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See detailEpigenetic control of the invasion-promoting MT1-MMP/MMP-2/TIMP-2 axis in cancer cells
Chernov, Andrei V.; Sounni, Nor Eddine ULg; Remacle, Albert G. et al

in Journal of Biological Chemistry (2009), 284(19), 12727-34

Membrane type-1 matrix metalloproteinase (MT1-MMP) is an activator of soluble MMP-2. The activity of both MMPs is regulated by their physiological inhibitor TIMP-2. An MT1-MMP/MMP-2/TIMP-2 axis plays a ... [more ▼]

Membrane type-1 matrix metalloproteinase (MT1-MMP) is an activator of soluble MMP-2. The activity of both MMPs is regulated by their physiological inhibitor TIMP-2. An MT1-MMP/MMP-2/TIMP-2 axis plays a key role in the invasive behavior of many cell types. Despite its importance, epigenetic control of this pro-invasive axis is insufficiently studied, and, as a result, its modification in a rational and clinically beneficial manner is exceedingly difficult. Therefore, we performed an epigenetic analysis of the MT1-MMP, MMP-2, and TIMP-2 gene promoters in highly migratory glioblastoma cells and in low migratory breast carcinoma MCF-7 cells. We determined, for the first time, that the epigenetic control leading to the transcriptional silencing of both MMPs includes hypermethylation of the corresponding CpG regions and histone H3 lysine-27 trimethylation (H3K27me3). In turn, undermethylation of the CpG islands and low levels of histone H3 lysine-27 trimethylation are features of transcriptionally active MT1-MMP and MMP-2 genes in invasive cancer cells. Additional histone modifications we have analyzed, including H3ac and H3K4me2, are present in both transcriptionally active and inactive promoters of both MMPs. Histone H3 lysine-4 trimethylation is likely to play no significant role in regulating MT1-MMP and MMP-2. The pattern of epigenetic regulation of TIMP-2 was clearly distinct from that of MMPs and included the coordinated methylation and demethylation of the two CpG regions in the promoter. Our results suggest that the epigenetic control plays an important role in both the balanced regulation of the MT1-MMP/MMP-2/TIMP-2 axis and the invasive behavior in cancer cells. [less ▲]

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See detailEpigenetic effects of omega-3 FA on the immune response of broiler breeder offspring
Koppenol, A.; Everaert, Nadia ULg; Franssens, L. et al

Conference (2014)

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See detailEpigenetic mechanisms underlying long-term programming effects of prenatal protein undernutrition by albumen removal in the chicken
Willems, E.; Guerrero-Bosagna, C.; Buyse, J. et al

Poster (2014, April)

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See detailEpigenetic modulators mitigate angiogenesis through a complex transcriptomic network
Shiva Shankar, T.V.; Willems, Luc ULg

in Vascular Pharmacology (2014), 60

In this review, we summarize the knowledge pertaining to the role of epigenetics in the regulation of angiogenesis. In particular, we show that lysine acetylation and cytosine methylation are important ... [more ▼]

In this review, we summarize the knowledge pertaining to the role of epigenetics in the regulation of angiogenesis. In particular, we show that lysine acetylation and cytosine methylation are important transcriptional regulators of angiogenic genes in endothelial cells. Lysine acetylation and cytosine methylation inhibitors idiosyncratically tune the transcriptome and affect expression of key modulators of angiogenesis such as VEGF and eNOS. Transcriptomic profiling also reveals a series of novel genes that are concomitantly affected by epigenetic modulators. The reversibility and overall tolerability of currently available epigenetic inhibitors open up the prospect of therapeutic intervention in pathologies where angiogenesis is exacerbated. This type of multitargeted strategy has the major advantage of overcoming the compensatory feedback mechanisms that characterize single anti-angiogenic factors. [less ▲]

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See detailEpigenetic regulation of angiogenesis
Shiva Shankar, Thammadihalli Veerasangaiah ULg; Sulka, Béatrice ULg; Willems, Luc ULg

Speech (2011)

DNA methylation and histone deacetylation are two key epigenetic modifications that play central role in regulation of gene expression. Several studies have shown that histone deacetylases (HDAC) and DNA ... [more ▼]

