Éric Solary

ORCID: 0000-0002-8629-1341
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Research Areas
  • Acute Myeloid Leukemia Research
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Chronic Lymphocytic Leukemia Research
  • Cell death mechanisms and regulation
  • Chronic Myeloid Leukemia Treatments
  • Cancer therapeutics and mechanisms
  • Epigenetics and DNA Methylation
  • Immune cells in cancer
  • Cancer Genomics and Diagnostics
  • Immune Cell Function and Interaction
  • Cancer-related Molecular Pathways
  • Heat shock proteins research
  • Acute Lymphoblastic Leukemia research
  • Lung Cancer Treatments and Mutations
  • Eosinophilic Disorders and Syndromes
  • Drug Transport and Resistance Mechanisms
  • Phagocytosis and Immune Regulation
  • Retinoids in leukemia and cellular processes
  • Autophagy in Disease and Therapy
  • Lymphoma Diagnosis and Treatment
  • Cancer-related gene regulation
  • Immunotherapy and Immune Responses
  • RNA Interference and Gene Delivery
  • Blood disorders and treatments
  • DNA Repair Mechanisms

Institut Gustave Roussy
2015-2024

Inserm
2015-2024

Université Paris-Saclay
2015-2024

Université Paris-Sud
2014-2024

Hôpital Avicenne
2024

Saint Louis University Hospital
2024

Hôpital Necker-Enfants Malades
1999-2023

Groupe Francophone des Myélodysplasies
1999-2022

Fondation ARC pour la Recherche sur le Cancer
2020-2022

Laboratoire d'études sur les monothéismes
2013-2021

Myeloid-derived suppressor cells (MDSCs) have been identified in humans and mice as a population of immature myeloid with the ability to suppress T cell activation. They accumulate tumor-bearing shown contribute cancer development. Here, we isolated tumor-derived exosomes (TDEs) from mouse lines that an interaction between TDE-associated Hsp72 MDSCs determines suppressive activity via activation Stat3. In addition, soluble factors triggered MDSC expansion Erk. Stat3 TLR2/MyD88-dependent...

10.1172/jci40483 article EN Journal of Clinical Investigation 2010-01-19

We investigated the mechanisms of immune tolerance raised by tumors comparing immunogenic and tolerogenic tumor cell clones isolated from a rat colon carcinoma. When injected into syngeneichosts, REGb cells yield that are rejected, while PROb progressive inhibit regression tumors. show here volume is correlated with an expansion CD4(+)CD25(+) regulatory T lymphocytes in lymphoid tissues. These delay vivo rejection vitro cell-mediated responses against through mechanism requires contact...

10.1002/eji.200324181 article EN European Journal of Immunology 2004-02-01

The mechanisms through which regulatory T cells accumulate in lymphoid organs of tumor-bearing hosts remain elusive. Our experiments indicate that the accumulation CD4+CD25+ (T reg cells) expressing FoxP3 and exhibiting immunosuppressive function originates from proliferation naturally occurring CD25+ requires signaling transforming growth factor (TGF)–β receptor II. During tumor progression, a subset dendritic (DCs) myeloid immature phenotype is recruited to draining lymph nodes. This DC...

10.1084/jem.20050463 article EN The Journal of Experimental Medicine 2005-09-26

PURPOSE The prognosis of invasive pulmonary aspergillosis (IPA) occurring in neutropenic patients remains poor. We studied whether new strategies for early diagnosis could improve outcome these patients. PATIENTS AND METHODS Twenty-three histologically proven and 14 highly probable IPAs 37 hematologic (neutropenic 36) were analyzed retrospectively. RESULTS most frequent clinical signs associated with IPA cough (92%), chest pain (76%), hemoptysis (54%). Bronchoalveolar lavage (BAL) was...

10.1200/jco.1997.15.1.139 article EN Journal of Clinical Oncology 1997-01-01

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

We have previously shown that the small heat shock protein HSP27 inhibited apoptotic pathways triggered by a variety of stimuli in mammalian cells. The present study demonstrates overexpression decreases U937 human leukemic cell sensitivity to etoposide-induced cytotoxicity preventing apoptosis. As observed for Bcl-2, delays poly(ADP-ribose)polymerase cleavage and procaspase-3 activation. In contrast with does not prevent cytochrome c release from mitochondria. cell-free system, addition...

10.1096/fasebj.13.14.2061 article EN The FASEB Journal 1999-11-01

The excision repair cross-complementation group 1 (ERCC1) protein is a potential prognostic biomarker of the efficacy cisplatin-based chemotherapy in non–small-cell lung cancer (NSCLC). Although several ongoing trials are evaluating level expression ERCC1, no consensus has been reached regarding method for evaluation.

10.1056/nejmoa1214271 article EN New England Journal of Medicine 2013-03-20

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
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