Received: September 23, 2011; Accepted: October 20, 2011.
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ABSTRACT
Purpose : Hepatocellular carcinoma (HCC) shows various molecular and genetic alterations in its development and
progression. The major tumor suppressor genes (TSGs) such as p16, PTEN, E-cadherin and p53 on chromosomes
9p21, 10q23, 16q22, 17p13 may play important roles in various regulation pathways as well as tumor suppression.
Microsatellite alteration such as loss of heterozygosity (LOH) has been reported is a predominant mechanism of
inactivation of TSGs. Also, LOH is known to be related with allelic loss of various TSGs. This study evaluated LOH
of 4 TSGs in HCCs and correlated these results with the clinicopathological factors.
Methods : LOH analysis was carried out using a polymerase chain reaction with 16 polymorphic microsatellite
markers of 4 chromosomes having TSGs in 50 surgically resected tumors and their non-tumorous counterparts.
Results : There was no detectable LOH in normal tissue. LOH was detected in 82% of 50 cases of HCCs. LOH of
9p21, 10q23, 16q22, 17p13 was detected in 36%, 54%, 38% and 66%, respectively. Advanced HCCs showed
significant LOH results of 9p21, 10q23 & 17p13. According to tumor grade, those of 10q23, 16q22, 17p13 correlated
with higher grade III. Vascular invasion & lymphatic emboli showed correlation with those of 9p21, 10q23, 17p13.
Cancer recurrence & metastasis significantly correlated with 9p21 LOH.
Conclusion : These results suggest that LOH of various chromosomes may be predominantly involved in
hepatocarcinogenesis and tumor invasion. Also, those LOH may be useful clinical indicator in determining the
poorer prognosis among patients with HCC.
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