Abstract
Some improvements are presented for the affected-pedigree-member method of linkage analysis, which is a generalization of the sib-pair method. The test statistic is extended to include contrasts between affected and unaffected pedigree members, so that it now utilizes marker information from all typed pedigree members rather than just the typed affected members. Computer simulation using a sample pedigree of 14 individuals shows that this modification can substantially increase statistical power where there is a direct association between marker variation and disease and where disease risk is elevated in carriers of the disease allele. Data on Huntington disease in 16 British families, which were analyzed previously using only the affected individuals, are reanalyzed with the unaffected individuals included. Strong rejection of the null hypothesis of no association between Huntington disease and the HindIII polymorphism is confirmed, but the particular families in which the association is significant differs from that obtained through an analysis based only on affected individuals and reflects more closely the results obtained from a lod-score analysis. The test statistic is also modified here to incorporate contrasts between individuals of zero kinship, if needed. This enables contrasts between individuals from different pedigrees, as well as contrasts involving individuals sampled from the general population, to be incorporated into the test of association. For population data, the methodology reduces to a type of contingency-table analysis, in which the rows of the table correspond to different marker-locus genotypes and in which the two columns categorize subjects into an "affected" group versus an "unaffected," or control, group. This aspect of the methodology is illustrated using two population data sets, the first relating APO-E genotype to the frequency of individuals undergoing maintenance hemodialysis and the second relating APO-B genotype to the frequency of coronary artery disease. The present methodology confirms the lack of association between marker and disease in the former data set and confirms the presence of association in the latter. Finally, the methodology is formulated here in terms of ordinary, multiperson kinship coefficients rather than in terms of the generalized kinship coefficients originally proposed. This greatly reduces the number of coefficients to be calculated, thereby enhancing the computational efficiency of the computer program.
MeSH Terms
Apolipoproteins B/genetics
Apolipoproteins E/genetics
Computer Simulation
Coronary Disease/genetics
Deoxyribonuclease HindIII
Female
Genetic Linkage
Humans
Huntington Disease/genetics
Male
Models, Genetic
Models, Statistical
Pedigree
Polymorphism, Restriction Fragment Length
Renal Dialysis
Risk Factors
Chemicals
Apolipoproteins B
Apolipoproteins E
Deoxyribonuclease HindIII
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Ward P J
Unité INSERM de Recherches en Epidémiologie des Cancers, U351, Institut Gustave Roussy, Villejuif, France.
References (20)
20 references, click to expand
-
The investigation of linkage between a quantitative trait and a marker locus.
Behav Genet. 1972 Mar;2(1):3-19
PMID: 4157472
-
Apolipoprotein B gene polymorphisms are associated with lipid levels in men of South Asian descent.
Atherosclerosis. 1991 Dec;91(3):267-75
PMID: 1789809
-
Sibling Method for Detecting HLA-linked genes in disease.
Tissue Antigens. 1977 Jan;9(1):31-5
PMID: 850916
-
A robust method for the detection of linkage in familial disease.
Am J Hum Genet. 1978 May;30(3):308-21
PMID: 677128
-
The generalized sib pair IBD distribution: its use in the detection of linkage.
Ann Hum Genet. 1978 Jul;42(1):87-94
PMID: 686687
-
A recursive algorithm for the calculation of identity coefficients.
Ann Hum Genet. 1981 Jul;45(Pt 3):299-305
PMID: 7305283
-
Studies of a DNA marker (G8) genetically linked to Huntington disease in British families.
Hum Genet. 1986 Aug;73(4):333-9
PMID: 3017842
-
The affected sib-pair method using identity by state relations.
Am J Hum Genet. 1986 Jul;39(1):148-50
PMID: 3463205
-
Apolipoprotein B-gene DNA polymorphisms associated with myocardial infarction.
N Engl J Med. 1986 Dec 11;315(24):1509-15
PMID: 3024002
-
The affected-pedigree-member method of linkage analysis.
Am J Hum Genet. 1988 Feb;42(2):315-26
PMID: 3422543
-
Restriction fragment length polymorphisms in the apo B gene in relation to coronary artery disease.
Atherosclerosis. 1989 Jun;77(2-3):193-201
PMID: 2568839
-
Linkage strategies for genetically complex traits. II. The power of affected relative pairs.
Am J Hum Genet. 1990 Feb;46(2):229-41
PMID: 2301393
-
The power of identity-by-state methods for linkage analysis.
Am J Hum Genet. 1990 Feb;46(2):254-65
PMID: 2301395
-
DNA polymorphisms of the apolipoprotein B gene in patients with premature coronary artery disease.
Atherosclerosis. 1990 May;82(1-2):7-17
PMID: 1972879
-
Linkage analysis assuming a single-locus mode of inheritance for traits determined by two loci: inferring mode of inheritance and estimating penetrance.
Genet Epidemiol. 1990;7(6):467-79
PMID: 2292371
-
Genetics of atherosclerosis.
Annu Rev Genet. 1990;24:171-87
PMID: 2088166
-
Metabolic factors in cancer susceptibility.
Cancer Surv. 1990;9(3):437-74
PMID: 2101721
-
Dissecting the genetic contribution to coronary heart disease.
Am J Hum Genet. 1991 Dec;49(6):1139-44
PMID: 1746548
-
Apolipoprotein E phenotypes and hyperlipidemia in patients under maintenance hemodialysis.
Hum Genet. 1992 Jan;88(3):307-12
PMID: 1733833
-
Disease susceptibility genes--their identification by multiple case family studies.
Tissue Antigens. 1976 AUG;8(2):109-19
PMID: 968896