Andrew R. Branagan

ORCID: 0000-0002-3868-9267
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About
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Research Areas
  • Chronic Lymphocytic Leukemia Research
  • Lymphoma Diagnosis and Treatment
  • Multiple Myeloma Research and Treatments
  • Immunodeficiency and Autoimmune Disorders
  • Chronic Myeloid Leukemia Treatments
  • Monoclonal and Polyclonal Antibodies Research
  • Glycosylation and Glycoproteins Research
  • CAR-T cell therapy research
  • Cancer Treatment and Pharmacology
  • Protein Degradation and Inhibitors
  • Influenza Virus Research Studies
  • Viral-associated cancers and disorders
  • Gastrointestinal Tumor Research and Treatment
  • Renal Diseases and Glomerulopathies
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Synthesis and Biological Evaluation
  • Neuroendocrine Tumor Research Advances
  • vaccines and immunoinformatics approaches
  • Hematopoietic Stem Cell Transplantation
  • Blood groups and transfusion
  • Cancer survivorship and care
  • Cancer therapeutics and mechanisms
  • SARS-CoV-2 and COVID-19 Research
  • Acute Myeloid Leukemia Research
  • Acute Lymphoblastic Leukemia research

Massachusetts General Hospital
2017-2025

Harvard University
2004-2024

Dana-Farber Cancer Institute
2003-2023

ABB (Switzerland)
2023

Metropolitan Hospital
2023

Janssen (Belgium)
2023

Pharmacyclics (United States)
2023

Karyopharm Therapeutics (United States)
2023

Adaptive Biotechnologies (United States)
2023

Palmetto Hematology Oncology
2023

Rituximab is an important therapeutic for Waldenstrom's macroglobulinemia (WM). Polymorphisms in FcgammaRIIIA (CD16) receptor expression modulate human immunoglobulin G1 binding and antibody-dependent cell-mediated cytotoxicity, may therefore influence responses to rituximab.Sequence analysis of the entire coding region was undertaken 58 patients with WM whose outcomes after rituximab were known.Variations five codons identified. Two commonly observed (FcgammaRIIIA-48 FcgammaRIIIA-158)...

10.1200/jco.2005.06.059 article EN Journal of Clinical Oncology 2005-01-19

Abstract Purpose: Waldenstrom's macroglobulinemia (WM) is a B-cell disorder. Despite advances in the therapy, WM remains incurable. As such, novel therapeutic agents are needed for treatment of WM. Experimental Design: In this multicenter study, 27 patients with received up to eight cycles bortezomib at 1.3 mg/m2 on days 1, 4, 8, and 11. All but one patient had relapsed/or refractory disease. Results: Following median serum IgM levels declined from 4,660 2,092 mg/dL (P < 0.0001). The...

10.1158/1078-0432.ccr-06-2511 article EN Clinical Cancer Research 2007-06-01

We report the long-term findings and final analysis of a pivotal multicenter trial ibrutinib monotherapy in previously treated patients with Waldenström macroglobulinemia (WM).Sixty-three symptomatic median prior therapies two (range, one to nine therapies), whom 40% were refractory their previous therapy, received at 420 mg/d. Dose reduction was permitted for toxicity.The follow-up 59 months, overall major response rates 90.5% 79.4%, respectively. At best response, serum immunoglobulin M...

10.1200/jco.20.00555 article EN cc-by-nc-nd Journal of Clinical Oncology 2020-09-15

BCL2 is overexpressed and confers prosurvival signaling in malignant lymphoplasmacytic cells Waldenström macroglobulinemia (WM). Venetoclax a potent antagonist triggers vitro apoptosis of WM cells. The activity venetoclax remains to be clarified.We performed multicenter, prospective phase II study patients with previously treated (NCT02677324). was dose-escalated from 200 mg maximum dose 800 daily for up 2 years.Thirty-two were evaluable, including 16 exposed Bruton tyrosine kinase...

10.1200/jco.21.01194 article EN cc-by-nc-nd Journal of Clinical Oncology 2021-11-18

Abstract Herein, we present the final report of a single-center, prospective phase II study evaluating ibrutinib 420 mg once daily in 30 treatment-naive patients with Waldenstrom macroglobulinemia (WM). The is registered ClinicalTrials.Gov (NCT02604511). With median follow-up 50 months, overall, major, and VGPR response rates were 100%, 87%, 30%. rate was numerically but not significantly lower than without CXCR4 mutations (14% vs. 44%; p = 0.09). time to minor 0.9 major 1.9 though longer...

10.1038/s41375-021-01417-9 article EN cc-by Leukemia 2021-09-16

Chimeric antigen receptor T cells (CAR T) are groundbreaking therapies but may cause significant toxicities including cytokine release syndrome (CRS), immune effector cell-associated neurotoxicity (ICANS), and cytopenias. Granulocyte colony-stimulating factor (G-CSF) is often used to mitigate neutropenia after CAR T, there no consensus recommended strategy due hypothesized, largely unknown risks of exacerbating toxicities. To investigate the impact G-CSF, we retrospectively analyzed 197...

10.1038/s41408-022-00741-2 article EN cc-by Blood Cancer Journal 2022-11-01

Abstract Purpose: Thalidomide and its more potent immunomodulatory derivative lenalidomide enhance rituximab-mediated antibody-dependent cell-mediated cytotoxicity. We therefore evaluated rituximab in symptomatic Waldenstrom's macroglobulinemia (WM) patients naive to either agent. Experimental Design: Intended therapy consisted of 48 weeks (25 mg/d for 3 then 1 week off) along with (375 mg/m2/wk) dosed on 2 5 13 16. Sixteen were enrolled, 12 whom previously untreated. Results: Unexpectedly,...

10.1158/1078-0432.ccr-08-0862 article EN Clinical Cancer Research 2008-12-31
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