Kapitolina Semenova, MD, University of California, Irvine
Jack Reid, MD, University of California, Irvine
Fabiola Quintero-Rivera, MD, University of California, Irvine
Cancer Sub-Classification / Subtype
Low-grade B-cell clonal neoplasm.
Definition / Description of Disease
Waldenström macroglobulinemia (WM) is a clinicopathological entity characterized by presence of Lymphoplasmacytic lymphoma (LPL) associated with any level of monoclonal immunoglobulin M (IgM) in the serum.
Synonyms / Terminology
Waldenström's macroglobulinemia, Waldenstrom macroglobulinemia, Macroglobulinemia.
Epidemiology / Prevalence
- Waldenström macroglobulinemia is a rare disorder with an age-adjusted incidence rate of 3.4 among the male population and 1.7 in the female population. 
- WL occurs most frequently in Caucasians and is less common in Asian and African-American populations. 
- WM is more common in men, with male to female ratio of approximately 2:1. 
- The median age of 60-70 years. 
- Approximately 2% of all hematologic malignancies with 1000-1500 new cases per year in the United States are represented by WM. 
- WM is an indolent disease with a wide variety of symptoms which could be divided in two categories: neoplastic organ involvement and IgM paraprotein-related symptoms. 
- Approximately 30% of patients are asymptomatic. 
- Symptomatic hyperviscosity is observed in patients with IgM levels >30 g/l. 
- Approximately 3% of patients have systemic amyloidosis, more often of immunoglobulin light chain (AL) type. 
|Signs and Symptoms||B-symptoms (fever, weight loss, fatigue, night sweats)
IgM related symptoms:
|Laboratory Findings||Anemia, usually mild normochromic and normocyticThrombocytopenia
Elevated beta2-microglobulin (increased in approximately 50% of patients)
High erythrocyte sedimentation rate
Hypoalbuminemia (<30.0 g/L)
High serum IgM
Cold agglutinin hemolytic anemia (rare, observed in 1.5% of patients)
Cryoglobulinemia (associated with concurrent hepatitis C infection)
Monoclonal immunoglobulin light chains (Bence-Jones proteins) in the urine in up to 80% of patients with WM.
Sites of Involvement
- By definition, diagnosis of Waldenström macroglobulinemia requires bone marrow involvement by Lymphoplasmacytic lymphoma.
- Lymphadenopathy and hepatosplenomegaly are more common at the time of relapse (up to 50%) rather than at the time of initial presentation (20%). 
- Peripheral blood may have lymphocytosis with small circulating neoplastic cells with condensed chromatin and inconspicuous nucleoli. Rouleaux formation is also observed. 
- Extramedullary involvement has been reported in <5% of patients with WM, with the lungs, soft tissue, central nervous system, kidneys, and bones being the most common sites. 
- The pulmonary system can be involved by WM in the form of malignant pleural effusion as well as an infiltration of the parenchyma of the lung. 
- Soft tissue involvement is reported in 21% of patients with an extramedullary presentation of WM and appears as a soft tissue mass in various locations. 
- Rare central nervous system involvement by WM lymphoplasmacytic infiltrate is known as Bing-Neel syndrome.  Bing -Neel syndrome is characterized by direct infiltration of the central nervous system and clinical symptoms such as headache, vertigo, ataxia, diplopia, impaired hearing. 
- Kidney involvement may present as nephrotic syndrome and demonstrate renal localization of the lymphoplasmacytic infiltrate of the WM. 
- Bone involvement is reported in 9% of patients with an extramedullary presentation of WM. 
- Bone marrow involvement by lymphoplasmacytic lymphoma is characterized by an interstitial, diffuse, or nodular patterns of infiltration. 
- Tumor burden of the bone marrow is variable with a wide range of percentage of involvement (5-95%). 
- Paratrabecular infiltration is composed of nodular aggregates or single cells along the bone trabeculae with peritrabecular fibrosis and is seen in 95% of cases. 
- Lymphoplasmacytic infiltrate is composed mainly of small monotonous lymphocytes with a various numbers of plasma cells and plasmacytoid lymphocytes. 
- An increased number of reactive mast cells in the background stroma of lymphoid infiltrates is often present. 
