Abstract: On multivariable analysis, males (OR = 4.51, 95%CI 1.78-11.4, p = 0.001), age>=40 (OR = 5.5, 95%CI 2.06-14.68, p = 0.001),
W4P/R/Y on
PreS1 (OR = 11.56, 95%CI 1.99-67.05, p = 0.006) and 4
S point-mutations as:
T47A/E/V/K (OR = 3.67, 95%CI 1.19-11.29, p = 0.023),
P120S/T (OR = 3.38, 95%CI 1.09-10.49, p = 0.035),
S174N (OR = 29.73, 95%CI 2.12-417.07, p = 0.012),
P203R (OR = 8.45, 95%CI 1.43-50.06, p = 0.019) were associated with
HCC.
Discussion: Recently, we identified the novel
W4P substitution in the
preS1 region of hepatitis B virus (HBV) related to
HCC that occurs exclusively in male patients.
Discussion: The phenotypes of male
Discussion: Therefore, further studies are necessary to demonstrate higher male susceptibility to
liver carcinogenesis in our
W4P TG mouse model and clarify its mechanism in the future.
Abstract: CDDO-me exerted cytotoxic activity against
W4P-
LHB-expressing NIH3T3 cells, HepG2 cells, and Huh7 cells, and induced apoptotic cell death in a dose-dependent manner, demonstrating its anti-cancer activity against
HCC.
Abstract: Furthermore, -CDDO-me administration significantly suppressed tumor growth induced by
W4P-
LHB-expressing NIH3T3 cells in nude mice, confirming its anti-cancer activity.
Abstract: In addition, CDDO-me treatment resulted in decreased cell migration and colony formation in in vitro assays using
W4P-
LHB-NIH3T3, HepG2, or Huh7 cell lines, supporting its anti-cancer activity through STAT3 inhibition.
Abstract: A critical role of interleukin (IL)-6 signaling in
W4P-mediated tumorigenicity was tested by inhibition of Jak2.
Abstract: CONCLUSIONS: This study suggests that the
W4P mutation during the natural course of
chronic hepatitis B infection may contribute to
HCC development, particularly in male patients, in an IL-6-dependent manner.
Abstract: IL-6 levels of
HCC patients with the
W4P variant were significantly higher than those of patients with WT
LHB.