AZT is considered the standard of care for the prevention of perinatal HIV from mother to child in pregnant women; it has reduced transmission rate by over two-thirds. Recently-collected data suggest that AZT can integrate into patient DNA and that in animal studies (mice) AZT causes an increase in tumors when mothers are treated with AZT during the last trimester. Presently, the question arises as to whether AZT treatment can cause possible genomic damages and whether this relates to tumorgenesis in the offspring. The proposed study is based on the hypothesis that perinatally-administered AZT is incorporated into the DNA of target organs in the offspring causing DNA damages with an increased risk of tumorigenesis in the infant. The Principal Investigator proposes to study a full range of samples obtained from an NIH-funded study of rats that have been exposed to perinatal AZT and control reagents which are known to induce tumors (ddI) in various doses. The planned experiments employ standard molecular biological cytogenetic and molecular morphological protocols. The findings in rats will be verified in selected human samples. The data will lead to the better understanding of important questions relating to the potential of carcinogenic risk of AZT in children who are exposed to the drug in the fetal and early neonatal period.
