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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Harty, L. C. Articles by Modi, W. S. Search for Related Content PubMed PubMed Citation Articles by Harty, L. C. Articles by Modi, W. S. Related Collections Neoplasia Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 January 2002, Vol. 99, No. 2, pp. 690-693 BRIEF REPORT HLA-DR, HLA-DQ, and TAP genes in familial Hodgkin disease Lea C. Harty, Albert Y. Lin, Alisa M. Goldstein, Elaine S. Jaffe, Mary Carrington, Margaret A. Tucker, and William S. Modi From the Genetic Epidemiology Branch and the Laboratory of Pathology, National Cancer Institute, Bethesda, MD; the Intramural Research Support Program, SAIC Frederick, National Cancer Institute-Frederick, MD; Stanford University School of Medicine, Palo Alto, CA; and the Division of Hematology/Oncology, Santa Clara Valley Medical Center, San Jose, CA. The HLA region has long been implicated in sporadic and familial Hodgkin disease (HD), with recent case-control studies suggesting that HLA class II loci predispose to sporadic nodular sclerosis HD (NSHD). To determine whether this predisposition extends to familial HD, HLA class II loci (DRB1, DQA1, DQB1, DRB3, DRB4, and DRB5) and transporter associated with antigen processing (TAP) loci (TAP1, TAP2) were investigated in 100 members of 16 families with at least 2 confirmed cases of HD. With the use of the transmission disequilibrium test, evidence for linkage disequilibrium with familial HD and, in particular, familial NSHD was obtained for the DRB1*1501-DQA1*0102-DQB1*0602 haplotype, the TAP1 allele encoding Ile at residue 333, and the DRB5-0101 allele. These 3 markers were in linkage disequilibrium and may not represent independent susceptibility regions. Use of a family-based approach excludes population stratification as an explanation for these findings. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. F. Skibola, J. D. Curry, and A. Nieters Genetic susceptibility to lymphoma Haematologica, July 1, 2007; 92(7): 960 - 969. [Abstract] [Full Text] [PDF] D. L. Friedman, N. S. Kadan-Lottick, J. Whitton, A. C. Mertens, Y. Yasui, Y. Liu, A. T. Meadows, L. L. Robison, and L. C. Strong Increased Risk of Cancer among Siblings of Long-term Childhood Cancer Survivors: A Report from the Childhood Cancer Survivor Study Cancer Epidemiol. Biomarkers Prev., August 1, 2005; 14(8): 1922 - 1927. [Abstract] [Full Text] [PDF] L R Goldin, M L McMaster, M Ter-Minassian, S Saddlemire, B Harmsen, G Lalonde, and M A Tucker A genome screen of families at high risk for Hodgkin lymphoma: evidence for a susceptibility gene on chromosome 4 J. Med. Genet., July 1, 2005; 42(7): 595 - 601. [Full Text] [PDF] H. Hjalgrim, S. Rasmussen, K. Rostgaard, N. M. Nielsen, N. Koch-Henriksen, L. Munksgaard, H. H. Storm, and M. Melbye Familial Clustering of Hodgkin Lymphoma and Multiple Sclerosis J Natl Cancer Inst, May 19, 2004; 96(10): 780 - 784. [Abstract] [Full Text] [PDF] W. Cozen, P. S. Gill, S. A. Ingles, R. Masood, O. Martinez-Maza, M. G. Cockburn, W. J. Gauderman, M. C. Pike, L. Bernstein, B. N. Nathwani, et al. IL-6 levels and genotype are associated with risk of young adult Hodgkin lymphoma Blood, April 15, 2004; 103(8): 3216 - 3221. [Abstract] [Full Text] [PDF]

	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020