Nathalie Droin

ORCID: 0000-0002-6099-5324
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About
Contact & Profiles
Research Areas
  • Acute Myeloid Leukemia Research
  • Chronic Lymphocytic Leukemia Research
  • Occupational and environmental lung diseases
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Medical Imaging and Pathology Studies
  • Chronic Myeloid Leukemia Treatments
  • Pleural and Pulmonary Diseases
  • Acute Lymphoblastic Leukemia research
  • Cell death mechanisms and regulation
  • Immune cells in cancer
  • Epigenetics and DNA Methylation
  • Cancer Genomics and Diagnostics
  • Immune Cell Function and Interaction
  • Pancreatic and Hepatic Oncology Research
  • CAR-T cell therapy research
  • Cancer-related Molecular Pathways
  • Lymphoma Diagnosis and Treatment
  • Autophagy in Disease and Therapy
  • Immune Response and Inflammation
  • Protein Degradation and Inhibitors
  • Immunodeficiency and Autoimmune Disorders
  • Immunotherapy and Immune Responses
  • Cancer-related gene regulation
  • DNA Repair Mechanisms
  • Ubiquitin and proteasome pathways

Institut Gustave Roussy
2016-2025

Inserm
2015-2024

Centre National de la Recherche Scientifique
2016-2024

Université Paris-Saclay
2015-2024

Université Paris-Sud
2011-2023

Université de Bourgogne
1999-2022

La Ligue Contre le Cancer
2016-2022

Institut de Recherche et de Documentation en Économie de la Santé
2022

Mayo Clinic in Arizona
2019

Contrôle transcriptionnel et épigénétique de l’hématopoïèse maligne
2017

The tumor suppressor p53 exerts its anti-neoplastic activity primarily through the induction of apoptosis. We found that cytosolic localization endogenous wild-type or trans-activation-deficient was necessary and sufficient for directly activated proapoptotic Bcl-2 protein Bax in absence other proteins to permeabilize mitochondria engage apoptotic program. also released both multidomain BH3-only [Proapoptotic family share only third homology domain (BH3)] were sequestered by Bcl-xL....

10.1126/science.1092734 article EN Science 2004-02-12

Purpose Several prognostic scoring systems have been proposed for chronic myelomonocytic leukemia (CMML), a disease in which some gene mutations—including ASXL1—have associated with poor prognosis univariable analyses. We developed and validated score overall survival (OS) based on mutational status standard clinical variables. Patients Methods genotyped ASXL1 up to 18 other genes including epigenetic (TET2, EZH2, IDH1, IDH2, DNMT3A), splicing (SF3B1, SRSF2, ZRSF2, U2AF1), transcription...

10.1200/jco.2012.47.3314 article EN Journal of Clinical Oncology 2013-05-21

Appropriate cancer care requires a thorough understanding of the natural history disease, including cell origin, pattern clonal evolution, and functional consequences mutations. Using deep sequencing flow-sorted populations from patients with chronic lymphocytic leukemia (CLL), we established presence acquired mutations in multipotent hematopoietic progenitors. Mutations affected known lymphoid oncogenes, BRAF, NOTCH1, SF3B1. NFKBIE EGR2 were observed at unexpectedly high frequencies, 10.7%...

10.1158/2159-8290.cd-14-0104 article EN Cancer Discovery 2014-06-12

The cytidine analogues azacytidine and 5-aza-2'-deoxycytidine (decitabine) are commonly used to treat myelodysplastic syndromes, with or without a myeloproliferative component. It remains unclear whether the response these hypomethylating agents results from cytotoxic an epigenetic effect. In this study, we address question in chronic myelomonocytic leukaemia. We describe comprehensive analysis of mutational landscape tumours, combining whole-exome whole-genome sequencing. identify average...

10.1038/ncomms10767 article EN cc-by Nature Communications 2016-02-24

The mechanisms of action and resistance to trastuzumab deruxtecan (T-DXd), an anti-HER2-drug conjugate for breast cancer treatment, remain unclear. phase 2 DAISY trial evaluated the efficacy T-DXd in patients with HER2-overexpressing (n = 72, cohort 1), HER2-low 74, 2) HER2 non-expressing 40, 3) metastatic cancer. In full analysis set population 177), confirmed objective response rate (primary endpoint) was 70.6% (95% confidence interval (CI) 58.3-81) 1, 37.5% CI 26.4-49.7) 29.7% 15.9-47) 3....

10.1038/s41591-023-02478-2 article EN cc-by Nature Medicine 2023-07-24

Abstract Cancer chemotherapy can induce tumor regression followed, in many cases, by relapse the long‐term. Thus this study was performed to assess determinants of such phenomenon using an vivo cancer model and vitro approaches. When animals bearing established are treated cisplatin, initially undergoes a dramatic shrinkage is characterized giant cells that do not proliferate but maintain DNA synthesis. After several weeks latency, resumes its progression consists small proliferating cells....

10.1016/j.cellbi.2008.04.021 article EN Cell Biology International 2008-05-04

Myelodysplastic syndromes and chronic myelomonocytic leukemia (CMML) are characterized by mutations in genes encoding epigenetic modifiers aberrant DNA methylation. methyltransferase inhibitors (DMTis) used to treat these disorders, but response is highly variable, with few means predict which patients will benefit. Here, we examined baseline differences mutations, methylation, gene expression 40 CMML who were responsive or resistant decitabine (DAC) order develop a molecular of predicting...

10.1172/jci78752 article EN Journal of Clinical Investigation 2015-03-29

Ischemia-reperfusion (IR) injury induces endoplasmic reticulum (ER) stress and cell death. Bax Inhibitor-1 (BI-1) is an evolutionarily conserved ER protein that suppresses death abundantly expressed in both liver kidney. We explored the role of BI-1 protection from IR by using bi - 1 knockout mice, employing models transient hepatic or renal artery occlusion. Compared to wild-type bi-1 mice subjected exhibited these characteristics: ( i ) increased histological injury; ii serum...

10.1073/pnas.0506854103 article EN Proceedings of the National Academy of Sciences 2006-02-14

Abstract TET2 somatic mutations occur in ∼10% of diffuse large B-cell lymphomas (DLBCL) but are unknown significance. Herein, we show that is required for the humoral immune response and a DLBCL tumor suppressor. loss function disrupts transit B cells through germinal centers (GC), causing GC hyperplasia, impaired class switch recombination, blockade plasma cell differentiation, preneoplastic phenotype. was linked to focal enhancer hydroxymethylation transcriptional repression genes mediate...

10.1158/2159-8290.cd-18-0657 article EN Cancer Discovery 2018-10-01
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