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Preoperative portal vein embolization (PVE) induces compensatory hyperplasia of the future liver remnants (FLR), thus increasing resectability in the non-cirrhotic patients with primary liver cancer (PLC). However, it is unclear if it is similar in patients with liver cirrhosis. Therefore, the present study investigated the PVE value prior to liver resection in patients with PLC, and the liver cirrhotic effects on the compensatory hypertrophy of FLRs following PVE. In the present study, 21 patients with PLC who successfully underwent hepatic resection subsequent to PVE, were retrospectively examined. The patients were divided into a non-cirrhosis group and a cirrhosis group according to the absence or presence of cirrhosis, respectively. The FLR volume between the two groups of patients was compared. There was a significant difference in the FLR volume for all patients prior to, and 4-6 weeks following, PVE (P<0.001). PVE induced significant compensatory hypertrophy in the FLRs whether in the non-cirrhosis group (P=0.002) or cirrhosis group (P<0.001). However, no significant difference was identified between the two groups with respect to FLR volume enlargement 4-6 weeks following PVE (P=0.373). In conclusion, PVE prior to hepatectomy may promote FLR compensatory hypertrophy and an increase in the resectability of PLC tumors. No significant effects of liver cirrhosis were identified on liver lobe hyperplasia following PVE. [ABSTRACT FROM AUTHOR]

Radiofrequency ablation (RFA) has been widely accepted as an alternative treatment for unresectable primary and metastatic hepatic tumors, with satisfactory rates of local response and significant improvements in rates of overall survival. Numerous large series studies have shown that RFA is safe and effective, with a low mortality rate and a low major complication rate. Major complications, including diaphragmatic perforation and hernia, have rarely been previously reported. The current case report presents a case of diaphragmatic hernia with perforation of the incarcerated colon in the thoracic cavity 12 months following hepatic RFA, and reviews nine previously reported cases of diaphragmatic hernia. Comprehensive analysis of the nine cases demonstrated possibilities leading to diaphragmatic hernia following diaphragmatic thermal injury as a consequence of hepatic RFA. Clinicians and radiologists must consider diaphragmatic thermal damage following hepatic RFA for liver tumors adjacent to the diaphragm, particularly for patients with symptoms of ileus, dyspnea, chest pain, pleural effusion and right shoulder pain. [ABSTRACT FROM AUTHOR]

α-fetoprotein (AFP)-producing colorectal adenocarcinoma is rare and typically not well recognized. In the present study, 3 cases of AFP-producing colorectal cancer are described. All 3 of these cases demonstrated increased levels of blood AFP associated with disease progression. Only case 2 exhibited classical histological hepatoid features. Following immunohistochemical tissue staining, all 3 cases were observed to be positive for AFP expression. In addition, the expression of hepatocyte growth factor (HGF), c-Met receptor and the transcription factor c-Myc were identified to be associated with the expression of AFP. The 3 cases demonstrated resistance to multiple drugs, including epidermal growth factor receptor inhibitors, despite the presence of wild-type Kirsten rat sarcoma viral oncogene homolog (K-RAS; codons 12 and 13), neuroblastoma-RAS (codons 12 and 13) and B-Raf proto-oncogene, serine/threonine kinase (V600E). We propose that hepatoid histological features or a positive AFP finding by immunohistochemistry are sufficient for a diagnosis of AFP-producing colorectal adenocarcinoma. Furthermore, we speculates that autocrine HGF/c-Met activation may be capable of inducing the dedifferentiation of common adenocarcinoma cells, reverting them to a cancer stem cell state and producing AFP or hepatoid differentiation. Consequently, therapy targeted to the HGF/c-Met signaling pathway may potentially be effective for the treatment of AFP-producing colorectal adenocarcinoma.

Peptic ulcers are an extremely common condition, usually occurring in the stomach and proximal duodenum. However, cases of peptic ulcers accompanied with multiple complications are extremely rare and hard to treat. The present case reinforces the requirement for the early recognition and correct treatment of peptic ulcers accompanied with multiple complications. A 67-year-old man presented with recurrent abdominal pain, fever and melena. The laboratory results showed anemia (hemoglobin 62 g/l) and hypoproteinemia (23 g/l). Abdominal imaging examinations revealed stones in the gallbladder and right liver, with air in the dilated intrahepatic and extrahepatic bile ducts. Endoscopic retrograde cholangiopancreatography failed due to a deformed pylorus. The patient was finally diagnosed with peptic ulcers accompanied with gastrointestinal (GI) bleeding, pylorus obstruction and cholangitis secondary to a choledochoduodenal fistula during an emergency pancreatoduodenectomy, which was performed due to a massive hemorrhage of the GI tract. The patient recovered well after the surgery.

Cytohesins have been identified as cytoplasmic ErbB receptor activators in certain cancers, exhibiting an important role in ErbB signaling. However, whether cytohesins are essential in colorectal cancer is unknown. The aim of the present study was to investigate whether cytohesins contribute to the epidermal growth factor (EGF) pathway in colorectal cancer cells. RT-PCR and immunofluorescence experiments were employed to detect the expression of cytohesins in colorectal cancer cell lines. The EGF pathway activation conditions were investigated by examining the phosphorylation of the epidermal growth factor receptor (EGFR) and intracellular signal-related kinases, with or without chemical inhibition (SecinH3) and knockdown of cytohesins. An MTT assay was conducted to examine the inhibitory effect of SecinH3 and cytohesin-specific siRNA in HT-29 cells. Results demonstrated that the four homologous members of the cytohesin family were expressed in the four colorectal cancer cell lines. Notably, a significantly higher expression level of cytohesin-2 (ARNO) compared with the other three homologous family members was observed. Stimulation with EGF and SecinH3, as well as knockdown of ARNO, are capable of reducing EGF pathway activation and proliferation of HT-29 cells. In conclusion, cytohesins play an essential role in the activation of the EGF pathway and may be a potential target in colorectal cancer therapy.