Methods: Tumor tissue samples obtained during curative surgery (n = 2028) were analyzed using both MLH1/MSH2 IHC and MSI assays. Clinicopathological parameters and survival outcomes were compared according to IHC and MSI results. The median follow-up period was 43 months (range: 1–85 months). Results: IHC identified 207 tumor samples (10.2%) with a loss of either MLH1 or MSH2 expression. The MSI analysis identified 203 tumor samples (10%) with high-frequency MSI (MSI-H). Patients with MMR defects were
younger, and had tumors characterized by right-colon predilection; large-size, infrequent lymph node metastasis; poorly-differentiated or mucinous histology, find more and synchronous adenomas (P < 0.001–0.008). Patients with MSI-H status had higher 4-year disease-free survival rates than patients with microsatellite stable status (90.8% vs 80.6%, Dabrafenib order P = 0.001). A multivariate analysis showed that MSI-H status was a good prognostic factor for recurrence (hazard ratio: 0.48, 95% confidence interval: 0.30–0.83, P = 0.007). Conclusions: Patients with MMR defects had distinct clinicopathological characteristics, including a lower risk of recurrence. IHC and MSI analyses provided complementary information regarding specific clinicopathological parameters and prognosis. “
“It has been reported that branched-chain amino acids (BCAA) supplementation can
improve nutritional status and reduce liver-related complications in patients with decompensated cirrhosis. BCAA supplementation reportedly reduces the incidence of hepatocellular carcinoma (HCC) in obese cirrhotic patients infected with hepatitis C virus (HCV). We investigated the effects of oral supplementation
with BCAA granules on hepatocarcinogenesis in patients with HCV-related cirrhosis using propensity score matching. A total of 60 patients with HCV-related cirrhosis and without history of HCC who were selected by one-to-one matching of propensity scores: MCE公司 30 patients receiving 12 g/day of BCAA granules for 3 months or more (BCAA group) and 30 being observed without BCAA supplementation (control group). The impact of BCAA supplementation was analyzed on the incidence of HCC. The 3- and 5-year rates of HCC development were 13.7% and 13.7% in the BCAA group and 35.1% and 44.5% in the control group, respectively. The BCAA group had a significantly lower rate of HCC than the control group (P = 0.032). Multivariate analysis for factors that were associated with hepatocarcinogenesis indicated that BCAA supplementation was independently associated with a reduced incidence of HCC (hazard ratio 0.131; 95% confidence interval, 0.032–0.530; P = 0.004) along with sex and serum α-fetoprotein. Obesity (body mass index, ≥25 kg/m2) was not significantly associated with an increased incidence of HCC.