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multiple endocrine neoplasia type 1/tyrosine
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A new mutation in the menin gene causes the multiple endocrine neoplasia type 1 syndrome with adrenocortical carcinoma.
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Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant tumor syndrome that may be caused by mutations in the MEN1 gene on 11q13. Loss of function of the tumor suppressor gene MEN1 leads to synchronous or metachronous appearance of neuroendocrine tumors arising from neuroendocrine cells
Genetic aspects of multiple endocrine neoplasia types 1 and 2.
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Multiple endocrine neoplasia (MEN) type 1 is an autosomal, dominantly inherited predisposition to develop neoplastic lesions of the parathyroid glands, the neuroendocrine pancreas-duodenum, and the anterior pituitary. The genetic defect was mapped to the centromeric part of the long arm of
Multiple endocrine neoplasia type 1 (MEN1) and type 4 (MEN4).
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Multiple endocrine neoplasia (MEN) is characterized by the occurrence of tumors involving two or more endocrine glands within a single patient. Four major forms of MEN, which are autosomal dominant disorders, are recognized and referred to as: MEN type 1 (MEN1), due to menin mutations; MEN2
Multiple endocrine neoplasia type 1 and 2: from morphology to molecular pathology 1997.
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Multiple Endocrine Neoplasia (MEN) is an inherited syndrome which appears in two major forms referred to as type 1 (MEN-1) and type 2 (MEN-2). MEN-1 is characterized by the occurrence of neuroendocrine parathyroid, pancreas, duodenum and pituitary lesions. In addition to these tumors adrenocortical,
Molecular pathology and genetics of pancreatic endocrine tumours.
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Pancreatic neuroendocrine tumours (PETs) are the second most frequent pancreatic neoplasms. Their poor chemosensitivity, high rate of metastatic disease and relatively long survival make PETs an ideal field to be explored for novel therapies based on specific molecular changes. PETs are generally
Menin represses malignant phenotypes of melanoma through regulating multiple pathways.
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Substantial genetic evidence suggests that chromosome 11q is involved in regulating initiation and progression of malignant melanomas. Mutations of the MEN1 gene, located in chromosome 11q13, predispose individuals to the multiple endocrine neoplasia type 1 (MEN1) familial syndrome. MEN1 patients
[Multiple endocrine neoplasia: genetic aspects].
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Multiple endocrine neoplasia type 1 (MEN1) and type 2 (MEN2) are major genetic disorders carrying a high risk of endocrine tumor development. The mutated genes were identified in 1993 (MEN2-RET) and 1997 (MEN1), enabling genetic testing and functional studies. Genetic analysis has led to new
Biological aspects of neuroendocrine gastro-enteropancreatic tumours.
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Carcinoid tumours may develop from enterochromaffin cells in the gastrointestinal tract. Benign insulin-producing tumours may develop from islet cells, whereas other islet cell tumours might derive from multipotent stem cells in the pancreatic ducts. The idea that multiple endocrine neoplasia type 1
The gene causing multiple endocrine neoplasia type 2 (MEN 2).
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Multiple endocrine neoplasia (MEN) types 1 and 2 are distinct dominantly inherited syndromes of cancer predisposition in man. MEN 1 involves the parathyroids, pituitary, and pancreatic islets; MEN 2 involves the thyroid C-cells, adrenal medulla and parathyroids. In some varieties of MEN 2 there are
Two novel mutations in the MEN1 gene in subjects with multiple endocrine neoplasia-1.
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Multiple endocrine neoplasia type 1 (MEN1) is characterized by parathyroid, enteropancreatic endocrine and pituitary adenomas as well as germline mutation of the MEN1 gene. We describe 2 families with MEN1 with novel mutations in the MEN1 gene. One family was of Turkish origin, and the index patient
Identification of two novel isoforms of the ZNF162 gene: a growing family of signal transduction and activator of RNA proteins.
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By differential screening of a cDNA library obtained from a GM-CSF-dependent human myeloid leukemia cell line (GF-D8), we identified two novel isoforms of the recently described ZNF162 gene, which is apparently linked to multiple endocrine neoplasia type 1. The shorter of these new isoforms, called
[Multiple endocrine neoplasia (MEN)].
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OBJECTIVE
Multiple endocrine neoplasia (MEN) types 1 and 2 are hereditary cancer syndromes. They are characterized by the occurrence of many benign and malignant tumor types.
METHODS
Carriers of a MEN1 or RET gene mutation can be identified before manifestation of the disease. Family screening
FGF receptor signaling at the crossroads of endocrine homeostasis and tumorigenesis.
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Multiple endocrine neoplasia (MEN) syndromes represent familial disorders characterized by endocrine cell growth and hormone production dysregulation. For several decades, the fibroblast growth factor (FGF) system has been suspected of playing a unique function in MEN-type I (MEN I). However,
Pharmacotherapy of Zollinger-Ellison syndrome.
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BACKGROUND
The role of pharmacotherapy in the management of patients with Zollinger-Ellison syndrome (ZES) is often equated with the medical management of acid hypersecretion. However, pharmacotherapy is also increasingly involved in the other management areas of these patients.
METHODS
This paper
Lung cancer cell migration is regulated via repressing growth factor PTN/RPTP β/ζ signaling by menin.
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Menin encoded by the multiple endocrine neoplasia type 1 (MEN1) gene is associated with chromatin and the nuclear matrix and exerts multiple biological functions including regulation of cell proliferation and adhesion. Men1 mutations increase the likelihood of lung cancer development in mice. Menin
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