With the assistance of the Scientific Advisory Board, a formal grant program has been established to support Junior Researchers and Trainees. The grant program’s goal is to promote interest in amyloid research and attract new young researchers to amyloidosis.
Grants will be awarded on a yearly basis. The AF will continue to promote interest in amyloid research and looks forward to many years of contributing to the medical research that is required to advance the treatment of all types of amyloidosis.
2008 Junior Research Grant Program
The grant program supports two area; basic scientific and translational research. Candidates will have completed their doctoral studies or clinical fellowship within seven (7) years prior to application.
The AF is pleased to announce the following recipients of the Symposium Travel Awards. These awards help to defer the travel costs for these researchers attendance at the XIth International Symposium on Amyloidosis.
Elizabeth Baden
Mayo Graduate School Atomic Resolution Studies of Cardiac Light Chain Amyloidosis
John Keeling, CMIAC, PhD
Saint Louis University Involvement of lysosomes in renal AL-amyloidosis
Ping Zhou, MD, PhD
Memorial Sloan-Kettering Cancer Center The inhibitory Fcy-receptor IIB (CD32B) is highly expressed on clonal plasma cells from patients with systemic light-chain (AL) amyloidosis and provides a target for monoclonal antibody therapy.
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The recipient of the 2007 Junior Researcher Grant is
Raymond Migrino, MD
Medical College of Wisconsin -
Milwaukee WI
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The role of oxidative stress and apoptosis in endothelial dysfunction in AL amyloidosis and protection using antioxidant (MitoQ) and antiapoptotic (Bax inhibitor peptide) therapy
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Primary systemic AL amyloidosis or PSA can be a fatal disease with involvement of the heart being associated with the worst outcomes. The disease involves the deposit of abnormal proteins (light chains) in the heart and blood vessels such as the coronary arteries, leading to abnormal function of the heart and heart failure. It is also associated with abnormal function of the blood vessels, or endothelial dysfunction. Our hypothesis is that exposure to light chains from PSA patients will result in abnormal function of the blood vessel as a result of the increased production of free radicals and induction of cell death, and novel antioxidant agent mitoQ and an agent that prevents cell death, bax inhibitor peptide can reduce the damage to blood vessels from exposure to amyloid light chains. We will measure the ability of normal human blood vessels to dilate or expand in the presence of light chains from patients with PSA, measure the amount of free radicals and cell death generated and determine if there will be improved results if mitoQ or bax inhibitor peptide is administered. The results will increase our understanding of the mechanism of injury to blood vessels and may lead to new ways of treating this disease.
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CD32B: a target for therapy on the surface of plasma cells from patients with AL amyloidosis
Memorial Sloan-Kettering Cancer Center
Raymond L. Comenzo, M.D. – Principal Investigator
Monoclonal antibodies are like magic bullets that can destroy their target cells. They attack proteins that stick out like flags on the surface of cancer cells, and cause the cells to die. Patients with breast cancer and others with lymphoma have benefited from modern monoclonal antibody therapy. In some patients, their cancers have been eliminated, and their lives have been improved and prolonged. In this presentation from Memorial Sloan-Kettering Cancer Center, data are presented that show that the protein CD32B has been found on the outside of the cells that cause systemic AL amyloidosis. CD32B then is a target for monoclonal antibody therapy for AL patients.
