Prognostic Relevance of 6q Deletion in Waldenström's Macroglobulinemia: A Multicenter Study

Chang, Hong; Qi, Connie; Trieu, Young; Jiang, Allan; Young, Ken H.; Chesney, Alden; Jani, Prashant; Wang, Chen; Reece, Donna; Chen, Christine

doi:10.3816/clm.2009.n.008

Cited by 47 publications

(24 citation statements)

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“…Low proliferative rates of WM cells, however, hinder cytogenetic analysis. While IgH rearrangements are rare, deletion on the long arm of chromosome 6 (del 6q) is detected in 40-50% of the patients, and is the most common recurrent cytogenetic abnormality [20,21]. Tumor suppressor genes, B lymphocyte-induced maturation protein 1 (BLIMP1) on 6q21 and tumor necrosis factor alpha induced protein 3 (TNFAIP3) on 6q23 may have a role in the pathogenesis of WM [22,23].…”

Section: Insights Into Pathophysiologymentioning

confidence: 99%

“…Tumor suppressor genes, B lymphocyte-induced maturation protein 1 (BLIMP1) on 6q21 and tumor necrosis factor alpha induced protein 3 (TNFAIP3) on 6q23 may have a role in the pathogenesis of WM [22,23]. Del 6q was previously considered to portend worse outcomes, but its prognostic relevance has recently been questioned [21]. Routine evaluation for del 6q at diagnosis is not necessary as it is not entirely specific for LPL [20].…”

Section: Insights Into Pathophysiologymentioning

confidence: 99%

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Waldenström macroglobulinemia: What a hematologist needs to know

et al. 2015

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Section: Insights Into Pathophysiologymentioning

confidence: 99%

Section: Insights Into Pathophysiologymentioning

confidence: 99%

Waldenström macroglobulinemia: What a hematologist needs to know

et al. 2015

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“…Although 6q deletion was significantly associated with complex karyotypes in our large series, and with adverse characteristics such as hypoalbuminemia and high b2-microglobulin levels, 6q deletion had no adverse impact on patients' outcome, thus confirming the results of smaller studies. 1,2 The minimal deleted region on 13q14 seems to be similar in WM and CLL, and includes the microRNA genes miRNA-15a and miRNA-16-1.…”

Section: 18mentioning

confidence: 99%

“…1,2,6,17,22 Two tumor-suppressor genes could be involved in the pathogenesis of WM: BLIMP-1 on 6q21 and TNFAIP3 on 6q23. 6,23 In our series, we detected 6q deletions in 30% of patients, a rate slightly lower than that reported in the literature.…”

Section: 18mentioning

confidence: 99%

Chromosomal aberrations and their prognostic value in a series of 174 untreated patients with Waldenstrom's macroglobulinemia

et al. 2012

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To address these issues, we conducted a cytogenetic study of a large series of untreated symptomatic patients enrolled in a prospective, randomized, open-label clinical trial. The WM1 study took place in 101 centers in five countries and enrolled 339 patients with WM, 37 patients with non-MALT marginal zone lymphoma (MZL), and 38 patients with lymphoplasmacytic lymphoma, who were all randomly assigned to receive chlorambucil or fludarabine. 7Here we report our cytogenetic findings in 174 of the WM patients enrolled in this trial.

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“…29 Despite an earlier study suggesting prognostic significance to 6q deletions in WM, a more recent study did not confirm such significance. 27,30 As such, routine cytogenetic testing is not advised at this time. An exception, however, is the use of cytogenetics to clarify the diagnosis of WM from suspected cases of IgM myeloma.…”

Section: Cytogenetic Studiesmentioning

confidence: 99%

How I treat Waldenström macroglobulinemia

Treon

2009

Blood

183

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Waldenströ m macroglobulinemia (WM) is a distinct B-cell disorder resulting from the accumulation, predominantly in the bone marrow, of clonally related IgMsecreting lymphoplasmacytic cells. Genetic factors play an important role, with 20% of patients demonstrating a familial predisposition. Asymptomatic patients should be observed. Patients with a disease-related hemoglobin level less than 10 g/L, platelet count less than 100 ؋ 10 9 /L, bulky adenopathy or organomegaly, symptomatic hyperviscosity, peripheral neuropathy, amyloidosis, cryoglobulinemia, cold-agglutinin disease, or evidence of disease transformation should be considered for therapy. Plasmapheresis should be considered for symptomatic hyperviscosity and for prophylaxis in patients in whom rituximab therapy is contemplated. The use of rituximab as monotherapy or in combination with cyclophosphamide, nucleoside analog, bortezomib, or thalidomide-based regimens can be considered for the first-line therapy of WM and should take into account specific treatment goals, future autologous stem cell transplantation eligibility, and long-term risks of secondary malignancies. In the salvage setting, the reuse or use of an alternative frontline regimen can be considered as well as bortezomib, alemtuzumab, and stem cell transplantation. Newer agents, such as bendamustine and everolimus, can also be considered in the treatment of WM. (Blood. 2009;114:2375-2385)

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Prognostic Relevance of 6q Deletion in Waldenström's Macroglobulinemia: A Multicenter Study

Cited by 47 publications

References 10 publications

Waldenström macroglobulinemia: What a hematologist needs to know

Waldenström macroglobulinemia: What a hematologist needs to know

Chromosomal aberrations and their prognostic value in a series of 174 untreated patients with Waldenstrom's macroglobulinemia

How I treat Waldenström macroglobulinemia

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