@article{fdi:010075252,
  title = {{E}arly-onset liver cancer in {S}outh {A}merica associates with low hepatitis {B} virus {DNA} burden},
  author = {{M}archio, {A}. and {C}erapio, {J}. {P}. and {R}uiz, {E}. and {C}ano, {L}. and {C}asavilca, {S}. and {T}erris, {B}. and {D}eharo, {E}ric and {D}ejean, {A}. and {B}ertani, {S}t{\'e}phane and {P}ineau, {P}.},
  editor = {},
  language = {{ENG}},
  abstract = {{I}n {P}eru, hepatocellular carcinoma ({HCC}) arises in young non-cirrhotic patients. {H}epatitis {B} virus ({HBV}) is suspected to be the prominent etiological agent. {W}e thus performed a comprehensive molecular study of {HBV} infection in 65 {P}eruvian {HCC} patients. {O}nly 51% were considered as persistently infected at the onset. {HBV} {DNA} was found by {PCR} in the tumor and/or matched non-tumor liver tissues in more than 80% of cases (n = 53/65). {HBV} {DNA} was significantly more abundant in livers of younger patients than in those of the older ones. {W}e consistently observed low viral {DNA} burden (0.1-6.5 copies for 100 cells), with viral genomes in younger patients displaying higher proportion of mutations at di-pyrimidines ({T}p{T} and {C}p{C}, {P} = 0.006). {A} drastic activation of multiple {DNA} repair pathways in tumors of younger patients was observed. {O}ur observations clearly challenge the current vision that associates high {HBV} {DNA} load with earlier tumor development. {W}e concluded that in {P}eru, and maybe in other populations with {A}mericas' indigenous ancestry, {HBV}-associated liver tumorigenesis might differ significantly from that generally observed in the rest of the world. {P}rocedures used to screen for {HCC} development in subjects at risk should be adapted to the local situation.},
  keywords = {{PEROU}},
  booktitle = {},
  journal = {{S}cientific {R}eports - {N}ature},
  volume = {8},
  numero = {},
  pages = {art. 12031 [14 p.]},
  ISSN = {2045-2322},
  year = {2018},
  DOI = {10.1038/s41598-018-30229-8},
  URL = {https://www.documentation.ird.fr/hor/fdi:010075252},
}