- Dutcher bodies (intracytoplasmic immunoglobulin inclusions) and Russell bodies (mucopolysaccharides and immunoglobulin inclusion in the rough endoplasmic reticulum) are often present within plasma cells. 
|Positive (universal)||CD22 (dim)|
|Negative (universal)||Cyclin D1|
- Lymphocytes express B cell antigens and are positive for CD19, CD20, CD79a, and CD22. Plasma cells express CD138 and CD38.
- The majority of lymphocytes express function-associated antigen (LFA-1). 
- Adhesion molecules such as L-selectin, ICAM-1, CD44, and CD11c are expressed in a subset of cases of WM.
- Up to 20% may express CD5, CD10, and CD23. 
Chromosomal Rearrangements (Gene Fusions)
- t(9;14)(p13;q32) has been initially identified in the extensive retrospective analysis and correlated with a plasmacytoid differentiation.  This translocation has not been observed in a newer study. 
- Rare cases associated with t(8;14), t(11;18), and t(14;18) were observed in rare case reports. 
Individual Region Genomic Gain/Loss/LOH
- Chromosome 6q deletion involving q13-q22 regions is the most frequent structural abnormality.
- Del6q is associated with adverse prognostic features.
- The presence of 6q deletion is suggested as a marker of transformation to large cell lymphomas. This region includes genes of several modulators such as NF-kappa-B, BCL2, apoptosis, and plasma cell differentiation, which can participate in the pathogenesis of the WM/LPL.
|Chr #||Gain / Loss / Amp / LOH||Minimal Region Genomic Coordinates [Genome Build]||Minimal Region Cytoband||Diagnostic Significance (Yes, No or Unknown)||Prognostic Significance (Yes, No or Unknown)||Therapeutic Significance (Yes, No or Unknown)||Notes|
|3||Gain||Trisomy 3; 3q21-23 to 3q25-29 are in the minimal overrepresented region||No||No||No||Trisomy 3 is reported in rare case series.|
|4||Gain||Trisomy 4||Yes||Yes||No||Trisomy 4 is associated with adverse clinical presentation.|
|5||Gain||Trisomy 5||No||No||No||Trisomy 5 is reported in rare case series.|
|6||Loss||Del(6q)||No||No||No||Deletion of chromosome 6q is the most frequent chromosomal abnormality reported in up to 60% in patients with WM. Deletion 6q has no prognostic importance; however it has been reported in associated with features of adverse prognosis.|
|12||Gain||Trisomy 12||No||No||No||Rare (<5%); Trisomy 12 associated with short progression-free survival.|
|17||Loss||Del(17p)||No||No||No||17p (T53) deletion is found in 8% of cases.|
Characteristic Chromosomal Patterns
- There are no characteristic chromosomal patterns in WM.
- Trisomy of chromosome 4 and trisomy of chromosome 18 was shown in association. 
Gene Mutations (SNV/INDEL)
- In symptomatic patients with WM, three or more copy number alterations (CNA) were reported with higher frequency than in asymptomatic patients.
|Gene; Genetic Alteration||Presumed Mechanism (Tumor Suppressor Gene [TSG] / Oncogene / Other)||Prevalence (COSMIC / TCGA / Other)||Concomitant Mutations||Mutually Exclusive Mutations||Diagnostic Significance (Yes, No or Unknown)||Prognostic Significance (Yes, No or Unknown)||Therapeutic Significance (Yes, No or Unknown)||Notes|
|TNFAIP3 gene; 6q MDRs||TSG||90% of patients have concomitant mutation such as gain of chromosome 4, gain of 6p, or deletion of 13q.||Unknown||Unknown||Unknown||Unknown|
|Potential involved genes CASP3, SETS7, CAMK2D; MAR1 (4q24), MAR2 (4q31-4q35)||Unknown||Unknown||Unknown||Unknown||Unknown||ATM gene plays in DNA damage response pathway.|
|ATM; deletion 11q22.3-q23||Unknown||Unknown||Unknown||Unknown||Unknown|
|DLEU7; methylation||Unknown||Unknown||Unknown||Unknown||Unknown||DLEU7 is a regulator of NF-kB pathway.|
|TP53; 17p13 deletion||Unknown||Unknown||Unknown||Unknown||Unknown|
|CD79B/CD79A||Unknown||Unknown||Unknown||Unknown||Unknown||Key component of BCR pathway; Mutations in CD79B/CD79A were observed in 15% of patients. No correlation with clinical data was identified.|
Note: A more extensive list of mutations can be found in cBioportal (https://www.cbioportal.org/), COSMIC (https://cancer.sanger.ac.uk/cosmic), ICGC (https://dcc.icgc.org/) and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.
