Spanish capable of predicting liver tumor up to 20 years before

José Tubio, researcher at the University of Santiago de Compostela (USC, in Galicia), has been working in collaboration with scientists from England, Japan and Spain. The goal of it: understand how it is possible for an infection by a virus can lead to cancer. Specifically, the hepatitis B virus (VHB). 20% of these patients end up dying by cirrhosis or liver cancer. What happens for this degeneration to occur? After months and months of research, this international group has managed to describe a phenomenon that explains this progression of virus to tumor.

As explained by the Spanish author to this newspaper, "We have found supermutations in liver cancer that are caused by hepatitis B virus", even "20 years before the tumor is diagnosed." An important advance that has just published the magazine 'Nature Communications'. The results obtained in this work "suggest that if treatment is advanced against the hepatitis B virus in patients infected with the virus, many people could be saved from developing a liver cancer."

At this point, it should be remembered that 4% of the world's population is affected by HBV, so "it is a lot of people (240 million people) who could potentially benefit from our discovery," says Spanish.

It is a hopeful news that sheds light where there were no answers, thanks to the study of a total of 296 liver carninomas. This is how the new phenomenon that could be behind the start and progression of this type of tumors has been described. "Using DNA sequencing tanning technologies, we have checked that, frequently, the virus DNA integrations are mediating alterations in the genome of liver cells," explains Paula Otero, co-author of the Article and Researcher of the Singular Medicine Research Center Molecular and chronic diseases (CIMUS).

That is, "in our genome we see another type of anomalies - such as losses of native DNA or mergers between different chromosomes - that, ultimately, make protective genes against cancer", continues explaining Otero. Therefore, it would be the absence of these genes (which under normal conditions prevent the cells from dividing uncontrollably) that could stimulate the formation of the tumor.

For decades it is known that, during the infection, as part of its natural cycle, the VHB introduces its own genetic material (its instruction manual) within the cells of the human liver. "That's what allows you to continue producing copies of yourself and extending the infection," explains the authors of work. This process, which is common to many other viruses, can sometimes end with the integration of VHB DNA within human DNA. "These virus DNA integrations can be harmful, but by themselves they did not allow explaining how VHB promotes tumor formation."

The Spanish researchers feel proud of this finding and have been surprised to verify that this phenomenon occurs very early, sometimes even two decades before the tumor is diagnosed. Precisely for this reason, it argues Otero, "We believe that this discovery could facilitate the early diagnosis of the disease and also help develop more effective therapeutic strategies."

This advance is the last finding of the CIMUS group of the USC 'genomes and disease' and has been made within the framework of an international consortium (PAN-CANCER) integrated by teams from England, Japan and Spain, which has used advanced technologies of DNA sequencing to describe a new tumor formation path as a result of the HBV activity, and its genetic behavior, with the formation of tumors. "This will allow us to see the exact moment in which these events take place, characterize them and analyze how they affect the structure of the genome. In this way we can have a global vision of the process of tumor development from an evolutionary point of view," concludes another Of the Spanish researchers, Eva G. Álvarez.