43 research outputs found
Adjuvant oxaliplatin- or irinotecan-containing chemotherapy improves overall survival following resection of metachronous colorectal liver metastases
Resection of hepatitis B virus-related hepatocellular carcinoma: Evolving strategies and emerging therapies to improve outcome
Can delayed primary wound closure decrease incidence of wound infection after appendectomy in patients with perforated appendicitis?
Analysis of NQO1 polymorphisms and p53 protein expression in patients with hepatocellular carcinoma
NAD(P)H: quinone oxidoreductase 1
(NQO1), a cytosolic enzyme which catalyzes the twoelectron
reduction of quinone compounds, has been
suggested to prevent the generation of semiquinone free
radicals and reactive oxygen species, thus protecting
cells from oxidative damage. However, the enzymatic
activity of NQO1 strongly depends on the individual
genetic polymorphism of the NQO1 gene. A common
NQO1 polymorphism is a C to T transition at position
609, which results in an inactive enzyme. Recent studies
showed that NQO1 is an important enzyme for
stabilizing p53 protein, which is involved in antitumorigenesis.
Thus, the lack of enzymatic activity in
the homozygous C609T NQO1 polymorphism may play
a pivotal role in tumor development.
This study aimed to investigate the relationship
between C609T NQO1 polymorphism and p53
expression in human hepatocellular carcinoma (HCC).
Genotyping of NQO1 was performed on 100 HCC
specimens by PCR-RFLP analysis. In addition, NQO1
and p53 protein expression in HCC samples at different
TNM stages was determined by immunohistochemistry.
Our data showed that (1) the frequency of C609T NQO1
was significantly increased in TNM stage III HCC
patients; (2) no significant association was found
between p53 expression and C609T polymorphism of
NQO1 gene; and (3) a tumor/non-tumor (T/N) ratio >
1.27 of NQO1 expression revealed by real-time qPCR
analyses was positively correlated with poorer survival
in patients with tumors >5 cm, suggesting that an increase of NQO1 expression may be an indicator of
advanced tumor progression. This study provides
important information about NQO1 genotypes and its
expression to HCC tumor development and progression
Risk of recurrence in chronic hepatitis B patients developing hepatocellular carcinoma with antiviral secondary prevention failure
<div><p>Background</p><p>Nucleos(t)ide analogues (NUCs) treatment can reduce the risk of hepatocellular carcinoma (HCC) development and recurrence in chronic hepatitis B (CHB) patients. However, the risk of recurrence in CHB patients who develop HCC despite NUC treatment remains unclear.</p><p>Methods</p><p>167 consecutive CHB patients receiving curative resection for HCC with NUC therapy after surgery were retrospectively enrolled. Thirty-eight patients who developed HCC despite NUC therapy for more than 1 year were defined as secondary prevention failure. The other 129 patients started NUC therapy after surgery. Factors associated with recurrence-free survival (RFS) and overall survival (OS) were evaluated.</p><p>Results</p><p>The 5-year RFS and OS rates were 44.7% and 77.3%, respectively. Sex, BMI, BCLC stage, AFP levels and cirrhosis status were the independent predictors of RFS, while microvascular invasion was the independent predictor of OS. The RFS was comparable between patients with and without NUC secondary prevention. In the subgroup analysis, the RFS was significantly worse in cirrhotic patients with secondary prevention failure (hazard ratio = 2.373, p = 0.009). Secondary prevention failure did not have adverse impact on OS. Among 84 patients with recurrence, 58.3% of the cases remained in BCLC stage A, and 53.6% received a second curative treatment. Long-term NUC therapy may lead to a decline of non-invasive indices of hepatic fibrosis in HCC patients.</p><p>Conclusions</p><p>In general, the risk of recurrence and survival are comparable between patients with and without secondary prevention failure. However, a higher risk of recurrence was observed in cirrhotic patients with secondary prevention failure.</p></div