MicroRNA-155 as well as other microRNAs (miRNA-184, -206, -363, -494, -542-3p) are upregulated in the cells derived from the bone marrow of patients with WM. Recent studies have demonstrated that miRNA act as a modulator of histone acetylation and therefore may be considered as an epigenetic alteration.
MicroRNA-155 loss of function were shown to correlate with:
- Decline in WM cell proliferation
- Downregulation of PI3K/AKT and MAPK/ERK signaling pathways
- Inhibition of NFkB activation
- Inhibition of WM cells adhesion to fibronectin
- Inhibition of WM cell migration to SDF-1
Partial methylation of DLEU7 gene, which regulates NF-kB pathway, was seen in all patients regardless of clinical status.
Genes and Main Pathways Involved
- MYD88 L265, a single point mutation at NM_002468:c.978T>C (rs387907272) resulting in a p.Leu265Pro (L265P) amino acid change is the most common somatic mutation in patients with WM reported in more than 90% of patients.  MYD88 is an adaptor protein for toll-like receptor 4 (TLR-4) and also for interleukin-1 and -2 receptors (IL-1R and IL-2R).
- MYD88 L265P mutation may not be enough to cause malignant transformation. It may represent a part of a preneoplastic landscape that, together with other genetic alterations, causes the progression to the disease. 
- C1013G/CXCR4 is the second most common somatic mutation identified in patients with Waldenström macroglobulinemia and lymphoplasmacytic lymphoma and presents in up to 40% of patients with WM. The C-X-C chemokine receptor type 4 (CXCR4) is a G-protein-coupled receptor that regulates cell trafficking in hematopoietic stem cells and clonal B cells. 
- The presence of CXCR4 mutations is associated with a higher bone marrow burden. Patients with nonsense CXCR4 mutation was reported in association with higher immunoglobulin M level and symptomatic hyperviscosity. 
- In cases with mutated ARID1A WM, CXCL13 was shown to be overexpressed and correlated with bone marrow involvement. 
- Recurrent somatic mutations in CD79B (8-15%) , KMPTD/MLL2 (mutated in 7%), T53 (mutated in 7%), MYBBP1A (mutated in 7%)  are also reported.
- Patients with wild-type MYD88 WM were shown to have somatic mutations such as TBL1XR1, PTPN13, MALT1, BCL10, NFKB2, NFKBIB, NFKBIZ, and UDRL1F associated with activation of NF-kB and other mutations associated with epigenomic dysregulation (KMT2D, KMT2C, and KDM6A), and mutations causing DNA damage repair (T53, ATM, TRRAP). 
- Patients with MYD88 wild-type WM show worse prognosis compare to patients with mutated MYD88 WM. Also, the BTK inhibitor ibrutinib is less effective in patients with wild-type MYD88 WM. 
|Gene; Genetic Alteration||Pathway||Pathophysiologic Outcome|
|MYD88 L265; Activating mutation||The transcription factor nuclear factor (NF)-kB pathway||Enhanced cell survival|
|CXCR4 C1013G; Activating mutation||Cytokine release and chemotaxis||WM cells homing; promote WM cells dissemination|
|ARID1A||Part of switch/sucrose nonfermentable family; Chromatin remodeling protein||Poorly understood, however some studies suggest a possible role in modulating TP53 gene with an epigenetic tumor suppressor function.Patients with ARID1A mutated WM show higher bone marrow disease compare to non-ARID1A mutated WM patients.|
Genetic Diagnostic Testing Methods
- Next-generation sequencing is used to detect recurrent somatic mutations such as MYD88, CXCR4, ARID1A, and CD79B.
- Allele-specific polymerase chain reaction (AS-PCR) can be used to detect MYD88 L265P mutated cells in the peripheral blood. 
- The majority of cases of WM are sporadic; however, approximately 20% of cases have been shown in association with WM in first-degree relatives, which may suggest an autosomal dominant or co-dominant mode of inheritance. 
- Kristinsson et al. showed a 20-fold increased risk of developing Lymphoplasmacytic lymphoma or WM in first-degree relatives with WM and an increased risk of acquiring other hematologic malignancies. 
- Certain germline variants and BCL2 overexpression have been suggested to be predisposing factors; however, further investigation is required. 
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