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High hepatocellular carcinoma risk among US‐born Hispanics

We were intrigued by the still unexplained greater risk of hepatocellular carcinoma (HCC) in US-born Hispanic men, but not females, compared with foreign-born Hispanic individuals, even after accounting for infection by hepatitis viruses, the excessive intake of alcohol and calories, and other factors. Herein, we highlight another factor that could be considered: an infection that has been experimentally and epidemiologically related to HCC in animals and humans, especially males, namely Helicobacter pylori and other Helicobacter species. Experimental infection with Helicobacter hepaticus consistently caused acute and chronic hepatitis and HCC in most male mice. Several researchers, including ourselves, have found a very high prevalence of H. pylori infection in European and Chinese male patients with HCC. Indeed, the cytotoxin-associated gene A protein product (CagA) of H. pylori is the paradigm for hit-and-run carcinogenesis, and circulates within exosomes in the bloodstream. The liver performs clearing of nearly everything from the splanchnic circulation, and receives these CagA-laden exosomes that can be delivered to hepatocytes. The CagA protein is known to bind E-cadherin on cell membranes, thereupon freeing b-catenin, which enters the nuclei and activates the c-JUN proto-oncogene. Moreover, once CagA has been translated into gastric epithelial cells, it is phosphorylated on tyrosine residues. Phosphorylated CagA activates phosphoinositide 3-kinase and the AKT pathway, again allowing bcatenin to enter the nuclei and activate a proliferative state in the host cell. The hepatitis C virus (HCV) correlates with HCC, but HCC did not develop 20 years after infection with HCV in the Leipzig cohort study, suggesting the need for a cocarcinogenic, proinflammatory status to exert HCVtransforming capabilities. A low-grade systemic inflammatory status usually is caused by H. pylori infection and is increased if the infecting organisms express CagA. Many cytokines are involved, including interleukin 6, which stimulates HCC in males, less so in females. Other mechanisms capable of worsening liver disease and driving transformation have been recognized and described, including epidermal growth factor polymorphism, as well interleukin 28 and PNPLA3. It is unlikely that either sex could carry differences in gene polymorphisms within a homogenous population. It could be worth examining the California cohort presented by Setiawan et al for differences with regard to proinflammatory status and infection by pathogenic strains of H. pylori.