Refine Search

New Search

Results: 18

(searched for: doi:10.3816/clml.2011.n.042)
Save to Scifeed
Page of 1
Articles per Page
by
Show export options
  Select all
Elizabeth B. Elimimian, Nadeem Bilani, Maria J. Diacovo, Skirmante Sirvaitis, Chieh Lin Fu
Published: 1 January 2021
Journal of Hematology, Volume 10, pp 25-29; doi:10.14740/jh767

Abstract:
Waldenstrom’s macroglobulinemia (WM) is an indolent B-cell non-Hodgkin lymphoma characterized by lymphoplasmacytic histology in the bone marrow with monoclonal IgM. Median survival can be in excess of 10 years. The 5-year cumulative incidence of death is low at about 10%. One-third of all-cause specific mortality is due to the lymphoma for which histologic transformation (HT) is rare. Here we present a case of a 60-year-old man with longstanding untreated WM, presenting with minimally symptomatic transformation to diffuse large B-cell lymphoma (DLBCL), with an accompanying review of the literature. Transformed WM, diagnosed greater than 5 years, has a reported survival period of 8 - 9 months. This case highlights that after a decade of continued stability in WM, not requiring treatment, an acute change in laboratory data with minimally progressive IgM levels, in the absence of B symptoms and clinical findings, may be the harbinger of transformation and at the time of diagnosis can have a rapidly deteriorating clinical course. In this case, the tripling of the lactate dehydrogenase (LDH) as the primary drastic change demonstrates the importance of the rapid increase in LDH as a singly reliable marker for HT. Late transformation has been borne out as a negative variable as the generally indolent course of WM is curtailed with the poor outcome in HT. Although MYD88 wildtype is a possible predictive factor for transformation, it is unclear if late transformation is clonally or non-clonally related and further molecular investigation is needed.
Saurabh Zanwar, Jithma P. Abeykoon M.D., , Rebecca King, Gabriela E. Perez Burbano M.S., Shaji Kumar, , , , , et al.
Published: 8 December 2019
by Wiley
American Journal of Hematology, Volume 95, pp 274-281; doi:10.1002/ajh.25697

The publisher has not yet granted permission to display this abstract.
, Cécile Tomowiak, Anne-Sophie Michallet, Jehan Dupuis, Bénédicte Hivert, Stéphane Leprêtre, Elise Toussaint, Sophie Godet, Fatiha Merabet, Eric Van Den Neste, et al.
Published: 2 August 2017
by Wiley
British Journal of Haematology, Volume 179, pp 439-448; doi:10.1111/bjh.14881

Abstract:
Histological transformation (HT) to diffuse large B‐cell lymphoma (DLBCL) is a rare and poorly reported complication of Waldenström macroglobulinaemia (WM). We performed a retrospective study of 77 WM patients with biopsy‐proven transformation to DLBCL. The median time from WM diagnosis to HT was 4·6 years and 16 patients (21%) had never been treated for WM. At HT, extranodal sites were observed in 91% of patients with a rather high incidence of central nervous system, cutaneous or testicular involvement. Fluorodeoxyglucose‐positron emission tomography was performed in half of the patients and the median maximum standardized uptake value was 15 for transformed disease. More than 80% of cases with available data for assessment by the Hans’ algorithm harboured a non‐germinal centre B‐cell phenotype. First‐line treatment for transformation consisted of R‐CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone)‐like regimen in 85% of patients. The overall response rate after first‐line treatment was 61% and the median overall survival was only 16 months for the entire cohort. Time to transformation above 5 years (P = 0·0004) and elevated LDH (P = 0·02) were associated with worse outcome. Based on these findings, HT should be considered and lead to a biopsy in WM patients presenting with extranodal involvement, elevated LDH and constitutional symptoms. The optimal therapeutic approaches remain to be defined.
Onyemaechi N Okolo, Ariel C Johnson, Seongseok Yun, Stacy J Arnold,
Published: 1 August 2017
Immunotherapy, Volume 9, pp 709-714; doi:10.2217/imt-2017-0027

The publisher has not yet granted permission to display this abstract.
, Zhang W, Lee V, Le Dt, Coffin R, Cooper S, Kuhn C, Weiner Hl, Daud Ai, Zane Lt, et al.
Published: 1 January 2017
Immunotherapy, Volume 9, pp 1-3; doi:10.2217/imt-2013-0201

, Andy C. Rawstron, Ruth M. de Tute
Waldenström’s Macroglobulinemia pp 3-19; doi:10.1007/978-3-319-22584-5_1

