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(searched for: doi:10.3816/clml.2011.n.032)
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Ricardo D. Parrondo, Tea Reljic, Madiha Iqbal, Ernesto Ayala, Han W. Tun, Mohamed A. Kharfan-Dabaja, Ambuj Kumar,
Clinical Lymphoma Myeloma and Leukemia, Volume 20; doi:10.1016/j.clml.2020.05.021

Abstract:
Waldenström macroglobulinemia (WM) is an IgM-producing lymphoproliferative disorder that remains incurable. Patients with high-risk disease have an overall survival (OS) of less than 3 years. Both autologous (AHCT) and allogeneic (allo-HCT) hematopoietic cell transplantation (HCT) are prescribed for treatment of WM despite a lack of randomized controlled studies. We performed a comprehensive literature search using PubMed/Medline and EMBASE on September 10, 2019. Data on clinical outcomes related to benefits and harms was extracted independently by 3 authors. Fifteen studies (8 AHCT [n = 278 patients], 7 allo-HCT [n = 311 patients]) were included in this systematic review/meta-analysis. Pooled OS, progression-free survival (PFS), and nonrelapse mortality (NRM) rates post AHCT were 76% (95% confidence interval [CI], 65%-86%), 55% (95% CI, 42%-68%), and 4% (95% CI, 1%-7%), respectively. Pooled OS, PFS, and NRM rates post allografting were 57% (95% CI, 50%-65%), 49% (95% CI, 42%-56%), and 29% (95% CI, 23%-34%), respectively. OS and PFS rates were reported at 3 to 5 years, and NRM was reported at 1 year in most studies. Pooled ORR (at day 100) post AHCT and allo-HCT were 85% (95% CI, 72%-94%) and 81% (95% CI, 69%-91%), respectively. Pooled complete response rates post AHCT and allo-HCT were 22% (95% CI, 17%-28%) and 26% (95% CI, 7%-50%), respectively. Relapse rates post AHCT and allo-HCT were 42% (95% CI, 30%-55%) and 23% (95% CI, 18%-28%), respectively. Our results show that both AHCT and allo-HCT are effective in the treatment of WM. A 2-fold lower relapse rate but a 7-fold higher NRM was noted for allo-HCT compared with AHCT. The role of transplant in WM needs to be addressed in the era of novel agents.
, Takehiko Mori, Hitoji Uchiyama, Hiroatsu Ago, Koji Iwato, Tetsuya Eto, Hiromi Iwasaki, Takahito Kawata, Hiroyuki Takamatsu, Satoshi Yamasaki, et al.
Annals of Hematology, Volume 99, pp 1635-1642; doi:10.1007/s00277-020-04078-3

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, Qing Zhang, Xenofon Papanikolaou, Caleb Stein, Al-Ola Abdallah, Bart Barlogie
Journal of Global Oncology, Volume 4, pp 1-8; doi:10.1200/jgo.2016.008003

Abstract:
Purpose Multiple myeloma (MM) is a clonal bone marrow disease characterized by the neoplastic transformation of differentiated postgerminal B cells. It is a heterogeneous disease both at the genetic level and in terms of clinical outcome. Immunoglobulin M (IgM) MM is a rare subtype of myeloma. Similar to Waldenström macroglobulinemia (WM), patients with MM experience IgM monoclonal gammopathy; however, both diseases are distinct in terms of treatment and clinical behavior. Materials and Methods To shed light on the presentation of IgM MM, its prognosis, and its gene expression profiling, we identified and characterized 21 patients with IgM MM from our database. Results One of these patients presented with a rare IgM monoclonal gammopathy of undetermined significance that progressed to smoldering myeloma. The median survival of the 21 patients was 4.9 years, which was comparable to a matched group of patients with non-IgM MM with similar myeloma prognostic factors (age, gender, albumin, creatinine, anemia, lactate dehydrogenase, β2-microglobulin, cytogenetics abnormalities), but much less than the median survival reported for patients with WM (9 years). We identified a cluster of genes that differ in their expression profile between MM and WM and found that the patients with IgM MM displayed a gene expression profile most similar to patients with non-IgM MM, confirming that IgM MM is a subtype of MM that should be differentiated from WM. Conclusion Because the prognosis of IgM MM and WM differ significantly, an accurate diagnosis is essential. Our gene expression model can assist with the differential diagnosis in controversial cases.
Published: 17 October 2018
by Wiley
American Journal of Hematology, Volume 94, pp 266-276; doi:10.1002/ajh.25292

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Morie A. Gertz
Published: 17 January 2017
by Wiley
American Journal of Hematology, Volume 92, pp 209-217; doi:10.1002/ajh.24557

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So Young Pyun,
Annals of Clinical Neurophysiology, Volume 19, pp 79-92; doi:10.14253/acn.2017.19.2.79

Expert Opinion on Investigational Drugs, Volume 26, pp 197-205; doi:10.1080/13543784.2017.1275561

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Rajshekhar Chakraborty, ,
Best Practice & Research Clinical Haematology, Volume 29, pp 229-240; doi:10.1016/j.beha.2016.08.018

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Amit M Oza,
Blood Cancer Journal, Volume 5; doi:10.1038/bcj.2015.28

Abstract:
Waldenstrom macroglobulinemia (WM) is a B-cell lymphoplasmacytic lymphoma characterized by monoclonal immunoglobulin M protein in the serum and infiltration of bone marrow with lymphoplasmacytic cells. Asymptomatic patients can be observed without therapy. First-line therapy should consist of the monoclonal anti-CD20 antibody, rituximab, given typically in combination with other agents. We prefer dexamethasone, rituximab, cyclophosphamide (DRC) as initial therapy for most patients with symptomatic WM. Other reasonable options are bortezomib, rituximab, dexamethasone (BoRD) or bendamustine plus rituximab (BR). All of these regimens are associated with excellent response and tolerability. Initial therapy is usually administered for 6 months, followed by observation. Response to therapy is assessed using the standard response criteria developed by the International Working Group on Waldenstrom macroglobulinemia. Relapse is almost inevitable in WM but may occur years after initial therapy. In symptomatic patients relapsing more than 1–2 years after initial therapy, the original treatment can be repeated. For relapse occurring sooner, an alternative regimen is used. In select patients, high-dose chemotherapy followed by autologous hematopoietic cell transplantation may be an option at relapse. Options for therapy of relapsed WM besides regimens used in the front-line setting include ibrutinib, purine nucleoside analogs (cladribine, fludarabine), carfilzomib and immunomodulatory agents (thalidomide, lenalidomide).
Published: 23 March 2015
by Wiley
American Journal of Hematology, Volume 90, pp 346-354; doi:10.1002/ajh.23922

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Published: 20 June 2013
by Wiley
American Journal of Hematology, Volume 88, pp 703-711; doi:10.1002/ajh.23472

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Anita D'souza, Stephen Ansell, ,
Published: 8 May 2013
by Wiley
British Journal of Haematology, Volume 162, pp 295-303; doi:10.1111/bjh.12367

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Published: 17 April 2012
by Wiley
American Journal of Hematology, Volume 87, pp 503-510; doi:10.1002/ajh.23192

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