Radiofrequency ablation (RFA) is a minimally invasive technique used to treat liver tumors. The current study presents the case of a patient with hepatocellular carcinoma who suffered from post-operative pericardial effusion following RFA treatment. We hypothesize that RFA thermal conduction may damage the diaphragm and pericardium, leading to local edema in the pericardium. RFA is a minimally invasive technique, however, adequate preparatory work must be performed prior to surgery, including a comprehensive assessment of the patient. During surgery, the location and extent of the region to receive RFA must be determined precisely in order to reduce the range of damage and to avoid post-operative complications. This study describes a case of pericardial effusion caused by RFA of liver cancer. We analyzed the causes and preventive measures for pericardial effusion in order to contribute to the prevention pericardial effusion that is complicated by RFA of liver cancer.
Activation of K-ras and inactivation of p16 are the most frequently identified genetic alterations in human pancreatic epithelial adenocarcinoma (PDAC). Mouse models engineered with mutant K-ras and deleted p16 recapitulate key pathological features of PDAC. However, a human cell culture transformation model that recapitulates the human pancreatic molecular carcinogenesis is lacking. In this study, we investigated the role of p16 in hTERT-immortalized human pancreatic epithelial nestin-expressing (HPNE) cells expressing mutant K-ras (K-rasG12V). We found that expression of p16 was induced by oncogenic K-ras in these HPNE cells and that silencing of this induced p16 expression resulted in tumorigenic transformation and development of metastatic PDAC in an orthotopic xenograft mouse model. Our results revealed that PI3K/Akt, ERK1/2 pathways and TGF? signaling were activated by K-ras and involved in the malignant transformation of human pancreatic cells. Also, p38/MAPK pathway was involved in p16 up-regulation. Thus, our findings establish an experimental cell-based model for dissecting signaling pathways in the development of human PDAC. This model provides an important tool for studying the molecular basis of PDAC development and gaining insight into signaling mechanisms and potential new therapeutic targets for altered oncogenic signaling pathways in PDAC.
Over-expression of integrin ?v?6 and increased numbers of cancer-associated fibroblasts (CAFs) play an important role in the development and progression of cancers. The aim of this study is to investigate the expression level of integrin ?v?6 and CAF numbers, their correlation with clinicopathologic features and their role in the prognosis of human gastric cancers. The expression levels of integrin ?v?6 and ?-SMA in CAFs were analyzed by immunohistochemistry. Their correlation with clinicopathologic features, the relationships and the survival time of patients were also analyzed. The integrin ?v?6 expression levels were analyzed mainly in gastric cancers. The ?-SMA expression levels were analyzed mainly in gastric cancers and paraneoplastic tissues. Patients with positive integrin ?6 and ?-SMA expression have a significantly lower overall survival rate than those with negative integrin ?6 and ?-SMA expression (P < 0.05). A multivariate analysis using a log-rank test indicated that patients with positive integrin ?6 and ?-SMA expression and/or a diffuse type of gastric cancer had a significantly poorer overall survival rate than did those with negative integrin ?6 expression (P < 0.05). Integrin ?6 expression correlated significantly with CAF numbers and served as a valuable prognostic indicator for human gastric cancers.
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