Dissecting the Enzymatic Activity of Anthracycline-Reductases in the Context of Coronary Heart Disease

Nicholas Cheung and Kyle Wieczorek

Common progression of heart failure .

Common progression of heart failure.

Undergraduate Student Project

Introduction

Cells in your body are always growing and one small mutation can cause a much bigger problem, cancer. Most people throughout their lives know or will know someone who has developed a form of cancer. My name is Nicholas Cheung and I am a senior majoring in pharmaceutical sciences. My current research takes place in the lab of Dr. Javier Blanco in the School of Pharmacy and Pharmaceutical Sciences. The labs primary focus is on genetic and epigenetic factors which contribute to variable drug response in relevant clinical settings. Our current research revolves around the study of drug toxicities to the heart. With cancer being such a prevalent disease, forms of chemotherapy are often employed as a way to target and prevent progression. One such chemotherapeutic agent is a small molecule drug called daunorubicin. This drug is often used in the treatment of various forms of leukemias and breast cancer. While this drug is popular to treat cancers, it has a nasty side effect which can cause heart damage if the dose given reaches a certain threshold. This project will hopefully help determine whether individuals with coronary heart disease are at a greater risk of experiencing these cardiotoxic side effects.

Abstract

Anthracycline related cardiotoxicity is a well-known adverse effect due to the cumulative use of these drugs. This research focuses primarily on daunorubicin (DAUN) which a cancer drug used to treat various forms of leukemias. In the body, DAUN is metabolized by Carbonyl Reductase's (CBRs) and Aldo-Keto Reductase's (AKRs) [1]. These enzymes metabolize DAUN into its alcohol metabolite known as daunorubicinol (DAUNol) which is believed to contribute to the cardiotoxicity of the drug. This experiment was conducted to research the enzymatic activity found in heart cytosols from donors with Coronary Heart Disease (CHD) and non-CHD to determine whether there is relationship between disease state and the formation of DAUNol.

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