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Rhumatologue

Docteur SANDRINE JOULIN-JOUSSE

📍 Brest (29)HospitalierRPPS 10003452041

✨ Profil synthétique

IA · 30/04/2026

Le Docteur Sandrine JoulIN-Jousse est rhumatologue hospitalier à Brest. Ses publications sur PubMed couvrent divers aspects de la rhumatologie, notamment les revues générales, les cas cliniques, l'épidémiologie et la pharmacovigilance. Elle a également publié sur des pathologies spécifiques comme le lupus et des populations particulières comme la pédiatrie.

Expertises présumées

  • Lupus érythémateux systémique
  • Rhumatologie pédiatrique
  • Pharmacovigilance en rhumatologie
  • Épidémiologie des maladies rhumatismales
  • Revue systématique de la littérature médicale
  • Cas cliniques en rhumatologie
  • Registres de maladies rhumatismales

Synthèse automatique à partir des sources publiques (HAL, OpenAlex, theses.fr, ClinicalTrials.gov, FAI²R, ANS). Pas une évaluation clinique. Le médecin peut corriger via son compte.

Diplômes

🎓 DES & spécialité ordinale

  • DES Rhumatologie
  • Rhumatologie (SM)

🎓 Diplômes

  • DE Docteur en médecine

Source : Annuaire Santé ANS (FHIR Practitioner.qualification) · Mises à jour quotidiennes.

Lieu de consultation

  • CHRU BREST SITE HOPITAL CAVALE BLANCHE

    Boulevard TANGUY PRIGENT, 29609 Brest

    ☎ 0298223333Hospitalier

Tarifs & secteur de conventionnement

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

📊 Comprendre le remboursement

Prendre rendez-vous & contact

🗓 Trouver sur Doctolib📇 Ajouter à mes contacts

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
    MUC1 and MUC16: critical for immune modulation in cancer therapeutics

    Frontiers in immunology · 2024

    📚 42 citations🎯 RCR 8.27Top 3% NIH🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    The Mucin (MUC) family, a range of highly glycosylated macromolecules, is ubiquitously expressed in mammalian epithelial cells. Such molecules are pivotal in establishing protective mucosal barriers, serving as defenses against pathogenic assaults. Intriguingly, the aberrant expression of specific MUC proteins, notably Mucin 1 (MUC1) and Mucin 16 (MUC16), within tumor cells, is intimately associated with oncogenesis, proliferation, and metastasis. This association involves various mechanisms, including cellular proliferation, viability, apoptosis resistance, chemotherapeutic resilience, metabolic shifts, and immune surveillance evasion. Due to their distinctive biological roles and structural features in oncology, MUC proteins have attracted considerable attention as prospective targets and biomarkers in cancer therapy. The current review offers an exhaustive exploration of the roles of MUC1 and MUC16 in the context of cancer biomarkers, elucidating their critical contributions to the mechanisms of cellular signal transduction, regulation of immune responses, and the modulation of the tumor microenvironment. Additionally, the article evaluates the latest advances in therapeutic strategies targeting these mucins, focusing on innovations in immunotherapies and targeted drugs, aiming to enhance customization and accuracy in cancer treatments.

  • 2
    TNKS1BP1 facilitates ubiquitination of CNOT4 by TRIM21 to promote hepatocellular carcinoma progression and immune evasion

    Cell death & disease · 2024

    📚 12 citations🎯 RCR 1.99🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    AbstractImmune checkpoint inhibitors, particularly PD-1/PD-L1 blockades, have been approved for unresectable hepatocellular carcinoma (HCC). However, high resistance rates still limit their efficacy, highlighting the urgent need to understand the underlying mechanisms and develop strategies for overcoming the resistance. In this study, tankyrasel binding protein 1 (TNKS1BP1) was found to interact with tripartite motif containing 21 (TRIM21) and mediated the ubiquitination of CCR4-NOT transcription complex subunit 4 (CNOT4) at the K239 residue via K48 and K6 linkage, which was essential for its tumorigenesis function. Autophagy and lipid reprogramming were identified as two possible mechanisms underlying the pro-tumor effect of TNKS1BP1. Upregulated TNKS1BP1 inhibited autophagy while induced lipid accumulation by inhibiting the JAK2/STAT3 pathway upon the degradation of CNOT4 in HCC. Importantly, knocking down TNKS1BP1 synergized with anti-PD-L1 treatment by upregulating PD-L1 expression on tumor cells via the JAK2/STAT3 pathway, and remodeling the tumor microenvironment by increasing infiltration of tumor-infiltrating lymphocytes as well as augmenting the effect of cytotoxic T lymphocytes. In conclusion, this study identified TNKS1BP1 as a predictive biomarker for patient prognosis and a promising therapeutic target to overcome anti-PD-L1 resistance in HCC.

  • 3
    Prevalence of Oral Submucous Fibrosis With Other Oral Potentially Malignant Disorders: A Clinical Retrospective Study

    Cureus · 2023

    📚 12 citations🎯 RCR 3.65Top 12% NIH🔓 Open Access📄 PDF gratuit ↗

Publications scientifiques (50) — classées par pathologie

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

Transversal27

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Revue générale5

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Case report / série3

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Épidémiologie & registres2

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Lupus2

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Pédiatrie2

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Pharmacovigilance2

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csDMARDs1

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Économie santé1

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Essai clinique1

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Génétique1

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IRM ostéo-articulaire1

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Revue / méta-analyse1

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Sclérodermie1

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Sjögren1

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Tendinopathies & SCC1

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