A5045617088- Chronic Lymphocytic Leukemia Research
- Galectins and Cancer Biology
- Lymphoma Diagnosis and Treatment
- Immunodeficiency and Autoimmune Disorders
- Phagocytosis and Immune Regulation
- Monoclonal and Polyclonal Antibodies Research
- Immune Cell Function and Interaction
- Acute Lymphoblastic Leukemia research
- CAR-T cell therapy research
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Viral-associated cancers and disorders
- Systemic Sclerosis and Related Diseases
- Neurogenetic and Muscular Disorders Research
- Pharmacological Effects and Toxicity Studies
- Hemoglobinopathies and Related Disorders
- Inflammatory Myopathies and Dermatomyositis
National Heart Lung and Blood Institute
2019-2024
National Institutes of Health
2019-2024
MRC Laboratory for Molecular Cell Biology
2018
University College London
2018
Sorbonne Paris Cité
2018
Inserm
2016
Université Sorbonne Paris Nord
2016
To study the role of B lymphocytes in systemic sclerosis (SSc).Peripheral cell subpopulations and production interleukin-6 (IL-6) transforming growth factor β (TGFβ) were analyzed using flow cytometry multiplex assay. The fibroblast proliferation rate upon incubation with supernatants from cells isolated SSc patients or healthy controls was assessed XTT, bromodeoxyuridine, Ki-67. Collagen a collagen assay.Ninety untreated (12 males) fulfilling American College Rheumatology/European League...
Chronic lymphocytic leukemia (CLL) is an immunosuppressive disease characterized by increased infectious morbidity and inferior antitumor activity of immunotherapies. Targeted therapy with Bruton's tyrosine kinase inhibitors (BTKis) or the Bcl-2 inhibitor venetoclax has profoundly improved treatment outcomes in CLL. To overcome prevent drug resistance extend duration response after a time-limited therapy, combination regimens are tested. Anti-CD20 antibodies that recruit cell-...
To determine the role of CD49d for response to Bruton's tyrosine kinase inhibitors (BTKis) in patients with chronic lymphocytic leukemia (CLL).In treated acalabrutinib (n=48), expression, VLA-4 integrin activation, and tumor transcriptomes CLL cells were assessed. Clinical responses BTKis investigated (n=48; NCT02337829), ibrutinib (n=73; NCT01500733) patients.In acalabrutinib, treatment induced lymphocytosis was comparable both subgroups but resolved more rapidly CD49d+ cases. Acalabrutinib...
Arthrogryposis-Renal dysfunction-Cholestasis syndrome (ARC, MIM#208085) is a rare multisystem disease due to mutations in the VPS33B and VIPAR genes, both involved maintaining apical-basolateral cell polarity. The correlation between phenotype ARC Syndrome not well described. We report on 6 year old patient who presented with severe renal Fanconi as first manifestation of related combined de novo mutation gene. A girl during life ARC-Syndrome. This case presents all defining features...
Despite numerous therapeutic options, safe and curative therapy is unavailable for most patients with chronic lymphocytic leukemia (CLL). A drawback of current therapies such as the anti-CD20 monoclonal antibody (mAb) rituximab elimination all healthy B cells, resulting in impaired humoral immunity. We previously reported identification a patient-derived, CLL-binding mAb, JML-1, identified sialic acid-binding immunoglobulin-like lectin-6 (Siglec-6) target JML-1. Although little known about...
<div>Abstract<p>Purpose: To determine the role of CD49d for response to Bruton’s tyrosine kinase inhibitors (BTKis) in patients with chronic lymphocytic leukemia (CLL). Methods: In treated acalabrutinib (n=48), expression, VLA-4 integrin activation, and tumor transcriptomes CLL cells were assessed. Clinical responses BTKis investigated (n=48; NCT02337829), ibrutinib (n=73; NCT01500733) patients. Results: acalabrutinib, treatment induced lymphocytosis was comparable both subgroups...
<p>Supplementary Figure S3. In vivo effect of acalabrutinib on the VLA-4 activation upon BCR and chemokine signaling</p>
<p>Supplementary Figure S5. Time to disease progression, prevalence of resistance mutations, and risk category by CLL-4 model</p>
<p>Supplementary Figure S3. In vivo effect of acalabrutinib on the VLA-4 activation upon BCR and chemokine signaling</p>
<p>Supplementary Figure S5. Time to disease progression, prevalence of resistance mutations, and risk category by CLL-4 model</p>
<p>Supplementary Methods</p>
<p>Supplementary Figure S4. Clinical impact of CD49d bimodal expression on durability BTKi therapy.</p>
<p>Supplementary Methods</p>
<p>Supplementary Figure S4. Clinical impact of CD49d bimodal expression on durability BTKi therapy.</p>