Virginie Trouplin

Institut de Neurosciences de la Timone

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ÉG

Éric Ghigo

Méditerranée Infection Foundation

Giovanna Mottola

Institut National de Recherche pour l'Agriculture, l'Alimentation et l'Environnement

Daniel Birnbaum

Centre National de la Recherche Scientifique

Julien Mozziconacci

Institut Paoli-Calmettes

Norbert Vey

Inserm

Frédéric Colland

Institut des Hautes Études Scientifiques

Véronique Gelsi‐Boyer

Institut Paoli-Calmettes

Nicolas Boucherit

Centre de Recherche en Cancérologie de Marseille

Max Chaffanet

Centre de Recherche en Cancérologie de Marseille

Alessandra Calabrese

Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale"

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Inserm

101

Centre National de la Recherche Scientifique

Aix-Marseille Université

Centre de Recherche en Cancérologie de Marseille

Institut Paoli-Calmettes

Hybrigenics (France)

Institut Pasteur

Université Paris Cité

Institut Curie

Institut Pprime

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Baseline Susceptibility of Primary Human Immunodeficiency Virus Type 1 to Entry Inhibitors

Journal of Virology (2002)

Béatrice Labrosse Jean‐Louis Labernardière Elisabeth Dam Virginie Trouplin Katharina Skrabal

ABSTRACT Human immunodeficiency virus type 1 plasma viruses from 29 entry inhibitor-naive patients were characterized for their susceptibilities to T-20, AMD3100, and RANTES. A strikingly wide range of susceptibilities to T-20 was observed that was influenced by coreceptor usage but not by the susceptibilities of the viruses to inhibitors that target the chemokine receptors or by polymorphisms in the gp41 N helix.

Chemokine receptor CCR5

10.1128/jvi.77.2.1610-1613.2003

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Citations (93)

ASXL1 mutation is associated with poor prognosis and acute transformation in chronic myelomonocytic leukaemia

British Journal of Haematology (2010)

Véronique Gelsi‐Boyer Virginie Trouplin Julien Roquain José Adélaı̈de Nadine Carbuccia

Chronic myelomonocytic leukaemia (CMML) is a haematological disease currently classified in the category of myelodysplastic syndromes/myeloproliferative neoplasm (MDS/MPN) because of its dual clinical and biological presentation. The molecular biology of CMML is poorly characterized. We studied a series of 53 CMML samples including 31 cases of myeloproliferative form (MP-CMML) and 22 cases of myelodysplastic forms (MD-CMML) using array-comparative genomic hybridisation (aCGH) and sequencing of 13 candidate genes including ASXL1, CBL, FLT3, IDH1, IDH2, JAK2, KRAS, NPM1, NRAS, PTPN11, RUNX1, TET2 and WT1. Mutations in ASXL1 and in the genes associated with proliferation (CBL, FLT3, PTPN11, NRAS) were mainly found in MP-CMML cases. Mutations of ASXL1 correlated with an evolution toward an acutely transformed state: all CMMLs that progressed to acute phase were mutated and none of the unmutated patients had evolved to acute leukaemia. The overall survival of ASXL1 mutated patients was lower than that of unmutated patients.

Chronic myelomonocytic leukemia

Monocytosis

PTPN11

IDH2

Myeloproliferative neoplasm

NPM1

10.1111/j.1365-2141.2010.08381.x

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Citations (214)

Staphylococcus aureus Promotes Smed-PGRP-2/Smed-setd8-1 Methyltransferase Signalling in Planarian Neoblasts to Sensitize Anti-bacterial Gene Responses During Re-infection

EBioMedicine (2017)

Cédric Torre Prasad Abnave Landry Laure Tsoumtsa Giovanna Mottola Catherine Lépolard

Little is known about how organisms exposed to recurrent infections adapt their innate immune responses. Here, we report that planarians display a form of instructed immunity to primo-infection by Staphylococcus aureus that consists of a transient state of heightened resistance to re-infection that persists for approximately 30 days after primo-infection. We established the involvement of stem cell-like neoblasts in this instructed immunity using the complementary approaches of RNA-interference-mediated cell depletion and tissue grafting-mediated gain of function. Mechanistically, primo-infection leads to expression of the peptidoglycan receptor Smed-PGRP-2, which in turn promotes Smed-setd8-1 histone methyltransferase expression and increases levels of lysine methylation in neoblasts. Depletion of neoblasts did not affect S. aureus clearance in primo-infection but, in re-infection, abrogated the heightened elimination of bacteria and reduced Smed-PGRP-2 and Smed-setd8-1 expression. Smed-PGRP-2 and Smed-setd8-1 sensitize animals to heightened expression of Smed-p38 MAPK and Smed-morn2, which are downstream components of anti-bacterial responses. Our study reveals a central role of neoblasts in innate immunity against S. aureus to establish a resistance state facilitating Smed-sted8-1-dependent expression of anti-bacterial genes during re-infection.

