Surgical timing for primary encapsulating peritoneal sclerosis: A case report and review of literature.

BACKGROUND: Primary encapsulating peritoneal sclerosis (EPS) is a rare but devastating disease that causes fibrocollagenous cocoon-like encapsulation of the bowel, resulting in bowel obstruction. The pathogenesis, prevention, and treatment strategies of EPS remain unclear so far. Since most patients are diagnosed during exploratory laparotomy, for the non-surgically diagnosed patients with primary EPS, the surgical timing is also uncertain. CASE SUMMARY: A 44-year-old female patient was referred to our center on September 6, 2021, with complaints of abdominal distention and bilious vomiting for 2 d. Physical examination revealed that the vital signs were stable, and the abdomen was slightly distended. Computerized tomography scan showed a conglomerate of multiple intestinal loops encapsulated in a thick sac-like membrane, which was surrounded by abdominal ascites. The patient was diagnosed with idiopathic EPS. Recovery was observed after abdominal paracentesis, and the patient was discharged on September 13 after the resumption of a normal diet. This case raised a question: When should an exploratory laparotomy be performed on patients who are non-surgically diagnosed with EPS. As a result, we conducted a review of the literature on the clinical manifestations, intraoperative findings, surgical methods, and therapeutic effects of EPS. CONCLUSION: Recurrent intestinal obstructions and abdominal mass combined with the imaging of encapsulated bowel are helpful in diagnosing idiopathic EPS. Small intestinal resection should be avoided.

CSN5 promotes the invasion and metastasis of pancreatic cancer by stabilization of FOXM1.

COP9 signalosome subunit 5 (CSN5) has been involved in the progression of diverse human cancers. MMP2 plays an important role in the metastasis of cancer cells. However, the roles and relationship of in pancreatic cancer (PC) is still unknown. Here, our data shown that both CSN5 and MMP2 were significantly upregulated in PC compared with the corresponding adjacent tissues, where a positive correlation in their expression and associated malignant characteristics were found. Further, silencing of CSN5 expression markedly inhibited PC invasion and metastasis in vitro and in vivo, accompanied by decreased MMP2 expression. Moreover, the anti-metastasis role of CSN5 silence was reversed by MMP2 overexpression, whereas knockdown of MMP2 decreased PC metastasis driven by upregulation of CSN5. Further investigation revealed that CSN5 regulated MMP2 expression via activation of FOXM1 in PC cells. Mechanistically, CSN5 directly bound FOXM1 and decreased its ubiquitination to enhance the protein stability of FOXM1. Taken together, the results indicate that CSN5 can contribute to PC invasion and metastasis through activation of FOXM1/MMP2 axis.

A recombinant adenovirus vector encoding the light chain of human coagulation factor VII and IgG1 Fc fragment to targeting tissue factor for colorectal cancer immunotherapy in the mouse model.

PURPOSE: Over expression of tissue factor (TF) occurs in more than 50 % of colorectal cancer (CRC). Therefore, TF represents an attractive target antigen for immunotherapy in CRC. METHODS: Here, we assessed the safety and efficacy of a recombinant adenovirus vector encoding the light chain of human coagulation factor VII (hfVII-LC) and human IgG1 Fc fragment (hIgG1-Fc), termed "benc vector," by targeting TF in the mouse model with colon cancer. Benc vector was administered intravenously or intratumorally in SCID mice with TF over-expressing HT-29 colon cancer. The safety and efficacy of benc vector were observed during animal experiments. RESULTS: Complete inhibition of tumor growth (5/5) was observed not only in the intravenously injection of benc vector group but also in the intratumorally of benc vector group. We also observed a precautionary effect on lung metastases of HT-29 cells by intratumoral injection of benc vector. In the control group of animals given empty control vector, all animals (5/5) developed lung tumors and exhibited a higher number of nodules after injection with HT-29 cells via the tail vein. In contrast, only three animals (3/5) in the treatment group receiving benc vector had any observable lung metastases and a lower number of nodules. No animals died and no bleeding was observed both in treatment groups and control groups. Moreover, only moderate liver damage was detected in mice receiving benc vector by intravenous injections. CONCLUSIONS: Benc vector encoding hfVII-LC and hIgG1-Fc can effectively inhibit tumor growth and metastases in SCID mice with TF over-expressing colon cancer and shows promise as an agent for CRC immunotherapy.