Steven L. Allen

ORCID: 0000-0002-3482-3182
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About
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Research Areas
  • Chronic Lymphocytic Leukemia Research
  • Immunodeficiency and Autoimmune Disorders
  • Lymphoma Diagnosis and Treatment
  • Monoclonal and Polyclonal Antibodies Research
  • Acute Myeloid Leukemia Research
  • Acute Lymphoblastic Leukemia research
  • Glycosylation and Glycoproteins Research
  • Immune Cell Function and Interaction
  • Chronic Myeloid Leukemia Treatments
  • Histone Deacetylase Inhibitors Research
  • T-cell and Retrovirus Studies
  • Hemoglobinopathies and Related Disorders
  • Cancer therapeutics and mechanisms
  • Retinoids in leukemia and cellular processes
  • Phagocytosis and Immune Regulation
  • Neutropenia and Cancer Infections
  • Lung Cancer Treatments and Mutations
  • Drug Transport and Resistance Mechanisms
  • Cytomegalovirus and herpesvirus research
  • Protein Degradation and Inhibitors
  • CAR-T cell therapy research
  • Cancer Treatment and Pharmacology
  • HIV/AIDS drug development and treatment
  • Cancer Genomics and Diagnostics
  • Cutaneous lymphoproliferative disorders research

Northwell Health
2016-2025

Feinstein Institute for Medical Research
2015-2024

Hofstra University
2014-2024

Royal Marsden Hospital
2024

North Shore Diabetes and Endocrine Associates
2024

Nova Scotia Health Authority
2024

North Shore University Hospital
2010-2023

United Kingdom Atomic Energy Authority
2023

University of Birmingham
2023

Cork University Hospital
2023

To better understand the stage(s) of differentiation reached by B-type chronic lymphocytic leukemia (B-CLL) cells and to gain insight into potential role antigenic stimulation in development diversification these cells, we analyzed rearranged VH genes expressed 83 B-CLL (64 IgM+ 19 non-IgM+). Our results confirm extend observations a bias use certain VH, D, JH among cells. In addition, they indicate that approximately 50% 75% non-IgM+ can exhibit somatic mutations. The presence mutation...

10.1172/jci3009 article EN Journal of Clinical Investigation 1998-10-15

PURPOSE Romidepsin (depsipeptide or FK228) is a member of new class antineoplastic agents active in T-cell lymphoma, the histone deacetylase inhibitors. On basis observed responses phase I trial, II trial romidepsin patients with lymphoma was initiated. PATIENTS AND METHODS The initial cohort limited to cutaneous (CTCL), subtypes mycosis fungoides Sézary syndrome, who had received no more than two prior cytotoxic regimens. There were limits on other types therapy. Subsequently, protocol...

10.1200/jco.2008.21.6150 article EN Journal of Clinical Oncology 2009-10-14

Due to its relatively slow clinical progression, B cell chronic lymphocytic leukemia (B-CLL) is classically described as a disease of accumulation rather than proliferation. However, evidence for various forms clonal evolution suggests that B-CLL clones may be more dynamic previously assumed. We used nonradioactive, stable isotopic labeling method measure kinetics in vivo. Nineteen patients drank an aliquot deuterated water (2H2O) daily 84 days, and 2H incorporation into the deoxyribose...

10.1172/jci23409 article EN Journal of Clinical Investigation 2005-03-01

Previous studies suggest that the diversity of expressed variable (V) region repertoire immunoglobulin (Ig)H chain B-CLL cells is restricted. Although limited examples marked constraint in primary structure H and L V regions exist, possibility this level restriction a general principle disease has not been accepted. This report describes five sets patients, mostly with unmutated or minimally mutated IgV genes, strikingly similar B cell antigen receptors (BCRs) arising from use common gene...

10.1084/jem.20040544 article EN The Journal of Experimental Medicine 2004-08-16

Infection with the human T-cell lymphotropic virus type I, a retrovirus, can cause distinctive cancer, adult leukemia–lymphoma. The median survival of patients acute and lymphomatous forms disease is short, despite use cytotoxic chemotherapy.