10.1016/j.ebiom.2017.04.031

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Citations (27)

Genome profiling of chronic myelomonocytic leukemia: frequent alterations of RAS and RUNX1genes

BMC Cancer (2008)

Véronique Gelsi‐Boyer Virginie Trouplin José Adélaı̈de Nicola Aceto Virginie Rémy

Abstract Background Chronic myelomonocytic leukemia (CMML) is a hematological disease close to, but separate from both myeloproliferative disorders (MPD) and myelodysplastic syndromes and may show either myeloproliferative (MP-CMML) or myelodysplastic (MD-CMML) features. Not much is known about the molecular biology of this disease. Methods We studied a series of 30 CMML samples (13 MP- and 11 MD-CMMLs, and 6 acutely transformed cases) from 29 patients by using Agilent high density array-comparative genomic hybridization (aCGH) and sequencing of 12 candidate genes. Results Two-thirds of samples did not show any obvious alteration of aCGH profiles. In one-third we observed chromosome abnormalities (e.g. trisomy 8, del20q) and gain or loss of genes (e.g. NF1 , RB1 and CDK6 ). RAS mutations were detected in 4 cases (including an uncommon codon 146 mutation in KRAS ) and PTPN11 mutations in 3 cases. We detected 11 RUNX1 alterations (9 mutations and 2 rearrangements). The rearrangements were a new, cryptic inversion of chromosomal region 21q21-22 leading to break and fusion of RUNX1 to USP16 . RAS and RUNX1 alterations were not mutually exclusive. RAS pathway mutations occurred in MP-CMMLs (~46%) but not in MD-CMMLs. RUNX1 alterations (mutations and cryptic rearrangement) occurred in both MP and MD classes (~38%). Conclusion We detected RAS pathway mutations and RUNX1 alterations. The latter included a new cryptic USP16-RUNX1 fusion. In some samples, two alterations coexisted already at this early chronic stage.

Chronic myelomonocytic leukemia

Comparative genomic hybridization

RUNX1

10.1186/1471-2407-8-299

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Citations (123)

Data from Small-molecule inhibitor of USP7/HAUSP ubiquitin protease stabilizes and activates p53 in cells

Frédéric Colland Étienne Formstecher Xavier Jacq Céline Reverdy Cécile Planquette

<div>Abstract<p>Deregulation of the ubiquitin/proteasome system has been implicated in the pathogenesis of many human diseases, including cancer. Ubiquitin-specific proteases (USP) are cysteine proteases involved in the deubiquitination of protein substrates. Functional connections between USP7 and essential viral proteins and oncogenic pathways, such as the p53/Mdm2 and phosphatidylinositol 3-kinase/protein kinase B networks, strongly suggest that the targeting of USP7 with small-molecule inhibitors may be useful for the treatment of cancers and viral diseases. Using high-throughput screening, we have discovered HBX 41,108, a small-molecule compound that inhibits USP7 deubiquitinating activity with an IC<sub>50</sub> in the submicromolar range. Kinetics data indicate an uncompetitive reversible inhibition mechanism. HBX 41,108 was shown to affect USP7-mediated p53 deubiquitination <i>in vitro</i> and in cells. As RNA interference-mediated USP7 silencing in cancer cells, HBX 41,108 treatment stabilized p53, activated the transcription of a p53 target gene without inducing genotoxic stress, and inhibited cancer cell growth. Finally, HBX 41,108 induced p53-dependent apoptosis as shown in p53 wild-type and null isogenic cancer cell lines. We thus report the identification of the first lead-like inhibitor against USP7, providing a structural basis for the development of new anticancer drugs.[Mol Cancer Ther 2009;8(8):2286–95]</p></div>

Deubiquitinating enzyme

HBx

10.1158/1535-7163.c.6532221.v1

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Citations (0)

Screening in Planarians Identifies MORN2 as a Key Component in LC3-Associated Phagocytosis and Resistance to Bacterial Infection

Cell Host & Microbe (2014)

Prasad Abnave Giovanna Mottola Grégory Gimenez Nicolas Boucherit Virginie Trouplin

Planarian

10.1016/j.chom.2014.08.002

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Citations (101)