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| http://dx.doi.org/10.1016/j.jid.2016.04.018 | DOI Listing |
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Lymphoma driver mutations at the root of somatic evolution of nerve-damaging autoantibodies in myelin associated glycoprotein neuropathy.
J Autoimmun
September 2025
Garvan Institute of Medical Research, Darlinghurst, NSW, Australia; Cellular Genomics Futures Institute & School of Biomedical Sciences, UNSW Sydney, Australia. Electronic address:
Background: In autoimmune disease it is not understood how self-reactive B cells escape immune tolerance checkpoints to produce pathogenic autoantibodies.
Objective: In patients with demyelinating polyneuropathy caused by IgM autoantibodies against myelin associated glycoprotein (MAG) and the sulphated trisaccharide CD57, we aimed to test the hypothesis that B cells making the autoantibody escaped tolerance by acquiring lymphoma driver somatic mutations.
Methods: Deep single-cell RNA, DNA, flow cytometric and antibody specificity analysis of blood from three patients with MAG neuropathy.
SOHO State of the Art Updates and Next Questions | The Optimal Management of Waldenström Macroglobulinemia.
Clin Lymphoma Myeloma Leuk
June 2025
Bing Center for Waldenström Macroglobulinemia, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA. Electronic address:
Waldenström macroglobulinemia (WM) is a rare IgM-secreting lymphoplasmacytic lymphoma with recurrent somatic mutations in MYD88 and CXCR4 observed in the malignant cells of >90% and 30% to 40% of the patients. Given its rarity, WM poses specific diagnostic and management challenges. The diagnosis of WM is clinicopathological and no pathognomonic findings exist.
View Article and Find Full Text PDFMutational Landscape of Bone Marrow CD19 and CD138 Cells in Waldenström Macroglobulinemia (WM) and IgM Monoclonal Gammopathy of Undetermined Significance (IgM MGUS).
Cancer Med
December 2024
Niguarda Hospital, Department of Hematology and Oncology, Milano, Italy.
Background: Despite recurrent and activating mutations, including MYD88, CXCR4, ARID1A, KMT2D, and CD79B were identified, the genetic basis for Waldenström's Macroglobulinemia (WM) and the risk of progression of IgM MGUS to WM remain to be fully elucidated.
Methods: We investigated the mutation status of WM (n = 8), sWM (n = 7), and IgM MGUS (n = 5) patients, by performing high-throughput targeted AmpliSeq NGS on 117 target genes. Specifically, we analyzed the CD19+ cells from 15 WM/sWM patients and five IgM MGUS patients.
Comparative analysis of somatic mutations in MYD88, CD79B, CARD11, and BTK between gastric marginal zone B-cell lymphoma of MALT and diffuse large B-cell lymphoma.
Ann Hematol
December 2024
Institute of Pathology, Ulm University, Albert-Einstein-Allee 23, 89081, Ulm, Germany.
Lasalocid A selectively induces the degradation of MYD88 in lymphomas harboring the MYD88 L265P mutation.
Blood
March 2025
Department of Medicine, Dan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX.
Article Synopsis
- MYD88 is a key protein involved in immune signaling and is commonly mutated (L265P) in blood cancers, leading to tumor progression.
- Researchers discovered lasalocid-A, a small molecule that selectively kills lymphoma cells with the MYD88 L265P mutation by promoting the degradation of the mutated protein.
- The study showed that lasalocid-A not only effectively works in lab models but also has potential benefits for treating resistant lymphoma types and can enhance the effects of other cancer drugs.