References of "Beckers, Albert"
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See detailProlactinomes résistants aux dopaminergiques
Beckers, Albert ULg

Scientific conference (2011, May 27)

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See detailBilan d'une masse hypophysaire non fonctionnelle
Beckers, Albert ULg

Scientific conference (2011, May 13)

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See detailLes maladies thyroïdiennes
Beckers, Albert ULg

Scientific conference (2011, April 26)

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See detailTo whom to offer genetic analysis in patients with pituitary adenoma ?
Beckers, Albert ULg

Scientific conference (2011, April)

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See detailHuman anti-animal antibodies interference in the Siemens Immulite chemiluminescent insulin immuno-assay: about one case
Cavalier, Etienne ULg; Huberty, Véronique; Carlisi, Ignazia ULg et al

in Clinica Chimica Acta (2011), 412(7-8), 668-669

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See detailTreatment outcomes in selected clinical conditions : Hot topics - Familial acromegaly
Beckers, Albert ULg

Scientific conference (2011, March 11)

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See detailNueva mutacion de AIP en adenomas hipofisarios familiares (FIPA)
Bilbao, I.; Daly, A. F.; Alvarez Coca, M. et al

in Abstract book - XIV congreso de la Sociedad de Endocrinologia, diabetes y nutricion de Euskadi (2011, March)

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See detailLes agonistes dopaminergiques peuvent-ils "guérir" un prolactinome ?
Beckers, Albert ULg

Scientific conference (2011, February 05)

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See detailAdénome hypophysaire
VROONEN, Laurent ULg; Beckers, Albert ULg

in Revue du Praticien (La) (2011)

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See detailDrospirenone and interference with renin-antiotensin system
VROONEN, Laurent ULg; Cavalier, Etienne ULg; Vranken, Laura ULg et al

in Annales d'Endocrinologie - 28ème congrès de la société Française d'Endocrinologie (2011)

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See detailInfluence of drospirenone on renin-angiotensin-aldosterone system evaluation
VROONEN, Laurent ULg; Cavalier, Etienne ULg; Vranken, Laura ULg et al

in Endocrine Abstracts - 13th European Congress of Endocrinology (2011)

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See detailGenetic screening for AIP mutations in Young patients with sporadic and Familial Pituitary Macroadenomas
Yaneva, M.; Elenkova, A.; Daly, Adrian ULg et al

in Endocrinologia = Endokrinologiia (2011), 16(1), 41-48

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See detailGenetic causes of familial pituitary adenomas
Vandeva, Silvia; Zacharieva, S.; Daly, Adrian ULg et al

in Growth Hormone Related Diseases and Therapy - Contemporary Endocrinology (2011)

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See detailHigh prevalence of AIP gene mutations following focused screening in young patients with sporadic pituitary macroadenomas.
Tichomirowa, Maria A; Barlier, Anne; Daly, Adrian ULg et al

in European Journal of Endocrinology (2011), 165(4), 509-15

BACKGROUND: Aryl hydrocarbon receptor interacting protein (AIP) mutations (AIPmut) cause aggressive pituitary adenomas in young patients, usually in the setting of familial isolated pituitary adenomas ... [more ▼]

BACKGROUND: Aryl hydrocarbon receptor interacting protein (AIP) mutations (AIPmut) cause aggressive pituitary adenomas in young patients, usually in the setting of familial isolated pituitary adenomas. The prevalence of AIPmut among sporadic pituitary adenoma patients appears to be low; studies have not addressed prevalence in the most clinically relevant population. Hence, we undertook an international, multicenter, prospective genetic, and clinical analysis at 21 tertiary referral endocrine departments. METHODS: We included 163 sporadic pituitary macroadenoma patients irrespective of clinical phenotype diagnosed at <30 years of age. RESULTS: Overall, 19/163 (11.7%) patients had germline AIPmut; a further nine patients had sequence changes of uncertain significance or polymorphisms. AIPmut were identified in 8/39 (20.5%) pediatric patients. Ten AIPmut were identified in 11/83 (13.3%) sporadic somatotropinoma patients, in 7/61 (11.5%) prolactinoma patients, and in 1/16 non-functioning pituitary adenoma patients. Large genetic deletions were not seen using multiplex ligation-dependent probe amplification. Familial screening was possible in the relatives of seven patients with AIPmut and carriers were found in six of the seven families. In total, pituitary adenomas were diagnosed in 2/21 AIPmut-screened carriers; both had asymptomatic microadenomas. CONCLUSION: Germline AIPmut occur in 11.7% of patients <30 years with sporadic pituitary macroadenomas and in 20.5% of pediatric patients. AIPmut mutation testing in this population should be considered in order to optimize clinical genetic investigation and management. [less ▲]

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See detailAcromégalie et apnées du sommeil : évaluations céphalométriques
BRUWIER, Annick ULg; Albert, Adelin ULg; Beckers, Albert ULg et al

in Annales d'Endocrinologie (2011)

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See detailUne nouvelle forme d'adénomes hypophysaires familiaux : les FIPA-Détection et prise en charge
Beckers, Albert ULg; PETROSSIANS, Patrick ULg; Auriemma, R. S. et al

in Correspondances en MHDN (2011)

