About 90% of humans have AAV2 in their blood. AAV2 present in the DNA of liver cells from patients with liver cancer either slowed or had no effect on tumor growth.
Leading researchers in the fields of gene therapy and molecular genetics rejected the conclusion drawn from a recent study that insertion of adeno-associated virus 2 (AAV2) into human DNA causes mutations leading to the development of hepatocellular carcinoma (HCC). Calling the conclusions of the study authors "an enormous leap from their data," the team of researchers challenge details of the experimental methods, interpretation of the findings, and limitations of the study design in an Editorial published in Human Gene Therapy.
‘Hepatocellular carcinoma is the most common type of liver cancer. It occurs predominantly in patients with underlying chronic liver disease and cirrhosis.’
Challenging a recent Letter in Nature Genetics by Nault et al., the authors of the HGT Editorial instead suggest that "AAV infection might indeed be a key factor in preventing HCC in humans." Up to 90% of humans have AAV2 in their blood, yet HCC affects only about 10/100,000 people in the U.S. In the Editorial, the authors assess the study design and data. They conclude that in most cases, AAV2 present in the DNA of liver cells from patients with HCC either slowed or had no effect on tumor growth, as it was detected in only 7% of HCC tumors and in 21% of adjacent normal liver tissue samples.
Source-Eurekalert