References of "Bours, Vincent"
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See detailThe influence of COMT single nucleotide polymorphism (rs4680) on the neural substrates of working memory representations maintenance in healthy aging
Manard, Marine ULiege; François, Sarah ULiege; Bahri, Mohamed Ali ULiege et al

Poster (2016, May 10)

The COMT val108/158met polymorphism was associated to the dopaminergic modulation in the brain, and therefore stimulated research on its influence for cognitive functioning and particularly working memory ... [more ▼]

The COMT val108/158met polymorphism was associated to the dopaminergic modulation in the brain, and therefore stimulated research on its influence for cognitive functioning and particularly working memory. First, a general advantage of carrying the met allele was reported. However, many studies used tasks that did not allow efficiently assessing the contribution of manipulation and maintenance processes in working memory, leading to divergent results, in both young and older populations, resulting in debates about the exact phenotypic effect of the COMT polymorphism. Using fMRI, this study was designed to assess the potential effect of the COMT polymorphism on age-related differences in working memory representations maintenance abilities (Sternberg paradigm). Partial Least Squares method was used to determine the brain-behavior correlations at low, intermediate, and high cognitive demands among young and older groups, homozygous for the val or for the met allele. First, young val/val showed some disadvantages at brain and behavioral level compared to their m/m counterparts. However, in older adults subgroups, the m/m participants tended to show greater age-related difference (when compared to younger adults with similar genotype), suggesting an advantage in carrying the val allele when dopamine signaling is not at optimal efficiency (optimal: young/middle adulthood vs suboptimal: childhood or older ages). These results will be discussed in regard to compensating theories and dopaminergic models accounting for the potential effect of COMT polymorphism on stability/flexibility abilities. [less ▲]

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See detailGenetic predisposition to breast cancer occurring in a male-to-female transsexual patient
Potorac, Iulia ULiege; CORMAN, Vinciane ULiege; Manto, Florence et al

Poster (2016, May)

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See detailSomatic mosaicism underlies X-linked acrogigantism (XLAG) syndrome in sporadic male subjects
Daly, Adrian ULiege; Yuan, Bo; Fina, Frederic et al

in Endocrine-Related Cancer (2016)

Somatic mosaicism has been implicated as a causative mechanism in a number of genetic and genomic disorders. X-linked acrogigantism (XLAG) syndrome is a recently characterized genomic form of pediatric ... [more ▼]

Somatic mosaicism has been implicated as a causative mechanism in a number of genetic and genomic disorders. X-linked acrogigantism (XLAG) syndrome is a recently characterized genomic form of pediatric gigantism due to aggressive pituitary tumors that is caused by submicroscopic chromosome Xq26.3 duplications that include GPR101. We studied XLAG syndrome patients (N=18) to determine if somatic mosaicism contributed to the genomic pathophysiology. Eighteen subjects with XLAG syndrome were identified with Xq26.3 duplications using high definition array comparative genome hybridization (HD-aCGH). We noted males with XLAG had a decreased log2 ratio compared with expected values, suggesting potential mosaicism, while females showed no such decrease. As compared with familial male XLAG cases, sporadic males had more marked evidence for mosaicism, with levels of Xq26.3 duplication between 16.1-53.8%. These characteristics were replicated using a novel, personalized breakpoint-junction specific quantification droplet digital PCR (ddPCR) technique. Using a separate ddPCR technique we studied the feasibility of identifying XLAG syndrome cases in a distinct patient population of 64 unrelated subjects with acromegaly/gigantism and identified one female gigantism patient that had increased copy number variation (CNV) threshold for GPR101 that was subsequently diagnosed as having XLAG syndrome on HD-aCGH. Employing a combination of HD-aCGH and novel ddPCR approaches, we have demonstrated that XLAG syndrome can be caused by variable degrees of somatic mosaicism for duplications at chromosome Xq26.3. Somatic mosaicism was shown to occur in sporadic males but not in females with XLAG syndrome, although the clinical characteristics of the disease were similarly severe in both sexes. [less ▲]

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See detailDouble genetic defect in a case of congenital hypogonadotropic hypogonadism
Potorac, Iulia ULiege; Pintiaux, Axelle ULiege; VALDES SOCIN, Hernan Gonzalo ULiege et al

in Abstract book - 17th World Congress of Gynecological Endocrinology (2016, March)

