References of "Beckers, Albert"
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See detailLe syndrome de Klinefelter : actualités cliniques et thérapeutiques
VALDES SOCIN, Hernan Gonzalo ULiege; Rey, R; COPPENS, Luc ULiege et al

in Vaisseaux, Coeur, Poumons (in press), 24(1),

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See detailCompound heterozygous mutations in the luteinizing hormone receptor signal peptide causing 46,XY disorder of sex development.
NECHIFOR - POTORAC, Iulia ULiege; Trehan, Ashutosh; Szymanska, Kamila et al

in European journal of endocrinology (2019)

Testosterone production by the fetal testis depends on a functional relationship between hCG and the LH/chorionic gonadotrophin receptor (LHCGR). Failure of the receptor to correctly respond to its ligand ... [more ▼]

Testosterone production by the fetal testis depends on a functional relationship between hCG and the LH/chorionic gonadotrophin receptor (LHCGR). Failure of the receptor to correctly respond to its ligand leads to impaired sexual differentiation in males. A phenotypically-female patient with pubertal delay, had a 46,XY karyotype and was diagnosed with 46X,Y disorder of sex development (DSD). Novel compound heterozygous LHCGR mutations were found in the signal peptide: a duplication p.L10_Q17dup of maternal origin, and a deletion (p.K12_L15del) and a p.L16Q missense mutation of paternal origin. cAMP production was very low for both the deletion and duplication mutations and was halved for the missense mutant. The duplication and missense mutations were both expressed intracellularly, but at very low levels at the cell membrane; they were most likely retained in the endoplasmic reticulum. The deletion mutant had a very limited intracellular expression, indicating impaired biosynthesis. There was reduced expression of all three mutants, which was most marked for the deletion mutation. There was also decreased protein expression of all three mutant receptors. In the deletion mutation, the presence of a lower molecular weight band corresponding to LHCGR monomer, probably due to lack of glycosylation, and a lack of bands corresponding to dimers/oligomers suggests absent ER entry. This novel case of 46X,Y DSD illustrates how three different LHCGR signal peptide mutations led to complete receptor inactivation by separate mechanisms. The study underlines the importance of specific regions of signal peptides and expands the spectrum of LHCGR mutations. [less ▲]

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See detailExcellent response to pasireotide therapy in an aggressive and dopamine-resistant prolactinoma.
Coopmans, Eva C.; van Meyel, Sebastiaan W. F.; Pieterman, Kay J. et al

in European journal of endocrinology (2019)

Prolactinomas are the most commonly encountered pituitary adenomas in the clinical setting. While most can be controlled by dopamine agonists, a subset of prolactinomas are dopamine-resistant and very ... [more ▼]

Prolactinomas are the most commonly encountered pituitary adenomas in the clinical setting. While most can be controlled by dopamine agonists, a subset of prolactinomas are dopamine-resistant and very aggressive. In such tumors, the treatment of choice is neurosurgery and radiotherapy, with or without temozolomide. Here, we report a patient with an highly aggressive, dopamine-resistant prolactinoma, who only achieved biochemical and tumor control during pasireotide long-acting release (PAS-LAR) therapy , a second-generation somatostatin receptor ligand (SRL). Interestingly, cystic degeneration, tumor cell necrosis, or both was observed after PAS-LAR administration suggesting an antitumor effect. This case shows that PAS-LAR therapy holds clinical potential in selective aggressive, dopamine-resistant prolactinomas that express somatostatin (SST) receptor subtype 5 and appears to be a potential new treatment option before starting temozolomide. In addition, PAS-LAR therapy may induce cystic degeneration, tumor cell necrosis, or both in prolactinomas. [less ▲]

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See detailHow do they grow so tall
Beckers, Albert ULiege

Scientific conference (2019, May 09)

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See detailWhat is new in Familial Isolated Pituitary Adenomas
BECKERS, Albert ULiege

Scientific conference (2019, March 29)

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See detailAIP and MEN1 mutations and AIP immunohistochemistry in pituitary adenomas in a tertiary referral center.
Daly, Adrian ULiege; Cano, David A.; Venegas, Eva et al

in Endocrine Connections (2019)

BACKGROUND: Pituitary adenomas have a high disease burden due to tumor growth/invasion and disordered hormonal secretion. Germline mutations in genes such as MEN1 and AIP are associated with early onset ... [more ▼]

