Primary intra­abdominal desmoid fibromatosis associated with familial adenomatous polyposis: A case report.

Desmoid fibromatosis (DF) is a clonal proliferative disorder of myofibroblasts, which arises, with a low incidence, in soft tissue, including within the abdomen. The incidence of DF is associated with familial adenomatous polyposis (FAP), and is more common following FAP surgery. It is rare for a patient to make his/her first visit to hospital due to DF symptoms associated with FAP. In the present report, a case of mesenteric DF associated with FAP is described. This case also had incomplete intestinal obstruction due to DF. By summarizing previous studies examining DF and FAP treatment, combined with the disease characteristics of this patient, the clinical treatment strategy for DF associated with FAP was explored.

Sevoflurane induces apoptosis and inhibits the growth and motility of colon cancer in vitro and in vivo via inactivating Ras/Raf/MEK/ERK signaling.

AIMS: To investigate the effects of sevoflurane on proliferation, cell cycle, apoptosis, autophagy, invasion and epithelial-mesenchymal transition of colon cancer cell line SW480, and to explore its possible mechanism. MATERIALS AND METHODS: SW480 and SW620 cells were treated with a mixture of 95% O2+5% CO2 containing different concentrations of sevoflurane (1.7% SAV, 3.4% SAV and 5.1% SAV) for 6 h. Meanwhile, we performed a rescue experiment by treating cells with the ERK pathway activator LM22B-10 prior to treatment of cells with 5.1% sevoflurane。 KEY FINDINGS: High concentration (5.1%) of sevoflurane significantly inhibited the proliferation and invasion of cells, causing G0/G1 phase arrest and promoted apoptosis and autophagy. 5.1% sevoflurane can participate in the regulation of EMT by regulating the expression of E-cadherin, Vimentin and N-cadherin proteins. LM22B-10 promoted proliferation and invasion of cancer cells and inhibited apoptosis and autophagy, while 5.1% sevoflurane could reverse the effect of LM22B-10 on the biological characteristics of cells. Sevoflurane can significantly inhibit tumor growth in SW480 cells transplanted nude mice. Moreover, 5.1% sevoflurane significantly increased the expression of p-Raf, p-MEK1/2, and p-ERK1/2 in SW480 cells and tumor tissues without affecting p-JNK and p-p38 proteins, meanwhile, 5.1% sevoflurane can inhibit the activation of ERK signaling pathway by LM22B-10 in vitro and in vivo. SIGNIFICANCE: Sevoflurane can inhibit the proliferation and invasion of colon cancer cells, induce apoptosis and autophagy, and participate in the regulation of epithelial-mesenchymal transition, which may be related to its inhibition of the ERK signaling pathway.