From this report we can see ETV or TDF at least reduce HCC risk especially on non-cirrhosis patients. So conflict with the lines above...
Impact of hbv therapy on hcc incidence , very good presentation
http://www.aphc.info/pdf/2014/pleniere_14012014/1430/Massimo_COLOMBO.pdf
Hbsag clearance before being 50 years old seems to have best prognosis. Age at which hbsag was cleared plays very important role.
By the way any study on nucs with less durability than 10 years is of zero significance for 2 reasons:
tumors take decades to escape immune detection and become visible to us
nucs take at least 5 years to change viral numbers in the liver, i d say even more than 5 years
Andrey is correct peg add on is the best solutions and peg is even active on liver tumors so in case of hbsag clearance its effect is very considerable
peg is a tumor therapy for melanoma and other tumors too
it is also interesting to see how nagalase goes once hbsag is cleared, my guess is that presence of nagalase during hbv infection is one of the main tumors effectors, afterall if immune system is fully functional we can have all the hcc we want in the liver...that it will get cleared by the immune system
To be honest, the article is quite general, no detailed information. After 42 months of NUCs, 7.7% patients developed HCC, too general.
Please see this link.
http://www.gastroenterologyupdate.com.au/latest-news/hcc-risk-remains-high-with-hep-b-antivirals
As I know, long-term TDF can also reduce cccDNA slowly, by 10 years, reduce to only 1%-10% volume compare with baseline. So HCC risk is reduced?
The only way to reduce risk significantly is hbsag clearance with or without seroconversion to anti-hbs. Nowadays the only way to obtain that status is through interferon therapy but unfortunately inf doesn't work for everyone.
What if one of the potential treatments currently being tested actually works to reduce HBsAg significantly, even if not a cure? Would that lower HCC risk significantly?
Some long-term studies found that even most potent NA (TDF) could not cut risk of HCC. Especially, when we have had this virus for a long time and it already integrated in our genome.
HCC is very complicated if cure (cccDNA - & anti-hbs +) could not achieve, the risk of HCC remains higher.
It's already very very low and no abnormal liver damage, why develops HCC? Generally we thought HCC is developing with long-term ALT abnormal?
Hbvdna is und in your blood stream but detectable inside liver
During the long-term ETV, HBVDNA keeps undetectable, no serious liver damages, how does HCC develops?
I assume all patients had und viral load if taking entecavir for long, would be interesting to see how hbsag levels corresponded to hcc occurrence!