Treatment of acute lymphoblastic leukemia and cancer in children is largely successful cure. Unfortunately, some children then had a dangerous heart disease. Suspected, the treatment of cancer has ever received that was the trigger.
In a report published peneltiian Journal of Clinical Oncology, researchers from the University at Buffalo trying to find answers to the underlying genetic why some victims of childhood cancer treated with strong antibiotics such as Adriamycin and daunomycin disorder called cardiomyopathy or heart muscle disease in later life.
"Anthracyclines are effective drugs used to treat a variety of childhood cancer, is also used to treat breast cancer and other malignant cancers in adults," said professor of pharmaceutical sciences University at Buffalo, Javier G. Blanco, PhD.
"After cancer, victims can suffer heart damage from a year to more than 15 years after initial chemotherapy with anthracyclines. Our knowledge of this drug's effectiveness in separating the effects of the poison is still narrow. The dose should be appropriate to achieve therapeutic effects without harm," Blanco said as quoted by Eurekalert . com, Tuesday (20/12/2011).
Blanco explained that the key to the success of drug therapy for each patient is to understand how individuals respond to the drug once it enters the body genetically, and then adjust the dose to be more precise again.
Working closely with Smita Bhatia, MD, MPH, chair of the Department of Population Sciences at City of Hope National Medical Center in California, Blanco decided to see how the drug is broken down by enzymes encoded by specific genes in the body.
Research that began seven years ago was to compare the genotype DNA of 170 child victims of cancer diagnosed heart muscle disease associated with anthracycline treatment control group consisted of 317 children who survived cancer without heart disease. Using a candidate gene approach, Blanco and his team were able to identify small gene variants associated with risk of cardiac toxicity.
Researchers focused on carbonyl reductases (CBR1 and CBR3), two enzymes that break down into metabolites alcohol cardiotoxic anthracyclines. Blanco noted that in mouse models, the CBR rate higher or more rapid action of the enzyme that will determine the metabolite levels higher and higher risk of heart poison.
