Malaria causes an estimated 500 million clinical cases worldwide with symptoms ranging from headache, high fevers and nausea to more than 1 million deaths annually.

Malaria has had a major effect on the evolution of our species. Mutations occurring in our genome that have helped us survive malaria have been selected for over tens of 1,000s of years of co-existing with this parasite. Understanding how these mutations make us more resistant to malaria can help us design innovative new strategies to prevent or treat severe malaria in places such as sub-Saharan Africa, says researcher Kevin Kain, a Professor out of the Department of Medicine at U of T and one of the lead researchers on the project. Our research shows that people who have an enzyme deficiency or those who carry the gene trait for this deficiency may be protected from severe and fatal malaria.

The team headed by Dr. Kain and which included researchers from McGill University found that a deficiency in an enzyme called pyruvate kinase, which is required for energy production in the body, provides protection against malaria infection.

The findings could lead to the design of new novel therapies to treat and prevent severe and fatal malaria through enhancing the body ™s protective pathways instead of inundating the body with drugs. The study was funded by the Canadian Institutes of Health Research (CIHR) Team grant in malaria.

The study findings were published in the April 24th issue of New England Journal of Medicine.

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Using the Brd4 gene signature, the researchers were able to predict survival and relapse of breast cancer patients in five separate datasets. They were also able to predict the survival of subsets of patients whose breast cancer had not spread to their lymph nodes and patients with estrogen-receptor positive tumors. Estrogen is known to play an important role in the development of breast cancer and about 70 percent of all breast cancers are estrogen-receptor positive. Further research is needed to determine the exact role of Brd4 in the progression of breast cancer, noted Hunter.

"The results of this study and other work in our laboratory suggests that people with inherited differences in Brd4 and the proteins that it induces have a genetic predisposition for developing cancer metastasis," he added. "A better understanding of this gene may lead to improved methods of diagnosing and treating cancer."

For more information on Hunter's research, please go to ccrncer/staff/staff.asp?profileid=13660.

For more information about cancer, please visit the NCI Web site at cancer, or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).

The NICHD sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. For more information, visit the Institute's Web site at nichd.nih.

Reference:Crawford NPS, Alsarraj J, Lukes L, Walker RC, Officewala J, Yang HH, Lee MP, Ozato K, and Hunter KW. 2008. Bromodomain 4 activation predicts breast cancer survival. PNAS. April 29, 2008.

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