The Experts below are selected from a list of 312 Experts worldwide ranked by ideXlab platform
Alfredo Quinones-hinojosa - One of the best experts on this subject based on the ideXlab platform.
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Expression of the Pituitary stem/progenitor marker GFRα2 in human Pituitary adenomas and normal Pituitary
Pituitary, 2015Co-Authors: Nestoras Mathioudakis, Ram Sundaresh, Alexandra Larsen, William Ruff, Jennifer Schiller, Hugo Guerrero-cazares, Roberto Salvatori, Peter Burger, Alfredo Quinones-hinojosaAbstract:Purpose Recent studies suggest that adult Pituitary stem cells may play a role in Pituitary tumorigenesis. We sought to explore whether the Glial cell-line derived neurotrophic factor receptor alpha 2 (GFRα2), a recently described Pituitary stem/progenitor marker, might be differentially expressed in Pituitary adenomas versus normal Pituitary. Methods The expression of GFRα2 and other members of the GFR receptor family (GFRα1, α3, α4) were analyzed using RT-PCR, western blot, and immunohistochemistry in 39 Pituitary adenomas, 14 normal Pituitary glands obtained at autopsy, and cDNA from 3 normal pituitaries obtained commercially. Results GFRα2 mRNA was ~2.6 fold under-expressed in functioning adenomas ( p
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Expression of the Pituitary stem/progenitor marker GFRα2 in human Pituitary adenomas and normal Pituitary.
Pituitary, 2014Co-Authors: Nestoras Mathioudakis, Ram Sundaresh, Alexandra Larsen, William Ruff, Jennifer Schiller, Hugo Guerrero-cazares, Peter C. Burger, Roberto Salvatori, Alfredo Quinones-hinojosaAbstract:Purpose Recent studies suggest that adult Pituitary stem cells may play a role in Pituitary tumorigenesis. We sought to explore whether the Glial cell-line derived neurotrophic factor receptor alpha 2 (GFRα2), a recently described Pituitary stem/progenitor marker, might be differentially expressed in Pituitary adenomas versus normal Pituitary.
Nestoras Mathioudakis - One of the best experts on this subject based on the ideXlab platform.
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Expression of the Pituitary stem/progenitor marker GFRα2 in human Pituitary adenomas and normal Pituitary
Pituitary, 2015Co-Authors: Nestoras Mathioudakis, Ram Sundaresh, Alexandra Larsen, William Ruff, Jennifer Schiller, Hugo Guerrero-cazares, Roberto Salvatori, Peter Burger, Alfredo Quinones-hinojosaAbstract:Purpose Recent studies suggest that adult Pituitary stem cells may play a role in Pituitary tumorigenesis. We sought to explore whether the Glial cell-line derived neurotrophic factor receptor alpha 2 (GFRα2), a recently described Pituitary stem/progenitor marker, might be differentially expressed in Pituitary adenomas versus normal Pituitary. Methods The expression of GFRα2 and other members of the GFR receptor family (GFRα1, α3, α4) were analyzed using RT-PCR, western blot, and immunohistochemistry in 39 Pituitary adenomas, 14 normal Pituitary glands obtained at autopsy, and cDNA from 3 normal pituitaries obtained commercially. Results GFRα2 mRNA was ~2.6 fold under-expressed in functioning adenomas ( p
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Expression of the Pituitary stem/progenitor marker GFRα2 in human Pituitary adenomas and normal Pituitary.
Pituitary, 2014Co-Authors: Nestoras Mathioudakis, Ram Sundaresh, Alexandra Larsen, William Ruff, Jennifer Schiller, Hugo Guerrero-cazares, Peter C. Burger, Roberto Salvatori, Alfredo Quinones-hinojosaAbstract:Purpose Recent studies suggest that adult Pituitary stem cells may play a role in Pituitary tumorigenesis. We sought to explore whether the Glial cell-line derived neurotrophic factor receptor alpha 2 (GFRα2), a recently described Pituitary stem/progenitor marker, might be differentially expressed in Pituitary adenomas versus normal Pituitary.
Shlomo Melmed - One of the best experts on this subject based on the ideXlab platform.
