{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T10:58:41Z","timestamp":1779101921685,"version":"3.51.4"},"reference-count":32,"publisher":"Hindawi Limited","license":[{"start":{"date-parts":[[2009,1,1]],"date-time":"2009-01-01T00:00:00Z","timestamp":1230768000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gastroenterology Research and Practice"],"published-print":{"date-parts":[[2009]]},"abstract":"<jats:p>Inflammatory bowel diseases (IBDs) comprising Crohn disease (CD) and ulcerative colitis (UC) are chronic inflammatory conditions with polygenic susceptibility. Interactions between TNF-alpha and TNF-alpha receptor play a fundamental role in inflammatory response. This study investigates the role that selected single nucleotide polymorphisms (SNPs) and haplotypes in the TNF-alpha receptor (TNSFRSF1B) gene play in the risk of IBD in a New Zealand Caucasian population. DNA samples from 388\u2009CD, 405\u2009UC, 27 indeterminate colitis patients, and 293 randomly selected controls, from Canterbury, New Zealand were screened for 3 common SNPs in TNSFRSF1B: rs1061622 (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:mtext>c<\/mml:mtext><mml:mn>.676<\/mml:mn><mml:mtext>T<\/mml:mtext><mml:mo>&gt;<\/mml:mo><mml:mtext>C<\/mml:mtext><\/mml:mrow><\/mml:math>), rs1061624 (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:mtext>c<\/mml:mtext><mml:msup><mml:mo>.<\/mml:mo><mml:mo>\u2217<\/mml:mo><\/mml:msup><mml:mn>1663<\/mml:mn><mml:mtext>A<\/mml:mtext><mml:mo>&gt;<\/mml:mo><mml:mtext>G<\/mml:mtext><\/mml:mrow><\/mml:math>), and rs3397 (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:mtext>c<\/mml:mtext><mml:msup><mml:mo>.<\/mml:mo><mml:mo>\u2217<\/mml:mo><\/mml:msup><mml:mtext>1690T<\/mml:mtext><mml:mo>&gt;<\/mml:mo><mml:mtext>C<\/mml:mtext><\/mml:mrow><\/mml:math>), using TaqMan technologies. Carrying the rs1061624 variant decreased the risk of UC in the left colon (OR 0.73, 95%\u2009<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:mtext>CI<\/mml:mtext><mml:mo>=<\/mml:mo><mml:mn>0.54<\/mml:mn><\/mml:mrow><\/mml:math>\u20131.00) and of being a smoker at diagnosis (OR 0.62; 95%\u2009<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:mtext>CI<\/mml:mtext><mml:mo>=<\/mml:mo><mml:mn>0.40<\/mml:mn><\/mml:mrow><\/mml:math>\u20130.96). Carrying the rs3397 variant decreased the risk of penetrating CD (OR 0.62, 95%\u2009<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:mtext>CI<\/mml:mtext><mml:mo>=<\/mml:mo><mml:mn>0.40<\/mml:mn><\/mml:mrow><\/mml:math>\u20130.95). Three marker haplotype analyses revealed highly significant differences between CD patients and control subjects (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:msup><mml:mi>\u03c7<\/mml:mi><mml:mn>2<\/mml:mn><\/mml:msup><mml:mo>=<\/mml:mo><mml:mn>29.9<\/mml:mn><\/mml:mrow><\/mml:math>,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:mtext>df<\/mml:mtext><mml:mo>=<\/mml:mo><mml:mn>7<\/mml:mn><\/mml:mrow><\/mml:math>,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>.0001<\/mml:mn><\/mml:mrow><\/mml:math>) and UC cases and controls (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:msup><mml:mi>\u03c7<\/mml:mi><mml:mn>2<\/mml:mn><\/mml:msup><mml:mo>=<\/mml:mo><mml:mn>46.3<\/mml:mn><\/mml:mrow><\/mml:math>,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:mtext>df<\/mml:mtext><mml:mo>=<\/mml:mo><mml:mn>7<\/mml:mn><\/mml:mrow><\/mml:math>,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mtext>.0001<\/mml:mtext><\/mml:mrow><\/mml:math>). We conclude that carrying a 3-marker haplotype in the TNSFRSF1B gene may increase (e.g., haplotype of GGC was 2.9-fold more in the CD or UCpatients) or decrease (e.g., TGT was 0.47-fold less in UC patients) the risk of IBD in a New Zealand Caucasian population.<\/jats:p>","DOI":"10.1155\/2009\/591704","type":"journal-article","created":{"date-parts":[[2009,5,3]],"date-time":"2009-05-03T09:47:51Z","timestamp":1241344071000},"page":"1-9","source":"Crossref","is-referenced-by-count":15,"title":["Tumor Necrosis Factor Receptor Superfamily, Member 1B Haplotypes Increase or Decrease the Risk of Inflammatory Bowel Diseases in a New Zealand Caucasian Population"],"prefix":"10.1155","volume":"2009","author":[{"given":"Lynnette R.","family":"Ferguson","sequence":"first","affiliation":[{"name":"Discipline of Nutrition, The University of Auckland, Private Bag 92019, Auckland 1023, New Zealand"},{"name":"Nutrigenomics New Zealand, New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dug Yeo","family":"Han","sequence":"additional","affiliation":[{"name":"Discipline of Nutrition, The University of Auckland, Private Bag 92019, Auckland 1023, New Zealand"},{"name":"Nutrigenomics New Zealand, New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Claudia","family":"Huebner","sequence":"additional","affiliation":[{"name":"Discipline of Nutrition, The University of Auckland, Private Bag 92019, Auckland 1023, New Zealand"},{"name":"Nutrigenomics New Zealand, New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ivonne","family":"Petermann","sequence":"additional","affiliation":[{"name":"Discipline of Nutrition, The University of Auckland, Private Bag 92019, Auckland 1023, New Zealand"},{"name":"Nutrigenomics New Zealand, New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Murray L.","family":"Barclay","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, Christchurch Hospital, Christchurch 8011, New Zealand"},{"name":"Department of Medicine, University of Otago Christchurch, New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard B.","family":"Gearry","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, Christchurch Hospital, Christchurch 8011, New Zealand"},{"name":"Department of Medicine, University of Otago Christchurch, New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alan","family":"McCulloch","sequence":"additional","affiliation":[{"name":"Nutrigenomics New Zealand, New Zealand"},{"name":"Crop and Food Research, Mosgiel 9053, New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pieter S.","family":"Demmers","sequence":"additional","affiliation":[{"name":"Nutrigenomics New Zealand, New Zealand"},{"name":"AgResearch Limited, 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