The publisher has not yet granted permission to display this abstract.
Vilhjálmur Steingrímsson, Ola Landgren,
Waldenström’s Macroglobulinemia pp 97-109; doi:10.1007/978-3-319-22584-5_9

The publisher has not yet granted permission to display this abstract.
, Joshua Gustine, Kirsten Meid, Toni Dubeau, ,
Published: 27 July 2016
by Wiley
American Journal of Hematology, Volume 91, pp 1032-1035; doi:10.1002/ajh.24477

The publisher has not yet granted permission to display this abstract.
, Ramon Garcia-Sanz, Evdoxia Hatjiharissi, Robert A. Kyle, Xavier Leleu, Mary McMaster, , Monique C. Minnema, Enrica Morra, Roger G. Owen, et al.
Published: 5 July 2016
by Wiley
British Journal of Haematology, Volume 175, pp 77-86; doi:10.1111/bjh.14196

Abstract:
The diagnosis of Waldenström macroglobulinaemia (WM) can be challenging given the variety of signs and symptoms patients can present. Furthermore, once the diagnosis of WM is established, the initial evaluation should be thorough as well as appropriately directed. During the 8th International Workshop for WM in London, United Kingdom, a multi‐institutional task force was formed to develop consensus recommendations for the diagnosis and initial evaluation of patients with WM. In this document, we present the results of the deliberations that took place to address these issues. We provide recommendations for history‐taking and physical examination, laboratory studies, bone marrow aspiration and biopsy analysis and imaging studies. We also provide guidance on the initial evaluation of special situations, such as anaemia, hyperviscosity, neuropathy, Bing‐Neel syndrome and amyloidosis. We hope these recommendations serve as a practical guidance to clinicians taking care of patients with a suspected or an established diagnosis of WM.
, Adam J. Olszewski, Sandra Kanan, Kirsten Meid, Zachary R. Hunter, Steven P. Treon
Published: 28 May 2015
by Wiley
American Journal of Hematology, Volume 90, pp 696-701; doi:10.1002/ajh.24052

The publisher has not yet granted permission to display this abstract.
Published: 10 March 2015
by Wiley
Cancer, Volume 121, pp 2230-2236; doi:10.1002/cncr.29334

The publisher has not yet granted permission to display this abstract.
, Guy Pratt, Rebecca L. Auer, Rita Flatley, Charalampia Kyriakou, , Francis Matthey, Helen McCarthy, Feargal P. McNicholl, Saad M. Rassam, et al.
Published: 15 February 2014
by Wiley
British Journal of Haematology, Volume 165, pp 316-333; doi:10.1111/bjh.12760

Roger Owen
Published: 18 December 2013
Myeloma pp 11-27; doi:10.1017/cbo9780511862465.002

Published: 9 September 2013
ISRN Hematology, Volume 2013, pp 1-25; doi:10.1155/2013/815325

Abstract:
Waldenström macroglobulinemia (WM) is a rare and currently incurable neoplasm of IgM-expressing B-lymphocytes that is characterized by the occurrence of a monoclonal IgM (mIgM) paraprotein in blood serum and the infiltration of the hematopoietic bone marrow with malignant lymphoplasmacytic cells. The symptoms of patients with WM can be attributed to the extent and tissue sites of tumor cell infiltration and the magnitude and immunological specificity of the paraprotein. WM presents fascinating clues on neoplastic B-cell development, including the recent discovery of a specific gain-of-function mutation in the MYD88 adapter protein. This not only provides an intriguing link to new findings that natural effector IgM+IgD+ memory B-cells are dependent on MYD88 signaling, but also supports the hypothesis that WM derives from primitive, innate-like B-cells, such as marginal zone and B1 B-cells. Following a brief review of the clinical aspects and natural history of WM, this review discusses the thorny issue of WM’s cell of origin in greater depth. Also included are emerging, genetically engineered mouse models of human WM that may enhance our understanding of the biologic and genetic underpinnings of the disease and facilitate the design and testing of new approaches to treat and prevent WM more effectively.
Ruth M. De Tute, ,
Clinical Lymphoma Myeloma and Leukemia, Volume 13, pp 211-213; doi:10.1016/j.clml.2013.02.018

The publisher has not yet granted permission to display this abstract.
, , Roger Owen, Nicola Mulholland, Ming Young Simon Wan, John Quinn, , Kevin D. Boyd, , Asim Khwaja, et al.
Published: 1 January 2013
Myeloma; doi:10.1017/cbo9780511862465

The publisher has not yet granted permission to display this abstract.
Page of 1
Articles per Page
by
Show export options
  Select all
Back to Top Top