multiple endocrine neoplasia/hypoxia

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De novo multiple endocrine neoplasia type 2B with noncardiogenic pulmonary edema as the presenting symptom.

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Multiple endocrine neoplasia (MEN) type 2B is a rare hereditary disorder characterized by medullary thyroid carcinoma, pheochromocytoma, and neuroma. Early signs of MEN 2B are usually neuroma, gastrointestinal problems, and medullary thyroid carcinoma. Noncardiogenic pulmonary edema is rare as a

Differential expression of erythropoietin and its receptor in von hippel-lindau-associated and multiple endocrine neoplasia type 2-associated pheochromocytomas.

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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. Previous studies

Distinct gene expression profiles in norepinephrine- and epinephrine-producing hereditary and sporadic pheochromocytomas: activation of hypoxia-driven angiogenic pathways in von Hippel-Lindau syndrome.

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Pheochromocytomas in von Hippel-Lindau (VHL) syndrome produce exclusively norepinephrine, whereas those in multiple endocrine neoplasia type 2 (MEN 2) produce epinephrine. This study examined the pathways activated in VHL-associated pheochromocytomas by comparing gene expression profiles in VHL and

Integrative analysis of neuroblastoma and pheochromocytoma genomics data.

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BACKGROUND Pheochromocytoma and neuroblastoma are the most common neural crest-derived tumors in adults and children, respectively. We have performed a large-scale in silico analysis of altogether 1784 neuroblastoma and 531 pheochromocytoma samples to establish similarities and differences using

[Genetics of neuroendocrine tumours, hereditary tumour syndromes].

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Neuroendocrine tumours occur in some hereditary tumour syndromes, and the molecular pathophysiological mechanisms involved in these are also important in their sporadic counterparts which representing the majority of neuroendocrine tumours. These syndromes include multiple endocrine neoplasia type

Deregulation of genetic pathways in neuroendocrine tumors.

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Complexity and redundancy of functional pathways controlled by the human genome explain that a single type of tumor can be induced by independant defective mutations in various genes that encode proteins acting in different parts of the cell physiology. Neuroendocrine tumors represent a powerful

Menin is a regulator of the stress response in Drosophila melanogaster.

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Menin, the product of the multiple endocrine neoplasia type I gene, has been implicated in several biological processes, including the control of gene expression and apoptosis, the modulation of mitogen-activated protein kinase pathways, and DNA damage sensing or repair. In this study, we have

Menin links the stress response to genome stability in Drosophila melanogaster.

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BACKGROUND The multiple endocrine neoplasia type I gene functions as a tumor suppressor gene in humans and mouse models. In Drosophila melanogaster, mutants of the menin gene (Mnn1) are hypersensitive to mutagens or gamma irradiation and have profound defects in the response to several stresses

Differential gene expression of p27Kip1 and Rb knockout pituitary tumors associated with altered growth and angiogenesis.

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Mice lacking the p27Kip1 Cdk inhibitor, like mice lacking Rb, develop pituitary tumors involving pars intermedia melanotrophs, yet p27(Kip1) tumors are genetically distinct from Rb derived tumors as they exhibit haploid insufficiency. We compared tumors from mice with p27( Kip1) constitutive and

Multiple microvascular alterations in pancreatic islets and neuroendocrine tumors of a Men1 mouse model.

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Vascular therapeutic targeting requires thorough evaluation of the mechanisms activated in the specific context of each particular tumor type. We highlight structural, molecular, and functional microvascular aberrations contributing to development and maintenance of pancreatic neuroendocrine tumors

15 YEARS OF PARAGANGLIOMA: Pheochromocytoma, paraganglioma and genetic syndromes: a historical perspective.

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The last decades have elucidated the genetic basis of pheochromocytoma (PC) and paraganglioma (PGL) (PCPGL)-associated hereditary syndromes. However, the history of these syndromes dates back at least another 150 years. Detailed descriptions by clinicians and pathologists in the 19th and 20th

18F-FDG avidity of pheochromocytomas and paragangliomas: a new molecular imaging signature?

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Our objective was to evaluate (18)F-FDG PET uptake in patients with nonmetastatic and metastatic chromaffin-derived tumors. METHODS Twenty-eight consecutive unrelated patients with chromaffin tumors, including 9 patients with genetically determined disease, were studied. A combination of

PRECISION MEDICINE: AN UPDATE ON GENOTYPE/BIOCHEMICAL PHENOTYPE RELATIONSHIPS IN PHEOCHROMOCYTOMA/PARAGANGLIOMA PATIENTS.

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OBJECTIVE Pheochromocytomas and paragangliomas (PPGLs) are rare neuroendocrine tumors known to produce and secrete high levels of circulating catecholamines and their metabolites. The biochemical characteristics of these tumors can be used to divide them into three major phenotypes. The adrenergic,

The pressure rises: update on the genetics of phaeochromocytoma.

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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

Pancreatic endocrine microadenomatosis in patients with von Hippel-Lindau disease: characterization by VHL/HIF pathway proteins expression.

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BACKGROUND Von Hippel-Lindau (VHL) disease is an inherited syndrome caused by germline mutation in the VHL tumor suppressor gene predisposing to pancreatic endocrine tumors (PET). Whether these tumors derive from preexisting endocrine microadenomatosis as in multiple endocrine neoplasia type 1

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