Anitschkow Prize Recipient 2015

Professor Aldons J. Lusis receives the Anitschkow Prize from EAS President Professor Alberico Catapano and presents the Anitschkow Lecture at the EAS Congress 2015 in Glasgow, UK.

EAS is pleased to announce that Professor Aldons J. Lusis will be the recipient of the Anitschkow Prize 2015. This prestigious Prize, awarded annually by EAS, recognizes outstanding research in the field of atherosclerosis and linked metabolic disturbances.

About the Laureate

Aldons J. Lusis, Ph.D.

The following biography highlights some of Prof Lusis’ achievements.

Developmental genetics (1975-1978)
During his postdoctoral fellowship with Kenneth Paigen in the Department of Molecular Biology at Roswell Park, Prof Lusis studied natural variation in mice to examine aspects of developmental genetics.

Regulation of hematopoiesis (1979-1986)
Upon accepting a faculty position at UCLA, he began working on two projects. One was a continuation of mouse geneics and the other was a collaborative study with David Golde and others to study hematopoietic regulation. At that time, hematopoietic growth factors such as mascrophage colony stimulating factor and erythropoietic had not yet been identified.

Development of the mouse as a model systems for studies of lipoprotein metabolism (1981-1989)
As a result of interactions with Verne Schumaker and Mike Schotz, Prof Lusis became interested in applying mouse genetics to understand lipid metabolism and atherosclerosis. At that time, the mouse was considered a poor system for such studies, since they tend to be resistant to atherosclerosis. Hence, there was very little that had been done.

Molecular cloning of genes for plasma lipid metabolism (1983-1990)
To carry out genetic studies of lipid metabolis, Prof Lusis & coworkers cloned a number of critical molecules in lipid metabolism. In particular, they were the first to clone apolipoprotein B, the primary protein of LDL, and liprotein lipase, the enzyme dedicating lipoprotein triglyceride hydrolysis.

Mapping genes for lipid metabolism (1983-1990)
Before the genome project, it was important to locate genes on chromosomes to begin to understand genetic regulartory circuits. Prof Lusis was involved in the original mapping of many of the genes controlling lipid metabolism and related traits.

Inflammation and atherosclerosis (1990-present)
By the early 1990s, there was accumulating evidence that atherosclerosis involved inflammatory aspets and Prof Lusis & coworkers applied molecular genetics to help elucidate these. In particular, their background in macrophage biology was helpful in this regard.

Genetics of complex traits (1993-2006)
With the development of genetic markers in the early 1990s, it became feasible to map genes for complex cardiovascular and metabolic traits. Prof Lusis & coworkers were among the first to apply this technology to both mouse and human studies.

Systems genetics and complex traits (2003-present)
With the development of “omics” technologies, such as expression arrays, it became possible to examine certain biologic scales on a global, or near global, level. Over the past decade, Prof Lusis has worked to integrate such “intermediate phenotypes” with genetics to attempt to better understand pathways and interactions in complex disease. He & his coworkers were among the first to map the genetics of gene expression (expression quantitative trait loci, or eQTL) and to model biologic networks with such data.

The Hybrid Mouse Diversity Panel (HMDP), a new tool for sytems analysis of complex traits.
The HMDP consists of about 100 common and recombinant inbred strains which have been entirely sequenced or densely genotyped. The HMDP strains are commercially available and, thus, can be assayed for multiple phenotypes by different laboratories, providing cumulative biological insights. This, of course, is ideal for a systems genetics approach, since multiple “intermediate phenotypes” such as transcript levels, protein levels, and metabolite levels, can be assayed in genetically identical animals and then integrated. The HMDP also has two additional very important advantages. First, the mapping resolution in the HMDP, which involves association, is much better, by at least an order of magnitude, than classical linkage analysis. Second, the HMDP is ideal for examining gene-by-environment interactions, since genetically identical animals can be examined before and after a particular environmental perturbation.

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