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No association of the NFKB1 promoter polymorphism with ulcerative colitis in a British case control cohort
  1. M M Mirza1,
  2. S A Fisher1,
  3. C Onnie1,
  4. C M Lewis1,
  5. C G Mathew1,
  6. J Sanderson2,
  7. A Forbes3
  1. 1Department of Medical and Molecular Genetics, Guy’s King’s and St Thomas’ School of Medicine, King’s College London, Guy’s Hospital, London, UK
  2. 2Department of Gastroenterology, St Thomas’ Hospital, London, UK
  3. 3St Mark’s Hospital, Northwick Park, Watford Rd, Harrow, Middlesex, UK
  1. Correspondence to:
    Professor C G Mathew
    Department of Medical and Molecular Genetics, GKT School of Medicine, 8th Floor Guy’s Tower, Guy’s Hospital, London SE1 9RT, UK; christopher.mathewgenetics.kcl.ac.uk

https://doi.org/10.1136/gut.2005.070029

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    Recently, Karban and colleagues1 reported an association of a common NFKB1 gene polymorphism, −94ins/delATTG, with ulcerative colitis (UC) in a non-Hispanic, non-Jewish North American population. The deletion was significantly associated with disease in both family based and case control studies: in the combined case control cohort, the allele frequency of −94delATTG (D) was significantly increased in 350 non-Jewish UC cases (45.3%) compared with 802 non-Jewish controls (38.8%, p = 0.002). In a recessive model of inheritance, the homozygous (DD) genotype was significantly increased in UC cases (21.4%) compared with controls (14.8%) (p = 0.0043), giving an odds ratio of 1.57 for the DD genotype (95% confidence interval 1.14–2.16).

    Nuclear factor κB (NFκB) is an important transcription factor implicated in the inflammatory response.2 The NFKB1gene, which encodes the p105/p50 subunit of the NFκB family of proteins, maps to chromosome 4q24, in a region showing linkage to inflammatory bowel disease3–5; a …

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    Footnotes

    • Conflict of interest: None declared.