10.1056/nejm199506293322603 article EN New England Journal of Medicine 1995-06-29

Purpose This phase I dose-escalation trial was performed to determine the maximum-tolerated dose, dose-limiting toxicities, and pharmacokinetics of CPX-351. Patients Methods CPX-351 induction administered on days 1, 3, 5 by 90-minute infusion 48 relapsed or refractory patients with acute myeloid leukemia (AML) high-risk myelodysplasia. Doses started at 3 units/m 2 dose doublings in single-patient cohorts until a pharmacodynamic effect (treatment-related adverse events reduction bone marrow...

10.1200/jco.2010.30.5961 article EN Journal of Clinical Oncology 2011-02-01

CD5-expressing B lymphocytes from patients with selected chronic lymphoproliferative disorders were used to determine whether monoclonal populations of CD5+ human cells produce autoantibodies. 19 lymphocytic leukemia (CLL) and one diffuse well-differentiated lymphoma (DWDL) cultured, without mitogenic stimulation, obtain Ig these cells. 17 the 20 samples produced in vitro. mAb nine reactive either IgG, ssDNA, or dsDNA. In every instance, autoantibodies displayed monotypic L chain usage that...

10.1084/jem.169.1.255 article EN The Journal of Experimental Medicine 1989-01-01

Studies of B cell antigen receptors (BCRs) expressed by leukemic lymphocytes from patients with chronic lymphocytic leukemia (B-CLL) suggest that some level BCR structural restriction become transformed. While analyzing rearranged VHDJH and VLJL genes 25 non–IgM-producing B-CLL cases, we found five IgG+ cases display strikingly similar BCRs (use the same H- L-chain V gene segments unique, shared heavy chain third complementarity-determining region [HCDR3] light [LCDR3] motifs). These...

10.1172/jci19399 article EN Journal of Clinical Investigation 2004-04-01

Chronic lymphocytic leukemia (CLL) represents the outgrowth of a CD5+ B cell. Its etiology is unknown. The structure membrane Ig on CLL cells unrelated patients can be remarkably similar. Therefore, antigen binding and stimulation could contribute to clonal selection expansion as well disease promotion. Initial studies suggest that mAbs bind autoantigens. Since apoptosis make autoantigens accessible for recognition by antibodies, also create neo-epitopes chemical modifications occurring...

10.2119/2008-00102.catera article EN cc-by Molecular Medicine 2008-11-01

Catastrophic antiphospholipid syndrome (CAPS) is characterized by histopathologic evidence of small vessel thrombosis, dysfunction multiple organs occurring over a short period time, and laboratory confirmation the presence antibodies (aPL). Treatment CAPS focuses on anticoagulation therapy removal aPL that promote thrombosis activating endothelial cells, monocytes, platelets. Studies in animal models support hypothesis more targeted intervention, such as complement inhibition, may be an...

10.1002/art.34440 article EN Arthritis & Rheumatism 2012-02-21

DNA from 135 patients with chronic myelogenous leukemia (CML) at various clinical stages and Philadelphia (Ph1) chromosome positive acute lymphoblastic was investigated for alterations in a variety of proto-oncogenes which have been implicated the evolution CML its phase to blast crisis. The most common genetic change found typical Ph1 crisis an alteration p53 gene involving either rearrangement, deletion, or point mutation coding sequence gene. Alterations were myeloid rare megakaryocytic...

10.1172/jci115234 article EN Journal of Clinical Investigation 1991-06-01

Abstract The failure of chemotherapeutic regimens to eradicate cancers often results from the outgrowth minor subclones with more dangerous genomic abnormalities or self-renewing capacity. To explore such intratumor complexities in B-cell chronic lymphocytic leukemia (CLL), we measured kinetics vivo by quantifying deuterium ( 2 H)-labeled cells as an indicator a cell that had divided. Separating CLL clones on basis reciprocal densities chemokine (C-X-C motif) receptor 4 (CXCR4) and cluster...

10.2119/molmed.2011.00360 article EN cc-by Molecular Medicine 2011-09-23
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