Marginal Zone Lymphoma (MZL) and Waldenström's Macroglobulinemia (WM) are indolent lymphomas that both arise from post germinal center lymphocytes. Both can secrete a monoclonal protein but high levels are mostly only seen in WM. The MYD88 L256P somatic mutation that is present in an estimated 95% of patients with WM has helped greatly in differentiating the two lymphomas.
View Article and Find Full Text PDFWaldenström's Macroglobulinemia (WM) is a rare type of indolent non-Hodgkin lymphoma (NHL) that remains incurable. Several effective agents such as monoclonal antibodies (in combination with chemotherapy), Bruton's tyrosine kinase inhibitors, proteasome inhibitors, and BCL2 inhibitors are (becoming) available for the treatment of relapsed and refractory WM. There is however no consensus on a preferred treatment in the relapsed setting.
View Article and Find Full Text PDFIntroduction: Treatment options for Waldenström's Macroglobulinemia (WM) have expanded rapidly in the last decades. However, there is no consensus on a preferred treatment. Therefore, patient preferences become increasingly important in making individualized treatment plans.
View Article and Find Full Text PDFWaldenström's macroglobulinemia (WM), a rare low-grade B-cell non-Hodgkin lymphoma (NHL), has a distinct clinical presentation and different treatment-related side effects compared with other NHL. Currently, a wide variety of therapeutic agents are available for the treatment of WM but there is no consensus on optimal treatment in first line and/or at relapse. The aim of this survey was to evaluate the current knowledge and perspectives of hematologists on diagnosis and treatment of WM.
View Article and Find Full Text PDFIntroduction: In anti-myelin-associated glycoprotein IgM paraprotein-related peripheral neuropathy (anti-MAG PN), there is a lack of reliable biomarkers to select patients eligible for therapy and for evaluating treatment effects, both in routine practice and in clinical trials. Neurofilament light chain (NfL) and contactin-1 (CNTN1) can serve as markers of axonal and paranodal damage. Complement activation is involved in the pathogenesis in anti-MAG PN.
View Article and Find Full Text PDF