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See detailUne forme compliquée d'hypercalcémie hypocalciurique familiale
Potorac, Iulia ULiege; BETEA, Daniela ULiege; MALAISE, Olivier ULiege et al

in Abstract book - Symposium "Perspectives in Endocrinology" (2016, January)

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See detailThe genetic causes of pituitary gigantism
Rostomyan, Liliya ULiege; Lysy, P; Desfilles, C et al

in Abstract book - Symposium "Perspectives in Endocrinology" (2016, January)

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See detailCancer thyroïdien familial non médullaire : actualités cliniques et génétiques
VALDES SOCIN, Hernan Gonzalo ULiege; Gonon Rodrigues Palmeira, Leonor ULiege; Burlacu, MC et al

in Revue Médicale de Liège (2016), 71(12), 557-561

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See detailLa cardiotoxicité des traitements anti-cancéreux
FRERES, Pierre ULiege; PONCIN, Aurélie ULiege; MOONEN, Marie ULiege et al

in Revue Médicale de Liège (2016), 71(9), 382-387

Les cancers sont de plus en plus fréquents et leurs traitements de plus en plus agressifs. En conséquence, les médecins se trouvent régulièrement confrontés aux effets secondaires des traitements ... [more ▼]

Les cancers sont de plus en plus fréquents et leurs traitements de plus en plus agressifs. En conséquence, les médecins se trouvent régulièrement confrontés aux effets secondaires des traitements cytotoxiques. La cardiotoxicité induite par les traitements anti-cancéreux est une complication gravissime, car elle peut être mortelle et provoque un arrêt temporaire, voire définitif, des traitements. Dans cet article, nous décrivons les mécanismes, le dépistage et la prise en charge multidisciplinaire de la cardiotoxicité des agents anti-cancéreux. [less ▲]

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See detailIkappaBzeta: an emerging player in cancer.
Willems, Marie; Dubois, Nadege; Musumeci, Lucia ULiege et al

in Oncotarget (2016), 7(40), 66310-66322

IkappaBzeta, an atypical member of the nuclear IkappaB family of proteins, is expressed at low levels in most resting cells, but is induced upon stimulation of Toll-like/IL-1 receptors through an IRAK1 ... [more ▼]

IkappaBzeta, an atypical member of the nuclear IkappaB family of proteins, is expressed at low levels in most resting cells, but is induced upon stimulation of Toll-like/IL-1 receptors through an IRAK1/IRAK4/NFkappaB-dependent pathway. Like its homolog Bcl3, IkappaBzeta can regulate the transcription of a set of inflamatory genes through its association with the p50 or p52 subunits of NF-kappaB. Long studied as a key component of the immune response, IkappaBzeta emerges as an important regulator of inflammation, cell proliferation and survival. As a result, growing evidence support the role of this transcription factor in the pathogenesis number of human hematological and solid malignancies. [less ▲]

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See detailNew perspective on maintenance therapies for platinum- sensitive recurrent ovarian cancer in women with germline and somatic mutations in BRCA1 and BRCA2 genes.
Vergote, I.; Bours, Vincent ULiege; Blaumeiser, B. et al

in Facts, Views and Vision in Obgyn (2016), 8(3), 161-167

Ovarian cancer (OC) is the seventh most common cancer in women. Although women diagnosed with OC are usually treated frontline with platinum-based chemotherapy, most of them relapse once treatment is ... [more ▼]

Ovarian cancer (OC) is the seventh most common cancer in women. Although women diagnosed with OC are usually treated frontline with platinum-based chemotherapy, most of them relapse once treatment is halted. Therefore, maintenance therapies have been developed to secure the response and delay further chemotherapy. There are two established maintenance therapies for women affected by platinum-sensitive recurrent OC: bevacizumab, a humanized monoclonal antibody targeting vascular endothelial growth factor, and olaparib, an inhibitor of poly (adenosine diphosphate [ADP]-ribose) polymerase (PARPi). Loss-of-function mutations in genes in the homologous recombination pathway, especially BRCA1 and BRCA2, predict higher rates of platinum sensitivity, better overall survival (OS), and better response to PARPi in women with OC. Among patients with platinum-sensitive recurrent OC, a BRCA mutation is the first genetically defined predictive marker for targeted therapy, since these patients are most likely to benefit from treatment with a PARPi, such as olaparib. In patients with platinum-sensitive recurrent OC without a BRCA mutation, bevacizumab currently seems to be the best maintenance option. Women with OC are progressively more routinely screened for germline BRCA mutations, and the implication of somatic BRCA mutations is increasingly being recognized in OC. Therefore, the recommendations should be updated to reflect the importance of both types of mutations. Together, these data highlight the fact that treatment of recurrent OC can be optimized using genomic contributions to individualize therapy and to improve treatment response. [less ▲]

