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Annals of Oncology Advance Access originally published online on December 15, 2005
Annals of Oncology 2006 17(3):488-494; doi:10.1093/annonc/mdj111
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© 2005 European Society for Medical Oncology

Characterization of familial Waldenström's macroglobulinemia

S. P. Treon1,3,*, Z. R. Hunter1, A. Aggarwal2, E. P. Ewen2, S. Masota2, C. Lee2,3, D. Ditzel Santos1,3, E. Hatjiharissi1,3, L. Xu1, X. Leleu1, O. Tournilhac1,3, C. J. Patterson1, R. Manning1, A. R. Branagan1 and C. C. Morton2,3

1 Bing Center for Waldenström's Macroglobulinemia, Dana Farber Cancer Institute, Boston; 2 Department of Pathology, Brigham and Women's Hospital, Boston; 3 Harvard Medical School, Boston MA, USA

* Correspondence to: Dr S. P. Treon, Bing Program for Waldenström's Macroglobulinemia, Dana Farber Cancer Institute, LG102, 44 Binney St, Boston, MA 02115 USA. Tel: +1 617 632 2681; Fax: +1 617 632 4862; E-mail: steven_treon{at}dfci.harvard.edu

Background: Familial clustering of B-cell disorders among Waldenström's macroglobulinemia (WM) patients has been reported, though the frequency and any differences in disease manifestation for familial patients remain to be defined.

Patients and methods: We therefore analyzed clinicopathological data from 257 consecutive and unrelated WM patients. Forty-eight (18.7%) patients had at least one first-degree relative with either WM (n = 13, 5.1%), or another B-cell disorder including non-Hodgkin's lymphoma (n = 9, 3.5%), myeloma (n = 8, 3.1%), chronic lymphocytic leukemia (n = 7, 2.7%), monoclonal gammopathy of unknown significance (n = 5, 1.9%), acute lymphocytic leukemia (n = 3, 1.2%) and Hodgkin's disease (n = 3, 1.2%). Patients with a familial history of WM or a plasma cell disorder (PCD) were diagnosed at a younger age and with greater bone marrow involvement.

Results: Deletions in 6q represented the only recurrent structural chromosomal abnormality and were found in 13% of patients, all non-familial cases. Interphase FISH analysis demonstrated deletions in 6q21-22.1 in nearly half of patients, irrespective of familial background.

Conclusions: The above results suggest a high degree of clustering for B-cell disorders among first-degree relatives of patients with WM, along with distinct clinical features at presentation based on familial disease cluster patterns. Genomic studies to delineate genetic predisposition to WM are underway.

Key words: Waldenström's macroglobulinemia, B-cell, familial clustering


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