Cell Viability of Human Cardiomyocytes in the Context of Daunorubicin and Doxorubicin

Kyle Wieczorek

This is a picture of the UB Pharmacy Building, where Kyle's research took place.

This is a picture of the UB Pharmacy Building, where Kyle's research took place.

Undergraduate Student Project

Introduction

Down Syndrome (DS) is one of the most common chromosome disorders causing developmental and intellectual delays. DS is a genetic disorder caused when abnormal cell division results in extra genetic material from chromosome 21.

My name is Kyle Wieczorek. I am a senior pharmaceutical sciences BS/MS major at UB, and I've worked under Dr. Javier Blanco as my research mentor for just over a year now.  Dr. Blanco's lab focuses on the systematic characterization of genetic and epigenetic factors that contribute to variable drug response in relevant clinical settings. Over this past year I have been analyzing two drugs, doxorubicin and daunorubicin, to discover more on their cardiotoxic effects.

People with Down Syndrome are more prone to certain types of cancers these drugs are used. This happens usually in early childhood stages and later in life these patients develop heart complications known to be an effect of these drugs. It is important to understand how these drugs work and to develop methods limit toxic effects.

Abstract

Down Syndrome (DS) is one of the most common chromosome disorders causing developmental and intellectual delays. DS is a genetic disorder caused when abnormal cell division results in extra genetic material from chromosome 21. Individuals with DS are more prone to leukemia and lymphoma compared to be people without DS. The anthracyclines daunorubicin (DAUN) and doxorubicin (DOX), are most common in treating these cancers. These anthracycline drugs are known to cause cardiotoxic effects which can cause complications later in life. In this study the effects of these two drugs on AC16 cells are analyzed using a dose response method.

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