Diagnostic value of endoscopic ultrasonography in periampullary duodenal tumours.

Introduction: The objective of this study was to investigate the diagnostic value of endoscopic ultrasonography (EUS) for tumours around the duodenal ampullary. Patients and Methods: A retrospective analysis was performed on cases diagnosed and treated in our hospital from October 2016 to August 2021 due to the lesions around the duodenal ampulla. All patients received EUS, abdominal enhanced computed tomography (CT) and magnetic resonance imaging combined with magnetic resonance cholangiopancreatography (MRI-MRCP). Pathological diagnosis was used to verify the accuracy of the imaging findings. The detection rates of periampullary tumours by EUS, abdominal enhanced CT and MRI-MRCP were determined and compared. Results: A total of 86 patients were included in this study. According to the pathological diagnosis, the detection rate of EUS was 87% (36/41) for periampullary tumour lesions with a tumour diameter <1 cm, which was significantly higher than that of MRI-MRCP (59%, 24/41) (P = 0.003) and CT (44%, 18/41) (P < 0.001). For periampullary tumour lesions with a tumour diameter ≥1 cm, the detection rate of MRI-MRCP was 93% (42/45), which was significantly higher than that of EUS (78%, 35/45) (P = 0.036) and CT (76%, 34/45) (P = 0.02). Conclusions: EUS can accurately detect tumour lesions around the ampullary part of the duodenum with minimal gas interference. For periampullary tumour lesions <1 cm, EUS has better diagnostic accuracy than abdominal-enhanced CT and MRI-MRCP. In addition, a biopsy of the lesion can be performed at the same time during the EUS examination. Therefore, EUS has an important clinical significance and value in the diagnosis of duodenal periampullary tumours.

Reduced N-cadherin expression is associated with metastatic potential and poor surgical outcomes of hepatocellular carcinoma.

BACKGROUND AND AIM: N-cadherin (N-cad), one of the classic cadherins, has been reported to be involved in tumor metastasis in some types of tumors. This study aims to investigate the expression status of N-cad in hepatocellular carcinoma (HCC) and the correlation between N-cad expression and metastatic potential, as well as the surgical outcomes of HCC. METHODS: N-cad expression in HCC and adjacent liver tissues, as well as normal liver tissues, was studied by immunohistochemistry and Western blot, and the relationship between N-cad expression and the clinicopathological features of HCC was evaluated. By using RNA interference technique, the correlation of N-cad expression and metastatic potential was investigated by downregulating N-cad expression in HCCLM3 cells, and the effects of N-cad downregulation on cell aggregation, migration, and invasion were then analyzed. Furthermore, the correlation between N-cad expression and the surgical outcomes of a cohort of HCC patients was analyzed. RESULTS: In liver tissues, N-cad was strongly expressed on cell-cell boundaries, whereas various reduced-expression patterns were observed in tumors. Of 64 HCC, 34 (53%) tumors showed reduced N-cad expression, compared with their adjacent liver tissues. The decreased expression of N-cad was significantly correlated with poorer tumor differentiation (P = 0.001) and vascular invasion (P = 0.003). N-cad knockdown in HCCLM3 cells resulted in decreased cell aggregation and increased cell migration and invasion. The decreased expression of N-cad in HCC was significantly associated with shorter postoperative disease-free survival (P = 0.039). CONCLUSIONS: N-cad expression is decreased in HCC, and the downregulation of N-cad is associated with the metastatic potential of HCC and poorer surgical prognosis.

[Influence of cirrhosis on long-term outcomes after liver resection in patients with a single small hepatocellular carcinoma].

OBJECTIVES: To compare the outcomes after liver resection for a single small hepatocellular carcinoma (HCC) (≤ 5 cm) between non-cirrhotic patients and cirrhotic patients, and to explore the influence of liver cirrhosis on recurrence and overall survival after liver resection in patients with a single small HCC. METHODS: A consecutive series of 256 patients with a single small HCC undergoing liver resection from April 2001 to October 2009 was retrospectively reviewed. Among the 256 patients, 227 patients were male, and 29 were female. The medium age was 49 years (ranged, 14 - 79 years); 224 (87.5%) patients were positive for hepatitis B surface antigen, 241 (94.1%) patients were with preoperative liver function of Child-Pugh grade A. The entire cohort were divided into non-cirrhosis group (n = 44) and cirrhosis group (n = 212). Univariate analysis and then multivariate analysis were performed to determine the prognostic factors of recurrence and overall survival after liver resection for all patients. RESULTS: The 1-, 3-, 5-year recurrence-free survival rates after liver resection were 93.0%, 85.3%, and 68.5%, respectively, in non-cirrhosis group, while 81.1%, 58.6%, and 45.0%, respectively, in cirrhosis group. The 1-, 3-, 5-year overall survival rates after liver resection were 100%, 92.5%, and 92.5%, respectively, in non-cirrhosis group, while 93.8%, 78.7%, and 67.8%, respectively, in cirrhosis group. Both the recurrence-free survival and overall survival of non-cirrhosis group were significantly better than those of cirrhosis group (χ(2) = 8.756, P = 0.003; χ(2) = 8.603, P = 0.003). Cirrhosis, absence of tumor capsule, presence of microvascular invasion and moderate/poor tumor differentiation were the independent adverse prognostic factors for recurrence-free survival and overall survival in patients with a single small HCC after liver resection. CONCLUSIONS: Cirrhosis is an important adverse prognostic factor for long-term survival in patients with a single small HCC after liver resection. Liver resection resulted in much worse survival for cirrhotic patients compared to non-cirrhotic patients.

Synergistic suppressive effect of PARP-1 inhibitor PJ34 and HDAC inhibitor SAHA on proliferation of liver cancer cells.

Poly (ADP-ribose) polymerase-1 (PARP-1) inhibitors and histone deacetylase (HDAC) inhibitors have recently emerged as promising anticancer drugs. The aim of this study was to investigate the effect of combination treatment with the PARP inhibitor PJ34 and HDAC inhibitor SAHA on the proliferation of liver cancer cells. Cell proliferation and apoptosis were assessed in three human liver cancer cell lines (HepG2, Hep3B and HCC-LM3) treated with PJ34 (8 µmol/L) and SAHA (1 µmol/L), alone or combined, by Cell Counting Kit-8 assay and flow cytometry, respectively. The nude mice bearing subcutaneous HepG2 tumors were administered different groups of drugs (10 mg/kg PJ34, 25 mg/kg SAHA, 10 mg/kg PJ34+25 mg/kg SAHA), and the inhibition rates of tumor growth were compared between groups. The results showed that combined use of PJ34 and SAHA could synergistically inhibit the proliferation of liver cancer cell lines HepG2, Hep3B and HCC-LM3. The apoptosis rate of HepG2 cells treated with PJ34+SAHA was significantly higher than that of HepG2 cells treated with PJ34 or SAHA alone (P<0.05). In vivo, the tumor inhibition rates were 53.5%, 61.4% and 82.6% in PJ34, SAHA and PJ34+SAHA groups, respectively. The combined use of PJ34 and SAHA could significantly inhibit the xenograft tumor growth when compared with use of PJ34 or SAHA alone (P<0.05). It was led to conclude that PJ34 and SAHA can synergistically suppress the proliferation of liver cancer cells.