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MYD88 L265P somatic mutation in Waldenström's macroglobulinemia.
TLDR
MYD88 L265P is a commonly recurring mutation in patients with Waldenström's macroglobulinemia that can be useful in differentiating WaldenStröm’s macrogalobulinesia and non-IgM LPL from B-cell disorders that have some of the same features. Expand
Ibrutinib in previously treated Waldenström's macroglobulinemia.
TLDR
Ibrutinib was highly active, associated with durable responses, and safe in pretreated patients with Waldenström's macroglobulinemia, and the effect of MYD88 and CXCR4 mutations on outcomes was investigated. Expand
The genomic landscape of Waldenstrom macroglobulinemia is characterized by highly recurring MYD88 and WHIM-like CXCR4 mutations, and small somatic deletions associated with B-cell lymphomagenesis.
TLDR
The CXCR4 and CNA findings were validated in independent expansion cohorts of 147 and 30 WM patients, respectively, and provide a genomic basis for understanding the pathogenesis of WM. Expand
MYD88 L265P in Waldenström macroglobulinemia, immunoglobulin M monoclonal gammopathy, and other B-cell lymphoproliferative disorders using conventional and quantitative allele-specific polymerase
TLDR
These studies identify MYD88 L265P as a widely present mutation in WM and IgM MGUS patients using highly sensitive and specific AS-PCR assays with potential use in diagnostic discrimination and/or response assessment. Expand
Primary therapy of Waldenström macroglobulinemia with bortezomib, dexamethasone, and rituximab: WMCTG clinical trial 05-180.
TLDR
It is demonstrated that BDR produces rapid and durable responses, along with high rates of response and complete remissions in WM, and alternative schedules for bortezomib administration that includes weekly dosing should be pursued. Expand
Guideline for the diagnosis, treatment and response criteria for Bing-Neel syndrome
TLDR
Prospective clinical trials on Bing Neel syndrome patients that employ uniform treatment along with appropriate laboratory cerebral spinal fluid assessments and standardized MRI protocols will be invaluable, constituting a significant step forward in delineating treatment outcome for this intriguing disease manifestation. Expand
A mutation in MYD88 (L265P) supports the survival of lymphoplasmacytic cells by activation of Bruton tyrosine kinase in Waldenström macroglobulinemia.
TLDR
Inhibition of BTK or interleukin-1 receptor-associated kinase 1 and 4 kinase activity induced apoptosis of WM cells, and their combination resulted in more robust inhibition of NF-κB signaling and synergistic WM cell killing. Expand
Carfilzomib, rituximab, and dexamethasone (CaRD) treatment offers a neuropathy-sparing approach for treating Waldenström's macroglobulinemia.
TLDR
CaRD offers a neuropathy-sparing approach for proteasome inhibitor-based therapy in WM patients naïve to bortezomib and rituximab and was not impacted by MYD88(L265P) or CXCR4(WHIM) mutation status. Expand
Response assessment in Waldenström macroglobulinaemia: update from the VIth International Workshop
TLDR
This report represents a further update of the consensus panel criteria for the assessment of clinical response in patients with Waldenström macroglobulinaemia and a number of key changes are proposed but challenges do however remain. Expand
Treatment recommendations from the Eighth International Workshop on Waldenström's Macroglobulinemia.
TLDR
A task force for treatment recommendations was impanelled to review recently published and ongoing clinical trial data as well as the impact of new mutations (MYD88 and CXCR4) on treatment decisions, indications for B-cell receptor and proteasome inhibitors, and future clinical trial initiatives for WM patients. Expand
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