Recurrent AAV2-related insertional mutagenesis in human hepatocellular carcinomas. JC Nault, S Datta, S Imbeaud, A Franconi, M Mallet, G Couchy, E Letouzé, C Pilati, B Verret, JF Blanc, C Balabaud, J Calderaro, A Laurent, M Letexier, P Bioulac-Sage, F Calvo, J Zucman-Rossi. Nat Genet 2015 Oct;47(10):1187-1193. “We found clonal integration of adeno-associated virus type 2 (AAV2) in 11 of 193 HCCs. These AAV2 integrations occurred in known cancer driver genes, namely CCNA2 (cyclin A2; four cases), TERT (telomerase reverse transcriptase; one case), CCNE1 (cyclin E1; three cases), TNFSF10 (tumor necrosis factor superfamily member 10; two cases) and KMT2B (lysine-specific methyltransferase 2B; one case), leading to overexpression of the target genes. Tumors with viral integration mainly developed in non-cirrhotic liver (9 of 11 cases) and without known risk factors (6 of 11 cases), suggesting a pathogenic role for AAV2 in these patients. In conclusion, AAV2 is a DNA virus associated with oncogenic insertional mutagenesis in human HCC.” Of the 11 patients, one had HCV, one HBV plus alcohol, and three tumors were alcohol-related. Three patients were female (Supplementary Table 2).
This discovery is important because there are so few HCCs that aren’t caused by those known viruses in the first place: Ding et al. found that markers of hepatitis viruses B and C were not found in only 6.2% of American cases, and about 5% overall. They observed a high prevalence (35.2%) of occult hepatitis B, and that “Histological findings of non-B, non-C HCC showed that 81% of cases were accompanied by liver cirrhosis and 62.5% had chronic inflammatory cell infiltration in the portal tracts of nontumorous regions, which findings suggested persistent infection by unknown virus(es).” (Geographic Characterization of Hepatitis Virus Infections, Genotyping of Hepatitis B Virus, and p53 Mutation in Hepatocellular Carcinoma Analyzed by In Situ Detection of Viral Genomes from Carcinoma Tissues: Comparison among Six Different Countries. X Ding, YN Park, TC Taltavull, SN Thung, X Jin, Y Jin, NS Trung, Y Edamoto, T Sata, K Abe. Jpn J Infect Dis 2003 Feb;56(1):12-18.) [The portal tracts are bundles of vessels consisting of an artery, a vein, a bile duct, a lymphatic vessel, and a nerve branch.]
And this in turn is important, because the charlatans who concoct pretexts to meddle in peoples’ lifestyles are committing scientific fraud by failing to diagnose a high proportion of virally-infected cases! Such as:
“A majority of American studies on HCC and hepatitis viruses were conducted in the United States (Figure 3), with two-thirds of HCC cases coming from a nation-wide linkage study for the Surveillance Epidemiology and End-Results Program. In the United States, 9% of HCC cases were HBsAg+ and 22% were anti-HCV+. The prevalence of HBV/HCV coinfection in HCC cases was 3.2% and a high proportion (67%) of HCC cases were seronegative for markers of both hepatitis viruses… More than half of HCC cases were both HBsAg− and anti-HCV− in the United States and some North European countries, thus pointing to the relative importance of heavy alcohol consumption and, possibly, smoking, obesity and diabetes mellitus (Yuan et al, 2004) in areas where hepatitis virus prevalence and HCC incidence are low.” (Worldwide variation in the relative importance of hepatitis B and hepatitis C viruses in hepatocellular carcinoma: a systematic review. SA Raza, GM Clifford, S Franceschi. Br J Cancer 2007 Apr 10;96(7):1127–1134.)
“(67%) of HCC cases were seronegative for markers of both hepatitis viruses,” they claim! And on that basis they proclaim ownership of that 67% on behalf of their lifestyle crap! Look at the discrepancy between that and the finding of only 6.2% negative for markers of HBV/HCV in actual tumors! And the discovery of integrated adeno-associated virus in non-B non-C hepatocellular carcinomas means that the lifestyle nazis can’t even make a reasonably confident claim to the full 6.2% of cases remaining that couldn’t be attributed to HBV or HCV.