD, SDHB and SDHC) cause susceptibility to head and neck paragangliomas, and may be found in approximately 20% of unselected patients. In addition, germline SDHD and SDHB mutations may cause phaeochromocytoma susceptibility with or without associated head and neck paragangliomas. Recent studies suggest that germline SDHD and SDHB mutations are an important cause of familial and isolated phaeochromocytoma. The mechanism by which SDH subunit mutations predispose to phaeochromocytomas has not been defined in detail, but dysregulation of hypoxia-responsive genes and impairment of mitochondria-mediated apoptosis have both been suggested.
Hum Mol Genet 2002 Oct 01
PMID:The pressure rises: update on the genetics of phaeochromocytoma. 1235 69

A robust and fast DNA chip method was developed in order to detect the various beta-lactam antibiotic-resistance genes in one slide. These genes included PSE, OXA, FOX, MEN, CMY, TEM, SHV, OXY, and AmpC. beta-lactam antibiotic-resistance genes were labeled with a fluorescent nucleotide by a multiplex polymerase chain reaction using a mixture of specific primer sets for each gene. This labeled target was hybridized with a DNA chip that contained the spots of the specific probe DNAs for each beta-lactam antibiotic-resistance gene. This technique made it possible to detect the specific resistance gene, even in a single bacterium.
Mol Cells 2002 Oct 31
PMID:Development of DNA chip for the simultaneous detection of various beta-lactam antibiotic-resistant genes. 1244 90

Menin is a protein encoded by the gene mutated in multiple endocrine neoplasia type 1 (MEN1) characterized by multiple endocrine tumors of the parathyroid glands, pancreatic islets and the anterior pituitary, especially prolactinoma. In this study, we examined the effects of menin on human prolactin (hPRL) expression. In rat pituitary GH3 cells stably expressing menin, both PRL gene expression/secretion and thymidine incorporation into DNA were inhibited as compared with mock-transfected cells. The transcriptional activity of PRL promoter in GH3 cells co-transfected with menin was significantly decreased. A deletion mutation (569 delC), which we identified in a Japanese MEN1 family, was introduced into menin. When GH3 cells were transfected with a mutant menin expression vector, inhibition of hPRL promoter activity was partially reversed. 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.
J Mol Endocrinol 2002 Dec
PMID:The multiple endocrine neoplasia type 1 gene product, menin, inhibits the human prolactin promoter activity. 1245 32

The aim of this study was to look for common ancestors among MEN 2A Portuguese families presenting with the same germ-line mutation of the RET proto-oncogene. To address this question from a genetic point of view, we performed haplotype analysis in six out of nine, apparently separate, MEN 2A families using four polymorphic markers. Three families carrying the C634R mutation and presenting the same phenotype shared the same haplotype surrounding the MEN 2A mutation. Moreover, these families were originally from the same geographic region although settled at different places along the country. Altogether, data suggested a common ancestral MEN 2A chromosome for three families. Since MEN 2A is a rare inherited cancer syndrome, identification of common ancestors may draw attention for specific geographic regions from where other affected families may arise at a higher chance and, therefore, termed 'hot regions'.
Int J Mol Med 2003 Jan
PMID:MEN 2A families: from hot spots to hot regions. 1246 21

Menin is a 70-kDa protein encoded by MEN1, the tumor suppressor gene disrupted in multiple endocrine neoplasia type 1. In a yeast two-hybrid system based on reconstitution of Ras signaling, menin was found to interact with the 32-kDa subunit (RPA2) of replication protein A (RPA), a heterotrimeric protein required for DNA replication, recombination, and repair. The menin-RPA2 interaction was confirmed in a conventional yeast two-hybrid system and by direct interaction between purified proteins. 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. This region of RPA2 contains a weak single-stranded DNA-binding domain, but menin had no detectable effect on RPA-DNA binding in vitro. Menin bound preferentially in vitro to free RPA2 rather than the RPA heterotrimer or a subcomplex consisting of RPA2 bound to the 14-kDa subunit (RPA3). 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. This finding was consistent with the extensive overlap in the nuclear localization patterns of endogenous menin, RPA2, and RPA1 observed by immunofluorescence.
Mol Cell Biol 2003 Jan
PMID:The 32-kilodalton subunit of replication protein A interacts with menin, the product of the MEN1 tumor suppressor gene. 1250 49

The incidence and mortality of pancreatic adenocarcinoma are nearly coincident having a five-year survival of less than 5%. Enormous advances have been made in our knowledge of the molecular alterations commonly present in ductal cancer and other pancreatic malignancies. One significant outcome of these studies is the recognition that common ductal cancers have a distinct molecular fingerprint compared to other nonductal or endocrine tumors. Ductal carcinomas typically show alteration of K-ras, p53, p16INK4, DPC4 and FHIT, while other pancreatic tumor types show different aberrations. Among those tumors arising from the exocrine pancreas, only ampullary cancers have a molecular fingerprint that may involve some of the same genes most frequently altered in common ductal cancers. Significant molecular heterogeneity also exists among pancreatic endocrine tumors. Nonfunctioning pancreatic endocrine tumors have frequent mutations in MEN-1 and may be further subdivided into two clinically relevant subgroups based on the amount of chromosomal alterations. The present review will provide a brief overview of the genetic alterations that have been identified in the various subgroups of pancreatic tumors. These results have important implications for the development of genetic screening tests, early diagnosis, and prognostic genetic markers.
Mol Cancer 2003 Jan 07
PMID:Genetic abnormalities in pancreatic cancer. 1253 85


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