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Asthma
The PHF11 gene is not associated with asthma or asthma phenotypes in two independent populations
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  1. J McClenaghan1,
  2. N M Warrington1,
  3. E F Jamrozik1,
  4. J Hui2,3,
  5. J P Beilby2,3,
  6. J Hansen4,
  7. N H de Klerk4,
  8. A L James5,6,
  9. A W Musk5,6,
  10. L J Palmer1,7,8
  1. 1
    Centre for Genetic Epidemiology and Biostatistics, University of Western Australia, Nedlands, Australia
  2. 2
    Clinical Biochemistry, PathWest Laboratory Medicine, Perth, Australia
  3. 3
    School of Surgery and Pathology, University of Western Australia, Perth, Australia
  4. 4
    Division of Biostatistics and Genetic Epidemiology, Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia, Perth, Australia
  5. 5
    West Australian Sleep Disorders Research Institute, Sir Charles Gardner Hospital, Nedlands, Australia
  6. 6
    School of Medicine and Pharmacology, University of Western Australia, Crawley, Australia
  7. 7
    Western Australian Institute for Medical Research and UWA Centre for Medical Research, University of Western Australia, Nedlands, Australia
  8. 8
    School of Population Health, University of Western Australia, Crawley, Australia
  1. Professor L J Palmer, University of Western Australia, Nedlands, WA 6009, Australia; lyle{at}cyllene.uwa.edu.au

Abstract

Background: Numerous areas of the human genome have previously been associated with asthma and asthma-related phenotypes, but few positive findings have been successfully replicated in independent populations. Initial studies have reported strong associations of variants in the plant homeodomain zinc finger protein 11 (PHF11) gene with serum IgE levels, asthma, airway hyper-responsiveness and childhood atopic dermatitis.

Objectives: To investigate the association of variants in the PHF11 gene with asthma and associated intermediate phenotypes in two independent Western Australian population-based samples.

Methods: A linkage-disequilibrium (LD)-tagging set of 20 single nucleotide polymorphisms (SNPs) was genotyped in PHF11 in two separate populations (total n = 2315), a family-based twin study consisting of 230 families (n = 992 subjects) and a population-based nested case-control study consisting of 617 asthma cases and 706 controls. Information regarding asthma, respiratory physiology, atopy and environmental exposures was collected. Transmission disequilibrium tests, variance components models and generalised linear models were used to test for association between PHF11 SNPs and selected asthma outcomes (including longitudinal change in lung function).

Results: After correction for multiple testing, no statistically significant (p<0.05) associations were found between PHF11 and either asthma or total serum IgE levels in either population. No statistically significant associations were found with any other asthma-associated phenotypes in either population.

Conclusions: Previously reported associations of PHF11 with asthma outcomes were not replicated in this study. This study suggests that PHF11 is unlikely to contain polymorphic loci that have a major impact on asthma susceptibility in our populations.

https://doi.org/10.1136/thx.2008.108985

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    Footnotes

    • ▸ Additional details are published online only at http://thorax.bmj.com/content/vol64/issue7

    • Funding: The authors acknowledge the assistance of the Western Australian DNA Bank (NHMRC Enabling Facility) with DNA samples for this study and the support provided by the Western Australian Genetic Epidemiology Resource (NHMRC Enabling Facility). They also gratefully acknowledge the support of the WA Health Promotion Foundation (Healthway) for providing the initial funds, allowing the establishment of the WATR, the Wind-Over-Water Foundation and the Australian National Health and Medical Research Council (NHMRC) for providing ongoing funding.

    • Competing interests: None.