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Pathogenesis of Pituitary tumors.
Progress in Brain Research, 2020Co-Authors: Run Yu, Shlomo MelmedAbstract:Pituitary tumors are common and mostly benign neoplasia which cause excess or deficiency of Pituitary hormones and compressive damage to adjacent organs. Oncogene activation [e.g. PTTG (Pituitary tumor-transforming gene) and HMGA2], tumor suppressor gene inactivation (e.g. MEN1 and PRKAR1A), epigenetic changes (e.g. methylation) and humoral factors (e.g. ectopic production of stimulating hormones) are all possible Pituitary tumor initiators; the micro-environment of Pituitary tumors including steroid milieu, angiogenesis and abnormal cell adhesion further promote tumor growth. Senescence, a cellular defence mechanism against malignant transformation, may explain the benign nature of at least some Pituitary tumors. We suggest that future research on Pituitary tumor pathogenesis should incorporate systems approaches, and address regulatory mechanisms for Pituitary cell proliferation, development of new animal models of Pituitary tumor and isolation of functional human Pituitary tumor cell lines.
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Etiology of Pituitary Tumours
Pituitary Disease, 2020Co-Authors: Anthony P. Heaney, Shlomo MelmedAbstract:Pituitary adenomas account for ≈10% of all clinical presentations with primary intracerebral tumors (1), are found incidentally in 3–27% of autopsies (2,3), and a further 10% of asymptomatic adults harbor Pituitary adenomas (4), making Pituitary adenomas the most common tumor in the central nervous system. This apparent vulnerability of the Pituitary gland to neoplastic change is somewhat at odds with the closely regulated, highly specialized cellular phenotypes, which characterize the anterior Pituitary. However, recent advancement in our understanding of the molecular mechanisms involved in Pituitary tumorigenesis suggest that the same highly specific hormones, growth factors and cytokines derived from intra-and extra-Pituitary sites, but under tight hypothalamic-Pituitary control, may contribute to pituicyte transformation.
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Senescence Mediates Pituitary Hypoplasia and Restrains Pituitary Tumor Growth
Cancer Research, 2007Co-Authors: Vera Chesnokova, Run Yu, Kalman Kovacs, Svetlana Zonis, Kolja Wawrowsky, Tami Rubinek, Anat Ben-shlomo, Shlomo MelmedAbstract:Understanding factors subserving Pituitary cell proliferation enables understanding mechanisms underlying uniquely benign Pituitary tumors. Pituitary tumor-transforming gene ( Pttg ) deletion results in Pituitary hypoplasia, low Pituitary cell proliferation rates, and rescue of Pituitary tumor development in Rb +/− mice. Pttg −/− Pituitary glands exhibit ARF/p53/p21-dependent senescence pathway activation evidenced by up-regulated p19, cyclin D1, and Bcl-2 protein levels and p53 stabilization. High Pituitary p21 levels in the absence of PTTG were associated with suppressed cyclin-dependent kinase 2 activity, Rb phosphorylation, and cyclin A expression, all required for cell cycle progression. Although senescence-associated β-galactosidase was enhanced in Pttg -deficient Pituitary glands, telomere lengths were increased. DNA damage signaling pathways were activated and aneuploidy was evident in the Pttg -deficient Pituitary, triggering senescence-associated genes. To confirm the p21 dependency of decreased proliferation and senescence in the Pttg -null Pituitary, mouse embryonic fibroblast (MEF) colony formation was tested in wild-type, Pttg −/− , Rb +/− , Rb +/− Pttg −/− , and Rb +/− Pttg −/− p21 −/− cells. Rb +/− Pttg −/− MEFs, unlike Rb +/− cells, failed to produce colonies and exhibited high levels of senescence. p21 deletion from Rb +/− Pttg −/− MEFs enhanced anchorage-independent cell growth, accompanied by a marked decrease in senescence. As cell proliferation assessed by bromodeoxyuridine incorporation was higher in Rb +/− Pttg −/− p21 −/− relative to Rb +/− Pttg −/− Pituitary glands, p21-dependent senescence provoked by Pttg deletion may underlie Pituitary hypoplasia and decreased tumor development in Rb +/− Pttg −/− mice. [Cancer Res 2007;67(21):10564–72]
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Pituitary tumor transforming gene overexpression facilitates Pituitary tumor development.
