📇 Rhumatologue · LA TESTE CEDEX · (33) · Mixte
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2 raisons identifiées
Disponibilité géographique
3 lieux d'exercice — choisissez celui qui vous arrange
Délais de RDV courts dans la région
144.4 rhumatos / 100 000 hab. — département bien doté
✨ Génération du profil synthétique IA en cours…
Indicateurs publics agrégés sur 250 M+ d'œuvres scientifiques (OpenAlex, PubMed). Traduits ici en langage patient.
Influence scientifique
Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.
11
11 articles ont été cités au moins 11fois par d'autres chercheurs — preuve que ses travaux sont repris par la communauté médicale.
h-index
Total citations reçues
408
Nombre de fois où d'autres équipes ont mentionné ses publications dans leurs propres travaux.
Publications totales
87
Articles, revues et chapitres référencés dans les bases académiques internationales.
Articles influents
13
Publications ayant marqué leur domaine — chacune citée au moins 10 fois par d'autres chercheurs.
i10-index
Thématiques principales
Affiliations FR : Centre National de la Recherche Scientifique · Inserm · Université Fédérale de Toulouse Midi-Pyrénées
Source : OpenAlex (CC0, OurResearch). Indicateurs académiques agrégés sur 250 M+ d'œuvres.
Articles déposés en accès libre sur l'archive ouverte des universités françaises (HAL) — gage d'activité de recherche en France.
Modeling the PAX5P80R Mutation Reveals HIF2α Activation as a Common Feature and Therapeutic Target in B-cell Acute Lymphoblastic Leukemia
2025ArticleCancer Research
Stem cell–like reprogramming is required for leukemia-initiating activity in B-ALL
2023ArticleJournal of Experimental Medicine
CELL QUIESCENCE AND REPROGRAMMING ARE DISTINCTIVE FEATURES OF PRE- LEUKEMIC STEM CELLS IN BACUTE LYMPHOBLASTIC LEUKEMIA
2022Congrès51st Annual Scientific Meeting of the International-Society-for-Experimental-Hematology (ISEH)
Spectrum of Kidney Disorders Associated with T-Cell Immunoclones
2022ArticleJournal of Clinical Medicine
The CADM1 tumor suppressor gene is a major candidate gene in MDS with deletion of the long arm of chromosome 11
2022ArticleBlood Advances
Impact of TP53 mutations in acute myeloid leukemia patients treated with azacitidine
2020ArticlePLoS ONE
Constitutive Activation of RAS/MAPK Pathway Cooperates with Trisomy 21 and Is Therapeutically Exploitable in Down Syndrome B-cell Leukemia
2020ArticleClinical Cancer Research
PAX5-ELN oncoprotein promotes multistep B-cell acute lymphoblastic leukemia in mice
2018ArticleProceedings of the National Academy of Sciences of the United States of America
Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).
CABINET DU DR STEPHANIE LAGARDE
POLE DE SANTE D'ARCACHON CLINIQUE D'ARCACHON AVENUE JEAN HAMEAU TSA 11100, 33164 LA TESTE CEDEX
HOPITAL PRIVE WALLERSTEIN
14 B BD JAVAL, 33740 ARES
CLINIQUE D'ARCACHON
AV JEAN HAMEAU TSA 11100, 33164 LA TESTE CEDEX
Secteur de conventionnement non disponible (médecin hospitalier ou non présent dans l'Annuaire santé CNAM des libéraux conventionnés).
Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).
Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
Abstract Purpose: Children with Down syndrome (constitutive trisomy 21) that develop acute lymphoblastic leukemia (DS-ALL) have a 3-fold increased likelihood of treatment-related mortality coupled with a higher cumulative incidence of relapse, compared with other children with B-cell acute lymphoblastic leukemia (B-ALL). This highlights the lack of suitable treatment for Down syndrome children with B-ALL. Experimental Design: To facilitate the translation of new therapeutic agents into clinical trials, we built the first preclinical cohort of patient-derived xenograft (PDX) models of DS-ALL, comprehensively characterized at the genetic and transcriptomic levels, and have proven its suitability for preclinical studies by assessing the efficacy of drug combination between the MEK inhibitor trametinib and conventional chemotherapy agents. Results: Whole-exome and RNA-sequencing experiments revealed a high incidence of somatic alterations leading to RAS/MAPK pathway activation in our cohort of DS-ALL, as well as in other pediatric B-ALL presenting somatic gain of the chromosome 21 (B-ALL+21). In murine and human B-cell precursors, activated KRASG12D functionally cooperates with trisomy 21 to deregulate transcriptional networks that promote increased proliferation and self renewal, as well as B-cell differentiation blockade. Moreover, we revealed that inhibition of RAS/MAPK pathway activation using the MEK1/2 inhibitor trametinib decreased leukemia burden in several PDX models of B-ALL+21, and enhanced survival of DS-ALL PDX in combination with conventional chemotherapy agents such as vincristine. Conclusions: Altogether, using novel and suitable PDX models, this study indicates that RAS/MAPK pathway inhibition represents a promising strategy to improve the outcome of Down syndrome children with B-cell precursor leukemia.
The Journal of experimental medicine · 2024
B cell acute lymphoblastic leukemia (B-ALL) is a multistep disease characterized by the hierarchical acquisition of genetic alterations. However, the question of how a primary oncogene reprograms stem cell–like properties in committed B cells and leads to a preneoplastic population remains unclear. Here, we used the PAX5::ELN oncogenic model to demonstrate a causal link between the differentiation blockade, the self-renewal, and the emergence of preleukemic stem cells (pre-LSCs). We show that PAX5::ELN disrupts the differentiation of preleukemic cells by enforcing the IL7r/JAK-STAT pathway. This disruption is associated with the induction of rare and quiescent pre-LSCs that sustain the leukemia-initiating activity, as assessed using the H2B-GFP model. Integration of transcriptomic and chromatin accessibility data reveals that those quiescent pre-LSCs lose B cell identity and reactivate an immature molecular program, reminiscent of human B-ALL chemo-resistant cells. Finally, our transcriptional regulatory network reveals the transcription factor EGR1 as a strong candidate to control quiescence/resistance of PAX5::ELN pre-LSCs as well as of blasts from human B-ALL.
Journal of clinical medicine · 2022
Large granular T-cell leukemia is a clonal hematological condition often associated with autoimmune disorders. Whether small-sized T-cell clones that are otherwise asymptomatic can promote immune kidney disorders remains elusive. In this monocentric retrospective cohort in a tertiary referral center in France, we reviewed characteristics of 29 patients with T-cell clone proliferation and autoimmune kidney disorders. Next-generation sequencing of the T-cell receptor of circulating T-cells was performed in a subset of patients. The T-cell clones were detected owing to systematic screening (mean count 0.32 × 109/L, range 0.13–3.7). Strikingly, a common phenotype of acute interstitial nephropathy was observed in 22 patients (median estimated glomerular filtration rate at presentation of 22 mL/min/1.73 m2 (range 0–56)). Kidney biopsies showed polymorphic inflammatory cell infiltration (predominantly CD3+ T-cells, most of them demonstrating positive phospho-STAT3 staining) and non-necrotic granuloma in six cases. Immune-mediated glomerulopathy only or in combination with acute interstitial nephropathy was identified in eight patients. Next-generation sequencing (n = 13) identified a major T-cell clone representing more than 1% of the T-cell population in all but two patients. None had a mutation of STAT3. Twenty patients (69%) had two or more extra-kidney autoimmune diseases. Acute interstitial nephropathies were controlled with corticosteroids, cyclosporin A, or tofacitinib. Thus, we showed that small-sized T-cell clones (i.e., without lymphocytosis) undetectable without specific screening are associated with various immune kidney disorders, including a previously unrecognized phenotype characterized by severe inflammatory kidney fibrosis and lymphocytic JAK/STAT activation.
Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).
The Journal of experimental medicine · 2024 · Journal Article
Fregona V, Bayet M, Bouttier M, Largeaud L, et al.
Journal of clinical medicine · 2022 · Journal Article
Piedrafita A, Vergez F, Belliere J, Prades N, et al.
Clinical cancer research : an official journal of the American Association for Cancer Research · 2020 · Journal Article
Laurent AP, Siret A, Ignacimouttou C, Panchal K, et al.