Clinical and prognostic implications of low or high level of von Willebrand factor in patients with Waldenström macroglobulinemia

Hivert, Bénédicte; Caron, Claudine; Petit, S.; Charpy, Cécile; Fankam-Siaka, Corinne; Lecocq, Stephanie; Zawadzki, Christophe; Susen, Sophie; Rusu, Manuela; Duhamel, Alain; Tournilhac, Olivier; Goudemand, Jenny; Morel, Pierre

doi:10.1182/blood-2011-11-388256

Cited by 53 publications

(44 citation statements)

References 39 publications

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“…Elevated levels of VWF have also been observed in other malignancies, including lymphoplasmacytic lymphoma/Waldenström macroglobulinemia, and have also been associated with outcome. 35,36 However, in our patients, there was no strong correlation of the bone marrow infiltration by plasma cells or the levels of the involved free light chains with the levels of VWF:Ag. only found an inverse association with NTproBNP levels, in accordance with the previous studies.…”

Section: Discussionmentioning

confidence: 58%

Clinical and prognostic significance of serum levels of von Willebrand factor and ADAMTS-13 antigens in AL amyloidosis

Kastritis

Papassotiriou²,

Terpos

et al. 2016

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Section: Discussionmentioning

confidence: 58%

Clinical and prognostic significance of serum levels of von Willebrand factor and ADAMTS-13 antigens in AL amyloidosis

Kastritis

Papassotiriou²,

Terpos

et al. 2016

Blood

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“…51 The use of ibrutinib in patients who require other anticoagulants or medicinal products that inhibit platelet function may increase the risk of bleeding, and particular care should be taken if anticoagulant therapy is used. Moreover, acquired von Willebrand disease associated with a high IgM level can be responsible for bleeding, 52 although patients with acquired von Willebrand disease showed benefit after treatment with ibrutinib. 48 The panel recommends that testing for von Willebrand activity in patients with a history of bleeding diathesis before starting ibrutinib is reasonable.…”

Section: B-cell Receptor (Bcr) Pathway Inhibitorsmentioning

confidence: 99%

Treatment recommendations from the Eighth International Workshop on Waldenström’s Macroglobulinemia

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Advani

et al. 2016

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Waldenström macroglobulinemia (WM) is a distinct B-cell lymphoproliferative disorder for which clearly defined criteria for the diagnosis, initiation of therapy, and treatment strategy have been proposed as part of the consensus panels of the International Workshop on Waldenström’s Macroglobulinemia (IWWM). At IWWM-8, 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. The panel concluded that therapeutic strategies in WM should be based on individual patient and disease characteristics. Chemoimmunotherapy combinations with rituximab and cyclophosphamide-dexamethasone, bendamustine, or bortezomib-dexamethasone provide durable responses and are still indicated in most patients. Approval of the BTK inhibitor ibrutinib in the United States and Europe represents a novel and effective treatment option for both treatment-naive and relapsing patients. Other B-cell receptor inhibitors, second-generation proteasome inhibitors (eg, carfilzomib), and mammalian target of rapamycin inhibitors are promising and may increase future treatment options. Active enrollment in clinical trials whenever possible was endorsed by the panel for most patients with WM.

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“…increased BM microvessel density and VEGF). 9 Because of the heterogeneity of WM, the treatment approach must consider several different clinical profiles. As currently defined, WM is heterogeneous and may include more than one type of B-cell lymphoma.…”

Section: Introductionmentioning

confidence: 99%

Molecular pathogenesis of Waldenstrom's macroglobulinemia

et al. 2012

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Waldenström's macroglobulinemia is an indolent, lymphoproliferative disease, characterized by a heterogeneous lymphoplasmacytic bone marrow infiltrate and high immunoglobulin M production. While technological advances over the past several decades have dramatically improved the possibilities of studying the molecular basis of Waldenström's macroglobulinemia, the pathogenesis of the disease remains fragmented. Undoubtedly, research has been successful in uncovering underlying aberrations and deregulated mechanisms in this disease, providing useful information for identifying biomarkers for disease diagnosis, risk stratification and therapeutic intervention, but there is still a long way to go before the pathogenesis of Waldenström's macroglobulinemia is fully revealed. In addition, the low number of in vitro or in vivo models significantly challenges extensive analysis. In this manuscript, we review the molecular basis of this disease.Key words: WM, NF-kB signaling pathway, Jak/STAT, PI3K/Akt, aCGH, IL-6. Waldenström's macroglobulinemia. Haematologica 2012;97(9):1281-1290. doi:10.3324/haematol.2012 This is an open-access paper. Citation: Braggio E, Philipsborn C, Novak A, Hodge L, Ansell S, and Fonseca R. Molecular pathogenesis of ABSTRACT © F e r r a t a S t o r t i F o u n d a t i o n © F e r r a t a S t o r t i F o u n d a t i o nagreed that initiation of therapy was appropriate for patients with constitutional symptoms, such as fever, night sweats or weight loss. The median survival ranges from five to more than ten years, depending on the series analyzed. 10-13The existence of somatic hypermutation in WM indicates a role for antigenic stimulation in the development of WM. [14][15][16] The IgH variable region genes are commonly mutated and the VH3 gene is often used, suggesting antigen exposure and selection. 14,17 Clonality studies have shown clonal IgH and IgL gene rearrangements. The IgH variable region is commonly mutated in WM, but intraclonal variation is usually absent and IgH switching usually does not occur. 18,19 Environmental and inherited factors may contribute to familial IgM-MGUS/WM clusters. Patients with monoclonal gammopathy of undetermined significance (MGUS) are at increased risk for progression to WM. 20 In a population-based study of 1,384 individuals with MGUS, researchers showed an increased risk factor of 46 for developing WM. 20 The rate of progression from IgM-MGUS to WM was further noted to be 1.5-2% a year. [21][22][23] While the development of WM is thought to be sporadic, there are a few studies demonstrating familial linkage and predisposition to the disease. 2,[24][25][26] Both familial clustering of WM and a notable increase (~10 fold) of IgM-MGUS frequency in first-degree relatives of WM patients is suggestive of familial risk. 27 Using the assumption that WM and IgM-MGUS share common susceptibility genes, strong linkages involving chromosomes 1q, 3q, and 4q have been identified. 21 A causal relationship between MGUS/WM and chronic antigenic stimulation has been suggested b...

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Clinical and prognostic implications of low or high level of von Willebrand factor in patients with Waldenström macroglobulinemia

Cited by 53 publications

References 39 publications

Clinical and prognostic significance of serum levels of von Willebrand factor and ADAMTS-13 antigens in AL amyloidosis

Clinical and prognostic significance of serum levels of von Willebrand factor and ADAMTS-13 antigens in AL amyloidosis

Treatment recommendations from the Eighth International Workshop on Waldenström’s Macroglobulinemia

Molecular pathogenesis of Waldenstrom's macroglobulinemia

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