A5083761456- CAR-T cell therapy research
- Immune Cell Function and Interaction
- Chronic Lymphocytic Leukemia Research
- Retinoids in leukemia and cellular processes
- Ubiquitin and proteasome pathways
- Acute Myeloid Leukemia Research
- Colorectal Cancer Treatments and Studies
- Histone Deacetylase Inhibitors Research
- Protein Degradation and Inhibitors
- Melanoma and MAPK Pathways
- T-cell and B-cell Immunology
- Genetic factors in colorectal cancer
- Gastric Cancer Management and Outcomes
- Circular RNAs in diseases
- Extracellular vesicles in disease
- Photoreceptor and optogenetics research
- Cytomegalovirus and herpesvirus research
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Helicobacter pylori-related gastroenterology studies
- Neuroscience and Neuropharmacology Research
- Receptor Mechanisms and Signaling
- MicroRNA in disease regulation
- Blood disorders and treatments
St Anna Children's Hospital
2023-2024
St. Anna Children's Cancer Research Institute
2023-2024
Université de Montpellier
2014-2022
La Ligue Contre le Cancer
2018-2022
Centre National de la Recherche Scientifique
2014-2022
Institut de Génétique Moléculaire de Montpellier
2014-2018
Institut de Génomique Fonctionnelle
2018
Cancer Research UK Manchester Institute
2015
University of Manchester
2015
Chemotherapeutic drugs used in the treatment of acute myeloid leukemias (AMLs) are thought to induce cancer cell death through generation DNA double-strand breaks. Here, we report that one their early effects is loss conjugation ubiquitin-like protein SUMO from its targets via reactive oxygen species (ROS)-dependent inhibition SUMO-conjugating enzymes. Desumoylation regulates expression specific genes, such as proapoptotic gene DDIT3, and helps apoptosis chemosensitive AMLs. In contrast,...
Differentiation therapies using all-trans retinoic acid (ATRA) are highly efficient at treating acute promyelocytic leukemia (APL), a subtype of myeloid (AML). However, their efficacy, if any, is limited in the case non-APL AML. We report here that inhibition SUMOylation, posttranslational modification related to ubiquitination, restores prodifferentiation and antiproliferative activities retinoids Controlled SUMOylation with pharmacologic inhibitors 2-D08 or anacardic acid, via...
Resistance to chemotherapeutic drugs is a major cause of treatment failure in acute myeloid leukemias (AML). To better characterize the mechanisms chemoresistance, we first identified genes whose expression dysregulated AML cells resistant daunorubicin or cytarabine, main used for induction therapy. The found be activated are mostly linked immune signaling and inflammation. Among them, strong upregulation NOX2 NAPDH oxidase subunit (CYBB, CYBA, NCF1, NCF2, NCF4 RAC2). ensuing increase NADPH...
<p>Supplementary Figure S7: Analysis of differentially accessible genes in NK cell resistant tumour cells.</p>
<p>Supplementary Figure S8: Secondary resistant B-ALL cell clones.</p>
<p>Supplementary Figure S3: Flow cytometric analyses of human data sets and the NK-cell receptor ligand on mouse B-ALL cell lines.</p>
<p>Supplementary Figure S9: Profiles of tumour cells co-cultured with WT, Prf1-/- or Ifng-/- NK cells.</p>
<div>Abstract<p>The term cancer immunoediting describes the dual role by which immune system can suppress and promote tumor growth is divided into three phases: elimination, equilibrium, escape. The of NK cells has mainly been attributed to elimination phase. Here, we show that play a in all phases immunoediting. Extended co-culturing DNA-barcoded mouse BCR/ABL<sup>p185+</sup> B-cell acute lymphoblastic leukemia (B-ALL) with allowed for quantitative measure...
<p>Supplementary Figure S10: Generation of Plaat3 KO B-ALL clones and their characterisation.</p>
<p>Supplementary Figure S2: Flow cytometric analysis and gating strategies shown in 5.</p>
<p>Supplementary Figure S5: Extended quantification of NK cell-mediated cancer immunoediting <i>in vitro</i>.</p>
<p>Supplementary Figure S6: Analysis of differentially expressed genes in NK cell resistant tumour cells.</p>
<p>Supplementary Figure S1: Flow cytometric analysis and gating strategies.</p>
<p>Supplementary Figure S11: The expression of LY6E on K562 does not impact IFN-γ or TNF-α production in NK cells.</p>
<p>Supplementary Figure S4: B-ALL cell line characterisation and details about the barcode library.</p>
Abstract MLK4 is a member of the mixed-lineage family kinases that regulate JNK, p38, and ERK kinase signaling pathways. mutations have been identified in various human cancers, including frequently colorectal cancer, where their function pathobiological importance uncertain. In this study, we assessed functional consequences colon tumorigenesis. Biochemical data indicated majority are loss-of-function (LOF) can exert dominant-negative effects. seeking to understand abrogated activity these...
Extracellular vesicles (EVs) are nanosized lipid bilayer-encapsulated particles secreted by virtually all cell types. EVs play an essential role in cellular crosstalk health and disease. The origin of determines their composition potential therapeutic effect. Mesenchymal stem/stromal (MSC)-derived have shown a comparable to donor cells, making them promising tool for regenerative medicine. application circumvents some safety concerns associated with the transplantation viable, replicating...
Abstract The term cancer immunoediting describes the dual role by which immune system can suppress and promote tumour growth is divided into three phases: elimination, equilibrium escape. of NK cells has mainly been attributed to elimination phase. Here we show that play a in all phases immunoediting. Extended co-culturing DNA barcoded mouse BCR/ABLp185+ B-cell acute lymphoblastic leukaemia (B-ALL) with allowed for quantitative measure cell–mediated Although most cell clones were efficiently...
<div>Abstract<p>MLK4 is a member of the mixed-lineage family kinases that regulate JNK, p38, and ERK kinase signaling pathways. MLK4 mutations have been identified in various human cancers, including frequently colorectal cancer, where their function pathobiological importance uncertain. In this study, we assessed functional consequences colon tumorigenesis. Biochemical data indicated majority are loss-of-function (LOF) can exert dominant-negative effects. seeking to understand...
<div>Abstract<p>MLK4 is a member of the mixed-lineage family kinases that regulate JNK, p38, and ERK kinase signaling pathways. MLK4 mutations have been identified in various human cancers, including frequently colorectal cancer, where their function pathobiological importance uncertain. In this study, we assessed functional consequences colon tumorigenesis. Biochemical data indicated majority are loss-of-function (LOF) can exert dominant-negative effects. seeking to understand...