BACKGROUND. Increased expression of the proto-oncogene c-myc is a common ph
enomenon in hepatocellular carcinoma (I-ICC). The proto-oncogenes c-fas and
c-jun are involved in cell cycle progression and cellular proliferation.
METHODS. The objective of this study was to elucidate the mechanism of hepa
tocarcinogenesis with regard to the expressions of c-myc, c;fos, and c-jun.
One hundred fifty biopsied HCC specimens were stained immunohistochemicall
y for the above phenotypic markers both in tumor tissue and in adjacent non
tumor tissue.
RESULTS, Although the expression of c-myc was high (74%) in tumor tissue, i
t was significantly less compared with tile expression in nontumor tissue (
100%; P = 0.0002). The expression of c-myc was inversely proportional to th
e grade of differentiation ill tumor tissue (P = 0.0108; correlation coeffi
cient [r] = -0.244); that is, tissue with poorer histologic differentiation
had a lower level of c-myc expression. There were inverse associations bet
ween the expression of c-myc and the expression of mutated p53 (P = 0.0017;
r = -0.285) as well as the expression of I;L167 (P = 0.057; r = -0.147). T
here was significantly high expression of c-fos ill tumor tissue compared w
ith the expression in nontumor tissue (91% vs. 0%; P < 0.0001). Both the tu
mor tissue and the nontumor tissue had high levels of expression of c-jun (
96.53% and 100%, respectively). There was a trend toward a positive associa
tion between the expression of c-fos and the expression of c-jun in tumor t
issue (P = 0.07: r = 0.162),
CONCLUSIONS. Because c-myc is a. known inducer of wild type p53, decreased
c-myc expression may lead to uncontrolled cell growth. because of the lack
of p53 expression that normally induces apoptosis, The coordinated expressi
on of c-fos and c-jun in HCC may reflect the coordinated tumor cell cycle o
f progression and proliferation; however, future studies are required to el
ucidate this possibility. <(c)> 2001 American Cancer Society.