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See detailConstitutive activation of casein kinase 2 in glioblastomas: Absence of class restriction and broad therapeutic potential.
Dubois, Nadege; Willems, Marie; Nguyen-Khac, Minh-Tuan et al

in International Journal of Oncology (2016), 48(6), 2445-52

Casein kinase II contributes to the growth and survival of malignant gliomas and attracts increasing attention as a therapeutic target in these tumors. Several reports have suggested that this strategy ... [more ▼]

Casein kinase II contributes to the growth and survival of malignant gliomas and attracts increasing attention as a therapeutic target in these tumors. Several reports have suggested that this strategy might be most relevant for specific subgroups of patients, namely Verhaak's classical and TP53 wild-type tumors. Using kinase assays and microarray genetic profiling in a series of 27 proprietary fresh frozen surgical glioma samples, we showed that constitutive CK2 kinase activation is not restricted to tumors that present increased copy numbers or mRNA expression of its catalytic or regulatory subunits, and can result from a functional activation by various cytokines from the glioma microenvironment. Using corresponding primary tumor and human astrocyte cell cultures as well as glioma cell lines, we confirmed that CK2 inhibition is selectively toxic to malignant glial tumors, without any restriction to tumor class or to TP53 status. We finally showed that while the contribution of CK2 to the constitutive NF-kappaB hyperactivation in malignant gliomas is at best moderate, a delayed activation of NF-kappaB may associate with the therapeutic resistance of glioma cells to CK2 inhibition. [less ▲]

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See detailInvolvement of Ikbζ in glioblastomas and its potential implication in radioresistance
Dubois, Nadège ULiege; Willems, Marie; Kroonen, Jérôme et al

Poster (2016)

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See detailMicroRNAs and Inflammation in Colorectal Cancer.
Josse, Claire ULiege; Bours, Vincent ULiege

in Slaby, Ondrej; Calin, George A. (Eds.) Non-coding RNAs in Colorectal Cancer (2016)

Colorectal cancers (CRC) are known to be related to inflammatory conditions, and inflammatory bowel diseases increase the relative risk for developing CRC. The use of anti-inflammatory drugs prevents the ... [more ▼]

Colorectal cancers (CRC) are known to be related to inflammatory conditions, and inflammatory bowel diseases increase the relative risk for developing CRC. The use of anti-inflammatory drugs prevents the development of colorectal cancer.Several molecular mediators are connecting the pathways that are involved in inflammatory conditions and in carcinogenesis. By the way these pathways are tightly interwoven, with the consequence that a deregulation at the level of any of these molecular mediators can affect the others.MiRNAs are demonstrated to be deregulated in inflammatory bowel diseases and in colorectal cancer. Moreover, they target several molecular mediators that connect inflammation to cancer, and they are thus implicated in the route from inflammation to colorectal cancer.This chapter will focus on the miRNAs that are jointly deregulated in inflammatory bowel disease and in colorectal cancer. Their role on the regulation of the molecular mediators and pathways that link inflammation to cancer will be described. [less ▲]

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See detailBreast cancer in a male to female transsexual patient with a BRCA2 mutation
CORMAN, Vinciane ULiege; Potorac, Iulia ULiege; Manto, Florence ULiege et al

in Endocrine-Related Cancer (2016), 23(5), 391-397

Breast cancer is rare in male patients. Certain predisposing factors, be they genetic (e.g., BRCA2 gene mutations) or hormonal (imbalance between estrogen and androgen levels), have been implicated in ... [more ▼]

Breast cancer is rare in male patients. Certain predisposing factors, be they genetic (e.g., BRCA2 gene mutations) or hormonal (imbalance between estrogen and androgen levels), have been implicated in male breast cancer pathophysiology. Male-to-female (MtF) transsexualism is a condition that generally involves cross-sex hormone therapy. Anti-androgens and estrogens are used to mimic the female hormonal environment and induce the cross-sex secondary characteristics. In certain situations, the change in the hormonal milieu can be disadvantageous and favor the development of hormonedependent pathologies, such as cancer. We report a case of a MtF transgender patient who developed breast cancer after 7 years of cross-sex hormonal therapy. The patient was found to be BRCA2 positive, and suffered recurrent disease. The patient was unaware of being a member of an established BRCA2 mutation-positive kindred. This represents the first case of a BRCA2 mutation predisposing to breast cancer in a MtF transgender patient. [less ▲]