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See detailResistant prolactinomas
Vasilev, V.; Daly, Adrian ULg; VROONEN, Laurent ULg et al

in Journal of Endocrinological Investigation (2011), 34

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See detailHyperplasia-adenoma sequence in pituitary tumorigenesis related to aryl hydrocarbon receptor interacting protein gene mutation.
Villa, C.; Lagonigro, M. S.; Magri, F. et al

in Endocrine-Related Cancer (2011)

Mutations of the aryl hydrocarbon receptor interacting protein (AIP) gene are associated with pituitary adenomas that usually occur as familial isolated pituitary adenomas (FIPA). Detailed pathological ... [more ▼]

Mutations of the aryl hydrocarbon receptor interacting protein (AIP) gene are associated with pituitary adenomas that usually occur as familial isolated pituitary adenomas (FIPA). Detailed pathological and tumor genetic data on AIP mutation-related pituitary adenomas are scarce. Non-identical twin females presented as adolescents to the emergency department with severe progressive headaches caused by large pituitary macroadenomas requiring emergency neurosurgery; one patient had incipient pituitary apoplexy. Post-surgically the patients were found to have silent somatotrope adenomas on pathological examination. Furthermore, the light microscopic, immunohistochemical and electron microscopic studies demonstrated tumors of virtually identical characteristics. The adenomas were accompanied by multiple areas of pituitary hyperplasia, which stained positively for growth hormone, indicating somatotrope hyperplasia. Genetic analyses of the FIPA kindred revealed a novel E216X mutation of the AIP gene, which was present in both affected patients and the unaffected father. Molecular analysis of surgical specimens revealed loss of heterozygosity (LOH) in the adenoma, but showed that LOH was not present in the hyperplasic pituitary tissue from either patient. AIP immunostaining confirmed normal staining in the hyperplastic tissue and decreased staining in the adenoma in the tumors from both patients. These results demonstrate that patients with AIP germline mutation can present with clinically silent somatotroph pituitary adenomas. The finding of somatotrope hyperplasia unaccompanied by AIP LOH, suggests that LOH at the AIP locus may be a late event in the progression from hyperplastic to adenomatous tissue. [less ▲]

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See detailGenetic susceptibility in pituitary adenomas : from pathogenesis to clinical implications
Jaffrain-Rea, Marie-Lise; Daly, Adrian ULg; Angelini, Mariolina et al

in Expert Review of Endocrinology & Metabolism (2011)

Pituitary adenomas (PA) usually present sporadically, with a multifactorial pathogenesis including somatic mutational events in cancer-related genes. Genetic predisposition implies the presence of ... [more ▼]

Pituitary adenomas (PA) usually present sporadically, with a multifactorial pathogenesis including somatic mutational events in cancer-related genes. Genetic predisposition implies the presence of germline DNA alterations with a variety of impacts on pituitary cell biology, translating into a variable penetrance of the disease. Genetic causes must be considered in the presence of specific clinical settings, such as familial occurrence of PA, with or without extrapituitary diseases, and may also be suspected in young patients with macroadenomas. We <br />review the clinical implications of genetic predisposition, with special attention to Multiple Endocrine Neoplasia type 1 (MEN1), Carney’s complex (CNC) and FIPA (Familial Isolated Pituitary Adenoma), and the scenario of genetic screening in selected patients with an apparently sporadic disease is discussed. [less ▲]

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See detailMutations of calcium-sensing receptor gene: two novel mutations and overview of impact on calcium homeostasis
Livadariu, E.; Auriemma, R. S.; Rydlewski, C. et al

in European Journal of Endocrinology (2011)

Objective: Genetic disorders of calcium metabolism arise in a familial or sporadic setting. The calcium-sensing receptor (CaSR) plays a key role in maintaining calcium homeostasis and study of the CASR ... [more ▼]

Objective: Genetic disorders of calcium metabolism arise in a familial or sporadic setting. The calcium-sensing receptor (CaSR) plays a key role in maintaining calcium homeostasis and study of the CASR gene can be clinically useful in determining etiology and appropriate therapeutic approaches. We report two cases of novel CASR gene mutations that illustrate the varying clinical presentations and discuss these in terms of the current understanding of CaSR function. Patients and Methods: A 16 yr-old patient had mild hypercalcemia associated with low-normal urinary calcium excretion and normal-to-high parathyroid hormone (PTH) levels. Because of negative family history, familial hypocalciuric hypercalcemia (FHH) was originally excluded. The second patient was a 54 yr-old man with symptomatic hypocalcemia, hyperphosphatemia, low PTH, and mild hypercalciuria. Familial investigation revealed the same phenotype in the patient's sister. The coding region of the CaSR gene was sequenced in both probands and their available first-degree relatives. Results: The first patient had a novel heterozygous inactivating CASR mutation in exon 4, which predicted a p.A423K change; genetic analysis was negative in the parents. The second patient had a novel heterozygous activating CASR mutation in exon 6, which predicted a p.E556K change; the affected sister of the proband was also positive. Conclusions: We reported two novel heterozygous mutations of the CASR gene, an inactivating mutation in exon 4 and the first activating mutation reported to date in exon 6. These cases illustrate the importance of genetic testing of CASR gene to aid correct diagnosis and to assist in clinical management. [less ▲]

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