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HLA-DR, HLA-DQ, and TAP genes in familial Hodgkin disease

  1. Author:
    Harty, L. C.
    Lin, A. Y.
    Goldstein, A. M.
    Jaffe, E. S.
    Carrington, M.
    Tucker, M. A.
    Modi, W. S.

  2. Author Address

    NCI, Genet Epidemiol Branch, DCEG, NIH, EPS MSC 7236, Bethesda, MD 20892 USA. NCI, Genet Epidemiol Branch, DCEG, NIH, EPS MSC 7236, Bethesda, MD 20892 USA. NCI, Pathol Lab, Bethesda, MD 20892 USA. NCI, Intramural Res Support Program, SAIC Frederick, Frederick, MD 21701 USA. Stanford Univ, Sch Med, Palo Alto, CA 94304 USA. Santa Clara Valley Med Ctr, Div Hematol Oncol, San Jose, CA 95128 USA. Goldstein AM NCI, Genet Epidemiol Branch, DCEG, NIH, EPS MSC 7236, Bethesda, MD 20892 USA.
    1. Year: 2002
  2. Journal: Blood
    1. 99
    2. 2
    3. Pages: 690-693
  4. Type of Article: Article
  1. Abstract:

    The HLA region has long been implicated in sporadic and familial Hodgkin disease (HD), with recent case-control studies suggesting that HLA class 11 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*15011-DQA1*0112-DQB1*0602 haplotype, the TAP1 allele encoding IIe 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. (Blood. 2002; 99:690-693) (C) 2002 by The American Society of Hematology.

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