ArticleAmerican journal of human genetics1999
A genome scan for familial combined hyperlipidemia reveals evidence of linkage with a locus on chromosome 11.
Article in American journal of human genetics, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 124 citations in OpenAlex.
- Hypertriglyceridemia-induced acute pancreatitis in children: A mini-review.Frontiers in pediatrics · 2022Review
- Association of C5L2 genetic polymorphisms with coronary artery disease in a Han population in Xinjiang, China.Oncotarget · 2017Article
- A novel mutation in C5L2 gene was associated with hyperlipidemia and retinitis pigmentosa in a Chinese family.Lipids in health and disease · 2014Article
- The genetics of familial combined hyperlipidaemia.Nature reviews. Endocrinology · 2012Review
- Genome-wide association studies in atherosclerosis.Current atherosclerosis reports · 2011Review
- Relationship between a novel polymorphism of the C5L2 gene and coronary artery disease.PloS one · 2011Article
- A nonsynonymous SNP within PCDH15 is associated with lipid traits in familial combined hyperlipidemia.Human genetics · 2010Article
- Familial combined hyperlipidemia is associated with alterations in the cholesterol synthesis pathway.Arteriosclerosis, thrombosis, and vascular biology · 2010Article
- Galanin preproprotein is associated with elevated plasma triglycerides.Arteriosclerosis, thrombosis, and vascular biology · 2009Article
- Abnormal Igf2 gene in Prague hereditary hypertriglyceridemic rats: its relation to blood pressure and plasma lipids.Molecular and cellular biochemistry · 2008Article
- A pleiotropic QTL on 2p influences serum Lp-PLA2 activity and LDL cholesterol concentration in a baboon model for the genetics of atherosclerosis risk factors.Atherosclerosis · 2008Article
- Linkage analysis of quantitative traits for obesity, diabetes, hypertension, and dyslipidemia on the island of Kosrae, Federated States of Micronesia.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Genome-wide linkage scans for prediabetes phenotypes in response to 20 weeks of endurance exercise training in non-diabetic whites and blacks: the HERITAGE Family Study.Diabetologia · 2005Article
- Linkage and association between distinct variants of the APOA1/C3/A4/A5 gene cluster and familial combined hyperlipidemia.Arteriosclerosis, thrombosis, and vascular biology · 2004Article
- Empirically derived phenotypic subgroups - qualitative and quantitative trait analyses.BMC genetics · 2003Article
- Search for genetic factors predisposing to atherogenic dyslipidemia.BMC genetics · 2003Article
- Evidence of linkage of HDL level variation to APOC3 in two samples with different ascertainment.Human genetics · 2003Article
- Combined analysis of genome scans of dutch and finnish families reveals a susceptibility locus for high-density lipoprotein cholesterol on chromosome 16q.American journal of human genetics · 2003Article
- Genome scans provide evidence for low-HDL-C loci on chromosomes 8q23, 16q24.1-24.2, and 20q13.11 in Finnish families.American journal of human genetics · 2002Article
- Searching for the mountains of the moon: genome scans for atherosclerosis.Current atherosclerosis reports · 2002Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Familial combined hyperlipidemia (FCHL) is a common familial lipid disorder characterized by a variable pattern of elevated levels of plasma cholesterol and/or triglycerides. It is present in 10%-20% of patients with premature coronary heart disease. The genetic etiology of the disease, including the number of genes involved and the magnitude of their effects, is unknown. Using a subset of 35 Dutch families ascertained for FCHL, we screened the genome, with a panel of 399 genetic markers, for chromosomal regions linked to genes contributing to FCHL. The results were analyzed by use of parametric-linkage methods in a two-stage study design. Four loci, on chromosomes 2p, 11p, 16q, and 19q, exhibited suggestive evidence for linkage with FCHL (LOD scores of 1.3-2.6). Markers within each of these regions were then examined in the original sample and in additional Dutch families with FCHL. The locus on chromosome 2 failed to show evidence for linkage, and the loci on chromosome 16q and 19q yielded only equivocal or suggestive evidence for linkage. However, one locus, near marker D11S1324 on the short arm of human chromosome 11, continued to show evidence for linkage with FCHL, in the second stage of this design. This region does not contain any strong candidate genes. These results provide evidence for a candidate chromosomal region for FCHL and support the concept that FCHL is complex and heterogeneous.
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