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Genetic analysis of melanoma suscept...

Gillanders, Elizabeth.

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Genetic analysis of melanoma susceptibility and evaluation of molecular haplotyping information in a family-based linkage study.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Genetic analysis of melanoma susceptibility and evaluation of molecular haplotyping information in a family-based linkage study./
作者:	Gillanders, Elizabeth.
面頁冊數:	246 p.
附註:	Source: Dissertation Abstracts International, Volume: 66-11, Section: B, page: 5790.
Contained By:	Dissertation Abstracts International66-11B.
標題:	Biology, Genetics. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3197153
ISBN:	9780542429651

Genetic analysis of melanoma susceptibility and evaluation of molecular haplotyping information in a family-based linkage study.
Gillanders, Elizabeth.

Genetic analysis of melanoma susceptibility and evaluation of molecular haplotyping information in a family-based linkage study. - 246 p.

Source: Dissertation Abstracts International, Volume: 66-11, Section: B, page: 5790.

Thesis (Ph.D.)--The Johns Hopkins University, 2006.

Complex traits such as heart disease and cancer represent a significant public health burden, and account for a majority of human morbidity and mortality. Therefore, further understanding of the genetic and environmental factors involved in their etiologies is essential. The primary goal of this dissertation was to further localize novel genes involved in cutaneous and ocular melanoma susceptibility. The secondary goal was to investigate a novel method for complex trait gene discovery studies in general.

ISBN: 9780542429651Subjects--Topical Terms:

1017730
Biology, Genetics.

Genetic analysis of melanoma susceptibility and evaluation of molecular haplotyping information in a family-based linkage study.
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245 1 0 $a Genetic analysis of melanoma susceptibility and evaluation of molecular haplotyping information in a family-based linkage study.
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520 $a Complex traits such as heart disease and cancer represent a significant public health burden, and account for a majority of human morbidity and mortality. Therefore, further understanding of the genetic and environmental factors involved in their etiologies is essential. The primary goal of this dissertation was to further localize novel genes involved in cutaneous and ocular melanoma susceptibility. The secondary goal was to investigate a novel method for complex trait gene discovery studies in general.
520 $a In this dissertation, we describe the first genome wide scan for linkage in families that segregate both cutaneous and ocular melanoma. Our hypothesis was that families that segregate both cutaneous and ocular melanoma represent a genetically homogeneous subset of familial melanoma cases. Using a clinical criterion to minimize genetic heterogeneity is a strategy that has proven critical to many of the successful complex trait gene mapping studies. In addition, in collaboration with members of the international Melanoma Genetics Consortium we further localize a novel melanoma susceptibility allele on chromosome 2 and provide evidence against susceptibility loci on chromosomes 8 and 9. These results provide researchers important information towards the identification of novel melanoma susceptibility genes.
520 $a This dissertation also provides several advances to the research field of complex trait genetics in general. First, we describe GeneLink, a database, which was developed to aid researchers in their search for complex trait genes. Second, we investigated a novel method, which improves upon the statistical power of conventional gene mapping studies for complex traits. Specifically, we aimed to evaluate, by simulation, the increased power of molecular haplotypes in the context of a family based linkage study. Our simulations showed that when genetic homogeneity is expected or marker data is complete it is not efficient to generate molecular haplotyping information. However, with levels of heterogeneity and missing data patterns typical of complex traits there is at least a 12% increase in the power to detect HLODs greater than 3.0 when affected individuals are molecularly haplotyped. Any improvement in researchers ability to identify genes involved in complex traits has the potential to be significant from the public health perspective.
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