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Blood, 1 December 2000, Vol. 96, No. 12, pp. 3982-3984

BRIEF REPORT

Linkage analysis for major histocompatibility complex-related genetic susceptibility in familial chronic lymphocytic leukemia

Stephen Bevan, Daniel Catovsky, Estella Matutes, Petar Antunovic, Martin J. Auger, Isaac Ben-Bassat, Andrew Bell, Alain Berrebi, Elizabeth J. Gaminara, Maria E. Júnior, Francesca R. Mauro, Klas Quabeck, Saad M. B. Rassam, Cecil Reid, Isabel Ribeiro, Pinhas Stark, Jacques J. M. van Dongen, Jennifer Wimperis, Susan Wright, Andrea Marossy, Martin R. Yuille, and Richard S. Houlston

From the Institute of Cancer Research, Sutton, United Kingdom; Regionsykenhuset I Tromsø, Tromsø, Norway; The Kings Mill Centre, Sutton-in-Ashfield, United Kingdom; Sheba Medical Centre, Sackler School of Medicine, Tel-Hashomer, Israel; Poole General Hospital, Poole, United Kingdom; Kaplan Medical Center, Rehovot, Israel; St Albans City Hospital, St Albans, United Kingdom; Hospital de Santa Cruz, Carnaxide, Portugal; La Sapienza University, Rome, Italy; Group Practice for Haematology and Oncology, Duisburg, Germany; Queen Mary's Hospital, Sidcup, United Kingdom; Northwick Park Hospital, Harrow, United Kingdom; Hospital de Egas Moniz, Lisboa, Portugal; Rabin Medical Centre, Petah-Tiqva, Israel; Erasmus University Rotterdam, Rotterdam, The Netherlands; Norfolk and Norwich Hospital, Norwich, United Kingdom; and Mater Misericordiae Hospitals, South Brisbane, Australia.

Chronic lymphocytic leukemia (CLL) shows evidence of familial aggregation, but the genetic basis is poorly understood. The existence of a linkage between HLA and Hodgkin lymphoma, another B-cell disorder, coupled with the fact that CLL is frequently associated with autoimmune disease, led to the question of whether the major histocompatibility complex (MHC) region is involved in familial cases of CLL. To examine this proposition, 5 microsatellite markers on chromosome 6p21.3 were typed in 28 families with CLL, 4 families with CLL in association with other lymphoproliferative disorders, and 1 family with splenic lymphoma with villous lymphocytes. There was no evidence of linkage in these families to chromosome 6p21.3. The best estimates of the proportions of sibling pairs with CLL that share 0, 1, or 2 MHC haplotypes were not significantly different from the null expectation. This implies that genes within the MHC region are unlikely to be the major determinants of familial CLL.

© 2000 by The American Society of Hematology.
 

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