Abstract
We have previously described a form of hepatocellular carcinoma (HCC) in non-cirrhotic liver (HCC-NC) developed by Peruvian patients. We analyzed the metallomic profile in hepatic tissues from two independent cohorts exhibiting HCC-NC. Clinical, histopathological data, and HCC and non-tumoral liver (NTL) samples of 38 Peruvian and 38 French HCC-NC patients, were studied. Twelve metals were quantified using ICP/MS: Mn, Fe, Cu, Co, Zn, As, Se, Rb, Mo, Cd, Pb, and Sn. Associations between metals and survival were assessed. Our data showed significant differences between cohorts. Mean ages were 40.6 ± 20, 67.5 ± 9 years old for Peruvians and French, respectively. Fifty percent of the Peruvian patients were positive for the HBsAg, versus 3% in French patients. Mn, Cu, Zn, As, Se, Rb, Mo, Cd, Sn metal concentrations were higher in NTL of Peruvians. Importantly, metal concentrations were lower in HCC areas compared to NTL tissues in both cohorts, except for Cu for which mean concentration was higher in HCC (p < 0.05). Se concentration in HCC was associated with extended survival only in Peruvians. Our data, obtained in Peruvian and French HCC-NC cohorts, highlights similarity in the metallomic profile of HCC compared to NTL during the hepatic tumorigenesis in these specific groups of patients.
Highlights
We have previously described a form of hepatocellular carcinoma (HCC) in non-cirrhotic liver (HCC-NC) developed by Peruvian patients
The development of HCC is commonly regarded as a sequential multistep pathogenic process initiated with inflammation-mediated liver tissue damages and hepatocyte necrosis that induce liver fibrogenesis towards cirrhosis, which in turn increases the risk for HCC2
We have previously described a peculiar clinical and molecular presentation of HCC-NC developed by patients from Peru[3]
Summary
We have previously described a form of hepatocellular carcinoma (HCC) in non-cirrhotic liver (HCC-NC) developed by Peruvian patients. We observed within the non-tumor liver (NTL) parenchyma the presence of foci of cellular alteration in which cells are smaller compared to regular hepatocytes and exhibit an altered nuclear-cytoplasmic r atio[8] These foci of cellular alteration showed some degree of congruence with the co-expression of glutamine synthetase. These findings suggest that the clinical epidemiological situation encountered is due to some biological features intrinsic to the natural history of HCC in a fraction of the population in South A merica[10] This observation prompted us to search for additional pathophysiological cofactors associated with HCC-NC that could enhance the risk of developing precociously HCC among Peruvian patients
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