DNA methylation and histone deacetylation are two key epigenetic modifications that play central role in regulation of gene expression. Several studies have shown that histone deacetylases (HDAC) and DNA methyltransferases (DNMT) inhibitors are potent anti-angiogenic compounds. Though combination of HDAC and DNMT inhibitors are now being examined in clinical trials of hematological malignancies, little work has been done to understand the effect of this combination on physiological and tumoral angiogenesis. We designed a family of twin drugs with intrinsic HDAC and DNMT inhibitory activities and tested in relevant models of angiogenesis in vitro (Human Umbilical Vein Endothelial Cells – HUVEC and aortic ring) and in vivo (chick chorioallantoic membrane and Zebrafish). We have identified a lead compound (EPI) affecting global histone acetylation and having quantifiable anti-angiogenic action without cytotoxic and apoptotic effect. In order to elucidate its anti-angiogenic mechanism, we characterized gene expression pattern simultaneously with the methylation profile of HUVEC cells treated with EPI and reference epigenetic modulators. This approach based on parallel microarray analyses permitted us to underscore a list of genes exclusively affected by EPI but not by other HDAC or DNMT inhibitors. These genes were then analyzed using the Ingenuity Pathway Analysis software revealing potential involvement of a subset of genes in angiogenesis. Our present aim is to validate the expression levels of a series of genes with respect to epigenetic mechanisms (histone modifications and DNA methylation). Finally, the biological relevance of the target genes will be explored by RNA silencing. Hence, we are using these novel epigenetic modulators as a tool to understand the regulatory mechanism of angiogenesis and to develop effective approaches to treat cancer. [less ▲]

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See detailEpigenetic regulation of angiogenesis
Shiva Shankar, Thammadihalli Veerasangaiah ULg

Doctoral thesis (2013)

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See detailEpigenetic Therapy of Lung Cancers: Anti-tumoral effect of valproate on small cell lung cancer
Hubaux, Roland ULg

Doctoral thesis (2011)

Lung cancer is the leading cause of cancer-related death worldwide. Among lung carcinomas, the outcome of small cell lung carcinoma (SCLC) patients is the poorest of any histological subtype with five ... [more ▼]

Lung cancer is the leading cause of cancer-related death worldwide. Among lung carcinomas, the outcome of small cell lung carcinoma (SCLC) patients is the poorest of any histological subtype with five-year survival rate of less than 20 and 5 % for limited and extensive stage respectively. Based on increasing evidence that inhibitors of histones deacetylases (HDAC) have anticancer properties, the goal of this study was to evaluate the ability of valproate (VPA) to improve efficacy of chemotherapeutic regimen in SCLC. We show that VPA directly induces apoptosis of SCLC cell lines at concentrations relevant for clinical uses. Furthermore, VPA synergizes with two chemotherapeutic regimen used in first (cisplatin + etoposide) and second line (cyclophosphamid + vindesine + doxorubicin) treatments. Both mitochondrial and death receptor pathways are involved in VPA-induced apoptosis. Although VPA promotes production of reactive oxygen species, free radical scavenger N-acetylcystein is not sufficient to inhibit apoptosis. As expected, VPA triggers hyperacetylation of histone H3 and increases expression of p21. VPA reduces levels of BclxL, induces cleavage of Bid, translocation of Bax to mitochondria, release of cytochrome c into cytosol and phosphorylation of Erk and H2AX. Transcriptomic analyses by microarrays and quantitative RT-PCR have underscored a series of genes candidates potentially implicated into sensitivity of SCLC to VPA. Among these, the Fzd7 receptor of the WNT pathway is essential for VPA proapoptotic activity. Efficiency of VPA combined to first and second line chemotherapeutic agents is supported by preclinical models of SCLC cells engrafted into SCID mice. The second line combination is presently tested in a clinical trial with patients presenting with refractory or relapsing small cell lung cancer (protocol 01081 at http://www.elcwp.org). [less ▲]

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See detailEpigenetics and local adaptation
Hanikenne, Marc ULg

Conference (2014, January 22)

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See detailEpigenetics, sirtuins and osteoarthritis.
Gabay, Odile; Sanchez, Christelle ULg

in Joint, bone, spine : revue du rhumatisme (2012), 79(6), 570-3

Epigenetics, modifications of the DNA other than changes on the DNA sequences, is frequently studied in cancer research and aging. DNA methylation, mi-RNA, and histones deacetylation are investigated in ... [more ▼]