Endocrinology, 2006Co-Authors: Ines Donangelo, Kalman Kovacs, Shiri Gutman, Eva Horvath, Kolja Wawrowsky, Michael Mount, Shlomo MelmedAbstract:Intrinsic and extrinsic stimuli result in profound Pituitary growth changes ranging from hypoplasia to hyperplasia. Pituitary tumor transforming gene (PTTG) abundance correlates with Pituitary trophic status. Mice with Pttg inactivation exhibit Pituitary hypoplasia, whereas targeted Pituitary PTTG overexpression driven by α-subunit glycoprotein (αGSU) promoter results in focal Pituitary hyperplasia. To test the impact of Pituitary hyperplasia on tumor development, we crossbred αGSU.PTTG with Rb+/− mice, which develop Pituitary tumors with high penetrance. Pituitary glands of resulting bitransgenic αGSU.PTTGxRb+/− mice were compared with monotransgenic αGSU.PTTG, Rb+/−, and wild-type mice. Confocal microscopy showed that PTTG-overexpressing cells have enlarged nuclei and marked redistribution of chromatin, and electron microscopy of αGSU.PTTG pituitaries showed enlarged gonadotrophs with prominent Golgi complexes and numerous secretory granules. These morphological findings were even more remarkable in αGS...
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Pituitary Hypoplasia in Pttg−/− Mice Is Protective for Rb+/− Pituitary Tumorigenesis
Molecular Endocrinology, 2005Co-Authors: Vera Chesnokova, Kalman Kovacs, Anna-valeria Castro, Svetlana Zonis, Shlomo MelmedAbstract:Pituitary tumor transforming gene (Pttg) is induced in Pituitary tumors and associated with increased tumor invasiveness. Pttg-null mice do not develop tumors, but exhibit Pituitary hypoplasia, whereas mice heterozygous for the retinoblastoma (Rb) deletion develop Pituitary tumors with high penetrance. Pttg-null mice were therefore cross-bred with Rb+/− mice to test the impact of Pituitary hypoplasia on tumor development. Before tumor development, Rb+/−Pttg−/− mice have smaller Pituitary glands with fewer cycling Pituitary cells and exhibit induction of Pituitary p21 levels. Pttg silencing in vitro with specific short hairpin interfering RNA in AtT20 mouse corticotrophs led to a marked induction of p21 mRNA and protein levels, decreased RB phosphorylation, and subsequent 24% decrease in S-phase cells. Eighty-six percent of Rb+/−Pttg+/+ mice develop Pituitary adenomas by 13 months, in contrast to 30% of double-crossed Rb+/−Pttg−/− animals (P < 0.01). Pituitary hypoplasia, associated with suppressed cell pr...
Roberto Salvatori - One of the best experts on this subject based on the ideXlab platform.
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Expression of the Pituitary stem/progenitor marker GFRα2 in human Pituitary adenomas and normal Pituitary
Pituitary, 2015Co-Authors: Nestoras Mathioudakis, Ram Sundaresh, Alexandra Larsen, William Ruff, Jennifer Schiller, Hugo Guerrero-cazares, Roberto Salvatori, Peter Burger, Alfredo Quinones-hinojosaAbstract:Purpose Recent studies suggest that adult Pituitary stem cells may play a role in Pituitary tumorigenesis. We sought to explore whether the Glial cell-line derived neurotrophic factor receptor alpha 2 (GFRα2), a recently described Pituitary stem/progenitor marker, might be differentially expressed in Pituitary adenomas versus normal Pituitary. Methods The expression of GFRα2 and other members of the GFR receptor family (GFRα1, α3, α4) were analyzed using RT-PCR, western blot, and immunohistochemistry in 39 Pituitary adenomas, 14 normal Pituitary glands obtained at autopsy, and cDNA from 3 normal pituitaries obtained commercially. Results GFRα2 mRNA was ~2.6 fold under-expressed in functioning adenomas ( p
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Detection of Pituitary antibodies by immunofluorescence: approach and results in patients with Pituitary diseases.
