Celera and Collaborators Present Data Demonstrating the Association of Increased Risk for Heart Attack for Carriers with the KIF6 Gene Variant in a Hispanic Population from Costa Rica
New study expands the number of populations where KIF6 has been shown to predict increased risk of a coronary event
FOR IMMEDIATE RELEASE
Alameda, CA - March 12, 2009
Celera (NASDAQ:CRA) and its collaborators today announced the presentation of data demonstrating increased risk of myocardial infarction (MI), or heart attack, in carriers of the KIF6 gene variant in a case-control study of a Hispanic population from Costa Rica. The data will be presented as poster #P204 in session 3 at the American Heart Association’s 49thCardiovascular Disease Epidemiology and Prevention Conference in Palm Harbor, FL. This follows Celera’s recent findings from six prospective studies that report the association of a variant of the gene encoding kinesin-like protein 6 with coronary events in whites and African American populations (1-5).
In this research study, carriers of the KIF6 gene variant (58 percent of control subjects) had an elevated risk for non-fatal MI when compared with non-carriers, and ethnicity had no apparent effect on the association between the KIF6 variant and non-fatal MI. As with the previous studies in other population groups, the increased risk of clinical events observed in KIF6 carriers was independent of other well-known CHD risk factors, including smoking, hypertension, cholesterol level, age and sex, which Celera believes further supports the conclusion that the KIF6 gene variant is a new, independent predictor of risk for CHD. This current observational study did not measure response to statin therapy according to KIF6 status.
“Given that genetic associations can vary among different populations, it is imperative to determine whether a genetic predictor for disease is replicated in various ethnic groups,” said Thomas White, Ph.D., Chief Scientific Officer at Celera. “The current findings provide us with important data that KIF6 predicts risk for heart disease in this segment of the large population of people of Hispanic origin in the Americas. We are continuing to perform studies toward replicating this association in other ethnic populations.”
“These findings provide us with a better understanding of genetic predisposition to coronary heart disease in the Hispanic population,” said Hannia Campos, Ph.D., Senior Lecturer at Harvard School of Public Health, Harvard University, and a senior author of this poster.
As part of this case-control research study, 4,142 subjects, who were Hispanics from Costa Rica, were genotyped for the KIF6 gene variant. The non-fatal MI cases were 1,988 men and women who had survived a first acute MI; controls were 2,154 subjects selected randomly from the population who had no history of MI and whose age, gender and area of residence were matched with cases.
Lance Bare, Ph.D., Assistant Director of Cardiovascular Disease Research at Celera, was the lead author of this genetic study, which was conducted with collaborators at Harvard School of Public Health, Boston, MA, Brigham and Women’s Hospital, Harvard Medical School, MA, and the University of Costa Rica.
Approximately 60 percent of studied populations are carriers of the KIF6 gene variant, and these carriers were shown to have up to a 55% increased risk of primary and recurrent coronary heart disease(1-5). These studies have shown that this risk is significantly reduced by statin therapy. The KIF6 (kinesin-like protein 6) gene encodes a protein involved in the transport of cargo such as organelles, protein complexes and mRNA from one part of the cell to another. Kinesins propel themselves along microtubules within a cell in an ATP dependent manner. The KIF6 kinesin is a dimer that has two coiled-coil structures.
About Coronary Heart Disease
According to the American Heart Association, coronary heart disease includes acute myocardial infarction and other acute ischemic coronary heart disease. This year an estimated 700,000 Americans will have a new coronary event. About 500,000 will have a recurrent event (ARIC, 1987–2000, NHLBI). It is estimated that an additional 175,000 silent first heart attacks occur each year. Coronary heart disease caused 1 of every 5 deaths in the United States in 2006. CHD is the largest killer of American males and females. Every 26 seconds an American will suffer a coronary event, and every minute someone will die from one. About 41 percent of those who experience a coronary event will die within a year.
Celera is a healthcare business delivering personalized disease management through a combination of products and services incorporating proprietary discoveries. Berkeley HeartLab, a subsidiary of Celera, offers services to predict cardiovascular disease risk and improve patient management. Celera also commercializes a wide range of molecular diagnostic products through Abbott and has licensed other relevant diagnostic technologies developed to provide personalized disease management in cancer and liver diseases. Information about Celera Corporation, including reports and other information filed by the company with the Securities and Exchange Commission, is available at http://www.celera.com.
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1Iakoubova et al., (2008) Association of the Trp719Arg polymorphism in kinesin-like protein 6 with myocardial infarction and coronary heart disease in 2 prospective trials: the CARE and WOSCOPS trials. J Am Coll Cardiol. 51: 435-43.
2 Iakoubova et al., (2008) Polymorphism in KIF6 gene and benefit from statins after acute coronary syndromes: results from the PROVE IT-TIMI 22 study. J Am Coll Cardiol. 51: 449-55.
3Shiffman et al., (2008) A kinesin family member 6 variant is associated with coronary heart disease in the Women's Health Study. J Am Coll Cardiol. 51: 444-8.
4Bare et al., (2007) Five common gene variants identify elevated genetic risk for coronary heart disease. Genetics in Medicine 9:682-689.
5Shiffman D. et al., (2008) Association of gene variants with incident myocardial infarction in the Cardiovascular Health Study.Arterioscler Thromb Vasc Biol. 28:173-9.
David Speechly, Ph.D.
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