BACKGROUND: Pituitary adenomas have a high disease burden due to tumor growth/invasion and disordered hormonal secretion. Germline mutations in genes such as MEN1 and AIP are associated with early onset of aggressive pituitary adenomas that can be resistant to medical therapy. AIMS: We performed a retrospective screening study using published risk criteria to assess the frequency of AIP and MEN1 mutations in pituitary adenoma patients in a tertiary-referral center. METHODS: Pituitary adenoma patients with pediatric/adolescent onset, macroadenomas occurring </=30 years of age, familial isolated pituitary adenoma (FIPA) kindreds, and acromegaly or prolactinoma cases that were uncontrolled by medical therapy were studied genetically. We also assessed whether immunohistochemical staining for AIP (AIP-IHC) in somatotropinomas was associated with somatostatin analogs (SSA) response. RESULTS: Fifty-five patients met the study criteria and underwent genetic screening for AIP/MEN1 mutations. No mutations were identified and large deletions/duplications were ruled out using MLPA. In a cohort of sporadic somatotropinomas, low AIP-IHC tumors were significantly larger (p=0.002) and were more frequently sparsely-granulated (p=0.046) than high AIP-IHC tumors. No significant relationship between AIP-IHC and SSA responses was seen. CONCLUSIONS: Germline mutations in AIP/MEN1 in pituitary adenoma patients are rare and the use of published risk criteria did not identify cases in a large tertiary-referral setting. In acromegaly, low AIP-IHC was related to larger tumor size and more frequent sparsely-granulated subtype but no relationship with SSA-responsiveness was seen. The genetics of aggressive, treatment-resistant and familial pituitary adenomas remain largely unexplained and screening criteria could be significantly refined. [less ▲]

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See detailEndocrine rare diseases
Beckers, Albert ULiege

Scientific conference (2019, February 19)

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See detailPituitary tumourigenesis - What's new
Beckers, Albert ULiege

Scientific conference (2019, February 15)

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See detailEpidemiology and Management Challenges in Prolactinomas.
VROONEN, Laurent ULiege; Daly, Adrian ULiege; Beckers, Albert ULiege

in Neuroendocrinology (2019)

Clinically relevant pituitary adenomas are present in about 1 per 1000 of the general population and prolactinomas are by far the most common clinical subtype of pituitary adenomas. Usually prolactinomas ... [more ▼]

Clinically relevant pituitary adenomas are present in about 1 per 1000 of the general population and prolactinomas are by far the most common clinical subtype of pituitary adenomas. Usually prolactinomas affect pre-menopausal women and present with typical symptoms of menstrual disturbance and/or galactorrhea. They are generally managed with dopamine agonists to restore fertility and to control symptoms and tumour size. In a subset of prolactinomas, however, management remains challenging. Studies in recent years have identified the factors related to dopamine agonist resistance, such as, male sex, genetic features, and aggressive tumor behaviour. Certain other patient groups represent particular challenges for management, such as pediatric patients and pregnant women. Treatment with dopamine agonists is usually safe and effective, and adverse effects such as clinically relevant cardiac valvular complications and impulse control disorders may occur in isolated instances. A number of important disease characteristics of prolactinomas remain to be explained, such as the difference in sex prevalence before and after menopause, the higher prevalence of macroadenomas in older males and the biochemical mechanisms of resistance to dopaminergic agonists. [less ▲]

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See detailLe secret des Géants
Beckers, Albert ULiege

Scientific conference (2019, January 18)

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See detailIntérêt de la génétique dans l'exploration du gigantisme hypophysaire
PETIGNOT, Sandrine ULiege; ROSTOMYAN, Liliya ULiege; Beckers, Albert ULiege

in Vaisseaux, Coeur, Poumons (2019), 24(2), 21-28

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See detailGenetic Testing in Pituitary Adenomas: What, How, and In Whom?
Daly, Adrian ULiege; Beckers, Albert ULiege

in Endocrinología, Diabetes y Nutrición (2019), 66(2), 71-73

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See detailThyroid dysfunction after Alemtuzumab treatment for multiple sclerosis : a report of four cases
Daniel, Sara ULiege; HANSEN, Isabelle ULiege; Dive, Dominique ULiege et al

in Acta Clinica Belgica (2018, December), 73(2),

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See detailHow do they grow so tall. Genetics of gigantism
Beckers, Albert ULiege

Scientific conference (2018, December)

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See detailElements du diagnostic initial de l'acromegale. Données d'une base internationale
Beckers, Albert ULiege

Scientific conference (2018, November 23)

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See detailFamilial Pituitary Tumors - Updates in Pituitary tumor diagnosis and management
Beckers, Albert ULiege

Scientific conference (2018, November)

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See detailDiagnostic de l'acromégalie : observations à partir d'une base de données internationales
Beckers, Albert ULiege; PETROSSIANS, Patrick ULiege

in Mises au point clinique d'Endocrinologie, nutrition et métabolisme 2018 (2018)

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