Page 79 - Read Online

Gitto et al. Hepatoma Res 2020;6:22 I http://dx.doi.org/10.20517/2394-5079.2019.50 Page 7 of 9

[19]
In particular, Villani et al. studied 103 patients treated with DAAs. Changes in levels of VEGF, epidermal
growth factor, and several interleukins were evaluated. Interestingly, the authors demonstrated that
VEGF increased 4-fold from baseline to week 4 of treatment. VEGF level continued to increase until the
end of treatment and returned to the pre-DAA level afterwards. Of note, VEGF induces angiopoietin-2
[29]
expression and can therefore promote DAA-induced carcinogenesis as described in . On the other hand,
interleukin-10 and tumor necrosis factor-alpha significantly decreased with HCV clearance. The authors of
the cited study concluded that DAAs can alter the balance between inflammatory and anti-inflammatory
processes, affecting antitumor surveillance of the host and favoring HCC onset after DAA therapy.

In conclusion, available data indicate that DAAs represent a great option for both patients without cancer
and subjects with effectively treated HCC. Further studies may confirm whether or not some high-risk
subgroups exist, which deserve a personalized surveillance approach.

DECLARATIONS
Authors’ contributions
Conceived and designed the study and wrote the article together: Gitto S, Villa E

Availability of data and materials
Not applicable.

Financial support and sponsorship
None.

Conflicts of interest
Both authors declared that there are no conflicts of interest.

Ethical approval and consent to participate
Not applicable.

Consent for publication
Not applicable.

Copyright
© The Author(s) 2020.

REFERENCES
1. Ferlay J, Soerjomataram I, Dikshit R, Eser S, Mathers C, et al. Cancer incidence and mortality worldwide: sources, methods and major
patterns in GLOBOCAN 2012. Int J Cancer 2015;136:E359-86.
2. Beste LA, Leipertz SL, Green PK, Dominitz JA, Ross D, et al. Trends in burden of cirrhosis and hepatocellular carcinoma by
underlying liver disease in US veterans, 2001-2013. Gastroenterology 2015;149:1471-82.
3. D’Ambrosio R, Della Corte C, Colombo M. Hepatocellular carcinoma in patients with a sustained response to anti-hepatitis C therapy.
Int J Mol Sci 2015;16:19698-712.
4. Fattovich G, Stroffolini T, Zagni I, Donato F. Hepatocellular carcinoma in cirrhosis: incidence and risk factors. Gastroenterology
2004;127:S35-50.
5. Thein HH, Yi Q, Dore GJ, Krahn MD. Estimation of stage-specific fibrosis progression rates in chronic hepatitis C virus infection: a
meta-analysis and meta-regression. Hepatology 2008;48:418-31.
6. Sangiovanni A, Del Ninno E, Fasani P, De Fazio C, Ronchi G, et al. Increased survival of cirrhotic patients with a hepatocellular
carcinoma detected during surveillance. Gastroenterology 2004;126:1005-14.
7. Yano H, Iemura A, Haramaki M, Ogasawara S, Takayama A, et al. Interferon alfa receptor expression and growth inhibition by
interferon alfa in human liver cancer cell lines. Hepatology 1999;29:1708-17.
8. Simmons B, Saleem J, Heath K, Cooke GS, Hill A. Long-term treatment outcomes of patients infected with hepatitis C virus: a systematic
review and meta-analysis of the survival benefit of achieving a sustained virological response. Clin Infect Dis 2015;61:730-40.
9. Conteduca V, Sansonno D, Russi S, Pavone F, Dammacco F. Therapy of chronic hepatitis C virus infection in the era of direct-acting