The Journal of Clinical Endocrinology and Metabolism, 2014Co-Authors: Adriana Ricciuti, Roberto Salvatori, Alessandra De Remigis, Melissa A. Landek-salgado, Ludovica De Vincentiis, Federica Guaraldi, Isabella Lupi, Shintaro Iwama, Gary S. Wand, Patrizio CaturegliAbstract:Context: Pituitary antibodies have been measured mainly to identify patients whose disease is caused or sustained by Pituitary-specific autoimmunity. Although reported in over 100 publications, they have yielded variable results and are thus considered of limited clinical utility. Objectives: Our objectives were to analyze all publications reporting Pituitary antibodies by immunofluorescence for detecting the major sources of variability, to experimentally test these sources and devise an optimized immunofluorescence protocol, and to assess prevalence and significance of Pituitary antibodies in patients with Pituitary diseases. Study Design and Outcome Measures: We first evaluated the effect of Pituitary gland species, section fixation, autofluorescence quenching, blockade of unwanted antibody binding, and use of purified IgG on the performance of this antibody assay. We then measured cross-sectionally the prevalence of Pituitary antibodies in 390 Pituitary cases and 60 healthy controls, expressing result...
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Expression of the Pituitary stem/progenitor marker GFRα2 in human Pituitary adenomas and normal Pituitary.
Pituitary, 2014Co-Authors: Nestoras Mathioudakis, Ram Sundaresh, Alexandra Larsen, William Ruff, Jennifer Schiller, Hugo Guerrero-cazares, Peter C. Burger, Roberto Salvatori, Alfredo Quinones-hinojosaAbstract:Purpose Recent studies suggest that adult Pituitary stem cells may play a role in Pituitary tumorigenesis. We sought to explore whether the Glial cell-line derived neurotrophic factor receptor alpha 2 (GFRα2), a recently described Pituitary stem/progenitor marker, might be differentially expressed in Pituitary adenomas versus normal Pituitary.
Ram Sundaresh - One of the best experts on this subject based on the ideXlab platform.
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Expression of the Pituitary stem/progenitor marker GFRα2 in human Pituitary adenomas and normal Pituitary
Pituitary, 2015Co-Authors: Nestoras Mathioudakis, Ram Sundaresh, Alexandra Larsen, William Ruff, Jennifer Schiller, Hugo Guerrero-cazares, Roberto Salvatori, Peter Burger, Alfredo Quinones-hinojosaAbstract:Purpose Recent studies suggest that adult Pituitary stem cells may play a role in Pituitary tumorigenesis. We sought to explore whether the Glial cell-line derived neurotrophic factor receptor alpha 2 (GFRα2), a recently described Pituitary stem/progenitor marker, might be differentially expressed in Pituitary adenomas versus normal Pituitary. Methods The expression of GFRα2 and other members of the GFR receptor family (GFRα1, α3, α4) were analyzed using RT-PCR, western blot, and immunohistochemistry in 39 Pituitary adenomas, 14 normal Pituitary glands obtained at autopsy, and cDNA from 3 normal pituitaries obtained commercially. Results GFRα2 mRNA was ~2.6 fold under-expressed in functioning adenomas ( p
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Expression of the Pituitary stem/progenitor marker GFRα2 in human Pituitary adenomas and normal Pituitary.
Pituitary, 2014Co-Authors: Nestoras Mathioudakis, Ram Sundaresh, Alexandra Larsen, William Ruff, Jennifer Schiller, Hugo Guerrero-cazares, Peter C. Burger, Roberto Salvatori, Alfredo Quinones-hinojosaAbstract:Purpose Recent studies suggest that adult Pituitary stem cells may play a role in Pituitary tumorigenesis. We sought to explore whether the Glial cell-line derived neurotrophic factor receptor alpha 2 (GFRα2), a recently described Pituitary stem/progenitor marker, might be differentially expressed in Pituitary adenomas versus normal Pituitary.
