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Treatment of acute lymphoblastic leukemia and cancer in children is largely successful cure. Unfortunately, some children then experience a dangerous cardiac disease. Suspected, the treatment for cancer has ever received that was the trigger.
In a report peneltiian who published the Journal of Clinical Oncology, researchers from the University at Buffalo seeks an answer to an underlying genetic why some survivors of childhood cancer treated with powerful antibiotics like Adriamycin and daunomisin 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 at the University at Buffalo, Javier G. Blanco, PhD.
"After cancer, victims can suffer heart damage from the year to more than 15 years after initial chemotherapy with anthracyclines. Our knowledge in separating the effectiveness of these drugs effect the poison is still narrow. The dosage should be precise to achieve a therapeutic effect without harm," said Blanco as reported EurekAlert .com
Blanco explained that the key to the success of drug therapy for each patient is to understand how individuals respond to the drug after it enters the body genetically, and then adjust the dose to be more precisely.
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 compared the DNA genotypes of 170 child victims of cancer diagnosed heart muscle disease associated with anthracycline treatment control group consisted of 317 children who survived cancer without experiencing heart disease. Using the candidate gene approach, Blanco and his team were able to identify minor variants of genes associated with the risk of cardiac toxicity.
Researchers zeroed in on carbonyl reductases (CBR1 and CBR3), two enzymes that break down anthracyclines into cardiotoxic alcohol metabolites. Blanco notes that in mouse models, higher levels of CBR or enzymes work faster will determine metabolite levels higher and higher risk of heart poison.
The results showed that the risk of cardiomyopathy increases significantly in individuals who had two copies of the gene CBR3 when exposed to low to moderate doses of anthracycline.
"If you stop using anthracyclines we will not be able to treat up to 90 percent of children suffering from acute lymphoblastic leukemia. Parents should continue to monitor the health of children after the cancer is cured to identify heart problems," said Blanco.
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