Epigenetics, modifications of the DNA other than changes on the DNA sequences, is frequently studied in cancer research and aging. DNA methylation, mi-RNA, and histones deacetylation are investigated in different pathologies, including inflammatory diseases and age-related diseases such as osteoarthritis (OA). In this review, we focus on the chromatin-modifying enzymes in arthritic pathologies, and more particularly on Sirtuins. We also review the role of Sirt1 in OA, which has been highlighted in recent publications, and examine the possible protective role Sirt1 could play in this disease. Moreover, we discuss the possible therapeutic target of such a protein, reviewing the potential inhibitors/activators of this enzyme and their properties. [less ▲]

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See detailEpigenetique, interface entre environnement et genes: ro1e dans les maladies complexes.
SCHEEN, André ULg; Junien, C.

in Revue Médicale de Liège (2012), 67(5-6), 250-7

Epigenetics is the study of heritable changes in gene expression or cellular phenotype caused by mechanisms other than changes in the underlying DNA sequence. Epigenetics is one of the major mechanisms ... [more ▼]

Epigenetics is the study of heritable changes in gene expression or cellular phenotype caused by mechanisms other than changes in the underlying DNA sequence. Epigenetics is one of the major mechanisms explaining the "Developmental Origin of Health and Diseases" (DOHaD). Besides genetic background inherited from parents, which confers susceptibility to certain pathologies, epigenetic changes constitute the memory of previous events, either positive or negative, along the life cycle, including at the in utero stage. The later exposition to hostile environment may reveal such susceptibility, with the development of various pathologies, among them numerous chronic complex diseases. The demonstration of such a sequence of events has been shown for metabolic diseases as obesity, metabolic syndrome and type 2 diabetes, cardiovascular disease and cancer. In contrast to genetic predisposition, which is irreversible, epigenetic changes are potentially reversible, thus giving targets not only for prevention, but possibly also for the treatment of certain complex diseases. [less ▲]

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See detailEpigraphes alphabétiques du pays de la Mer
Colonna d'Istria, Laurent ULg

in Nouvelles Assyriologiques Brèves et Utilitaires (2012)

Detailed reference viewed: 40 (3 ULg)
See detailL'épigraphie au service de l'histoire médicale
Nissen, Cécile ULg

Scientific conference (2010, March 19)

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See detailEpigraphie latine
Dubuisson, Michel; Famerie, Etienne ULg

Learning material (2009)

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See detailEpigraphique grecque. Bibliographie
Famerie, Etienne ULg

Learning material (2009)

Detailed reference viewed: 30 (4 ULg)
See detailEpilepsie
Martin, Didier ULg

Scientific conference (2005, March)

Detailed reference viewed: 23 (5 ULg)
See detailEpilepsie a paroxysmes rolandiques de l'enfant
CARLIER, Gérard; Misson, Jean-Paul ULg; Dubru, Jean-Marie ULg

in Comptes Rendus de la Société Belge de Neurologie Infantile (1983)

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See detailEpilepsie chez des enfants infirmes moteurs-cérébraux
Peduzzi, M.; Defontaine, E.; Misson, Jean-Paul ULg

in Revue Médicale de Liège (2006), 61(4), 237-239

The incidence of epilepsy in 110 patients with cerebral palsy (the majority with spastic tetraplegia) was 46,4%. Almost half of the patients with spastic tetraplegia (45%) and hemiplegia (52%) had ... [more ▼]

The incidence of epilepsy in 110 patients with cerebral palsy (the majority with spastic tetraplegia) was 46,4%. Almost half of the patients with spastic tetraplegia (45%) and hemiplegia (52%) had epilepsy. The incidence was lower in patients with spastic diplegia (32%). Half of epilepsy in spastic hemiplegia were partial seizures and the other half consisted of generalized seizures, while generalized tonic-clonic episodes predominated in all other forms of C.P. A high incidence of West syndrome was observed in patients with spastic tetraplegia. Etiological factors of C.P. were perinatal in 75%. 16,65% had neonatal antecedents of convulsions; most of them had spastic tetraplegia (75%) and a significant mental retardation. A low intelligence quotient (I.Q.) was seen in most of the children with epilepsy, and patients with tetraplegia had significantly lower intelligence quotient than other groups. [less ▲]

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See detailL'épilepsie de Vincent VAN GOGH
Blumer, Dietrich; Stassart, Martine ULg

in Cahiers du CEP (Centre d'Etudes Pathoanalytiques) (1994), 4(4), 3-10

Though he never had typical "grand mal" crisis, Vincent VAN GOGH was really epileptic. The symptomatology of epileptic seizures was better known in the XIXd Century than today.

Detailed reference viewed: 75 (0 ULg)