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MYD88 L265P somatic mutation in Waldenström's macroglobulinemia.
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.
Ibrutinib in previously treated Waldenström's macroglobulinemia.
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.
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.
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.
MYD88 L265P in Waldenström macroglobulinemia, immunoglobulin M monoclonal gammopathy, and other B-cell lymphoproliferative disorders using conventional and quantitative allele-specific polymerase…
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.
Guideline for the diagnosis, treatment and response criteria for Bing-Neel syndrome
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.
Primary therapy of Waldenström macroglobulinemia with bortezomib, dexamethasone, and rituximab: WMCTG clinical trial 05-180.
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.
A mutation in MYD88 (L265P) supports the survival of lymphoplasmacytic cells by activation of Bruton tyrosine kinase in Waldenström macroglobulinemia.
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.
Carfilzomib, rituximab, and dexamethasone (CaRD) treatment offers a neuropathy-sparing approach for treating Waldenström's macroglobulinemia.
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.
Response assessment in Waldenström macroglobulinaemia: update from the VIth International Workshop
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.
Attainment of complete/very good partial response following rituximab‐based therapy is an important determinant to progression‐free survival, and is impacted by polymorphisms in FCGR3A in Waldenstrom…
The attainment of CR/VGPR was associated with significantly longer PFS in rituximab‐naïve WM patients undergoing ritudine‐based therapy, and was predicted by polymorphisms in FCGR3A.