Docteur SYLVIE PRIGENT

Bibliographie

• Sigma 1 Receptor is Overexpressed in Hepatocellular Adenoma: Involvement of ERα and HNF1α

  2020

  ArticleCancers

• Rat hepatocytes express functional P2X receptors.

  2007

  ArticleFEBS Letters

• Identification of the LIM Protein FHL2 as a Coactivator of β-Catenin

  2003

  ArticleJournal of Biological Chemistry

• Altered expression of E-cadherin in hepatocellular carcinoma: Correlations with genetic alterations, β-catenin expression, and clinical features

  2002

  ArticleHepatology

• Identification of three distinct regions of allelic deletions on the short arm of chromosome 8 in hepatocellular carcinoma

  1999

  ArticleOncogene

Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).

Lieu de consultation

• CHIC QUIMPER

  14 Avenue YVES THEPOT, 29107 Quimper

  ☎ 0298526060Hospitalier🏥 Voir cet établissement

Tarifs & secteur de conventionnement

Secteur de conventionnement non disponible (médecin hospitalier ou non présent dans l'Annuaire santé CNAM des libéraux conventionnés).

Prendre rendez-vous & contact

Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).

Top publications · les plus citées

• 1

  Altered expression of E-cadherin in hepatocellular carcinoma: correlations with genetic alterations, beta-catenin expression, and clinical features

  Hepatology (Baltimore, Md.) · 2002

  📚 143 citations🎯 RCR 2.73Top 18% NIH

  Lire l'abstract Crossref ↓

  E-cadherin is a key cell adhesion protein implicated as a tumor/invasion suppressor in human carcinomas and a binding partner of β-catenin, which plays a critical role in Wnt signaling and in tumorigenesis. Here we report genetic and expression studies of E-cadherin and β-catenin in hepatocellular carcinoma (HCC). Immunohistochemical analysis of E-cadherin expression in 37 HCCs and adjacent nontumor tissues revealed important variations among tumor samples, ranging from complete or heterogeneous down-regulation in 35% of cases to marked overexpression in 40% of tumors. Loss of E-cadherin expression was closely associated with loss of heterozygosity (LOH) at the E-cadherin locus and methylation of CpG islands in the promoter region (P < .002), predominantly in hepatitis B virus (HBV)-related tumors (P < .005). No mutation of the E-cadherin gene could be detected in the tumors examined, suggesting the requirement for reversible mechanisms of E-cadherin down-regulation. In most HCCs, including E-cadherin-positive and -negative cases, β-catenin was strongly expressed at the cell membrane and nuclear accumulation of the protein was correlated with the presence of mutations in the β-catenin gene itself, but not with E-cadherin loss. At difference with a number of epithelial cancers, vascular invasion was frequently noted in HCCs showing enforced expression of the membranous E-cadherin/β-catenin complex. In conclusion, these data support the notion that E-cadherin might play diverse and seemingly paradoxic roles in HCC, reflecting specific requirements for tumor growth and spread in the liver environment.

• 2

  Identification of the LIM protein FHL2 as a coactivator of beta-catenin

  The Journal of biological chemistry · 2003

  📚 122 citations🎯 RCR 1.96🔓 Open Access📄 PDF gratuit ↗
• 3

  The blocking of capacitative calcium entry by 2-aminoethyl diphenylborate (2-APB) and carboxyamidotriazole (CAI) inhibits proliferation in Hep G2 and Huh-7 human hepatoma cells

  Cell calcium · 2004

  📚 68 citations🎯 RCR 1.43

Publications scientifiques (11) — classées par pathologie

Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).

Partager cette fiche