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See detailGrowth hormone releasing hormone excess and blockade in X-LAG syndrome.
Daly, Adrian Francis ULiege; Lysy, Philippe; Defilles, Celine et al

in Endocrine-related cancer (2016)

X-linked acrogigantism (X-LAG) syndrome is a newly-described form of inheritable pituitary gigantism that begins in early childhood and is usually associated with markedly elevated growth hormone (GH) and ... [more ▼]

X-linked acrogigantism (X-LAG) syndrome is a newly-described form of inheritable pituitary gigantism that begins in early childhood and is usually associated with markedly elevated growth hormone (GH) and prolactin secretion by mixed pituitary adenomas/hyperplasia. Microduplications on chromosome Xq26.3 including the GPR101 gene cause X-LAG syndrome. In individual cases random GH-releasing hormone (GHRH) levels have been elevated. We performed a series of hormonal profiles in a young female sporadic X-LAG syndrome patient and subsequently undertook in vitro studies of primary pituitary tumor culture following neurosurgical resection. The patient demonstrated consistently elevated circulating GHRH levels throughout preoperative testing, which was accompanied by marked GH and prolactin hypersecretion; GH demonstrated a paradoxical increase following TRH administration. In vitro, the pituitary cells showed baseline GH and prolactin release that was further stimulated by GHRH administration. Co-incubation with GHRH and the GHRH receptor antagonist, acetyl-(D-Arg(2))-GHRH (1-29) amide, blocked the GHRH-induced GH stimulation; the GHRH receptor antagonist alone significantly reduced GH release. Pasireotide, but not octreotide, inhibited GH secretion. A ghrelin receptor agonist and an inverse agonist led to modest, statistically significant increases and decreases in GH secretion, respectively. GHRH hypersecretion can accompany the pituitary abnormalities seen in X-LAG syndrome. These data suggest that the pathology of X-LAG syndrome may include hypothalamic dysregulation of GHRH secretion, which is in keeping with localization of GPR101 in the hypothalamus. Therapeutic blockade of GHRH secretion could represent a way to target the marked hormonal hypersecretion and overgrowth that characterizes X-LAG syndrome. [less ▲]

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See detailGPR101 mutations are not a frequent cause of congenital isolated growth hormone deficiency
Castinetti, F; Daly, Adrian ULiege; Stratakis, CA et al

in Hormone & Metabolic Research (2016)

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See detailPrognostic relevance of epilepsy at presentation in glioblastoma patients.
Berendsen, Sharon; Varkila, Meri; Kroonen, Jerome et al

in Neuro-oncology (2016)

BACKGROUND: Epileptogenic glioblastomas are thought to convey a favorable prognosis, either due to early diagnosis or potential antitumor effects of antiepileptic drugs. We investigated the relationship ... [more ▼]

BACKGROUND: Epileptogenic glioblastomas are thought to convey a favorable prognosis, either due to early diagnosis or potential antitumor effects of antiepileptic drugs. We investigated the relationship between survival and epilepsy at presentation, early diagnosis, and antiepileptic drug therapy in glioblastoma patients. METHODS: Multivariable Cox regression was applied to survival data of 647 consecutive patients diagnosed with de novo glioblastoma between 2005 and 2013 in order to investigate the association between epilepsy and survival in glioblastoma patients. In addition, we quantified the association between survival and valproic acid (VPA) treatment. RESULTS: Epilepsy correlated positively with survival (HR: 0.75 (95% CI: 0.61-0.92), P < .01). This effect is independent of age, sex, performance status, type of surgery, adjuvant therapy, tumor location, and tumor volume, suggesting that this positive correlation cannot be attributed solely to early diagnosis. For patients who presented with epilepsy, the use of the antiepileptic drug VPA did not associate with survival when compared with patients who did not receive VPA treatment. CONCLUSION: Epilepsy is an independent prognostic factor for longer survival in glioblastoma patients. This prognostic effect is not solely explained by early diagnosis, and survival is not associated with VPA treatment. [less ▲]

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