Hypoalbuminemia is a predictor of poor surgical outcomes of colon cancer and is a poor prognosis factor for long-term survival of colon cancer after curative operation.

Although patients afflicted with IMA node metastasis revealed a rather high incidence of tumor recurrence/metastasis, 25.6% of these patients remained disease free following IMA node dissection after a minimum 5-year follow-up. We consider that IMA node dissection is more beneficial in patients with non-disseminated sigmoid pT4 tumor.

To our knowledge, stercoral perforation of the colon is rarely seen with fewer than 90 cases reported in the literature till date. We explored the principles of management to prevent impending mortality in five patients with this condition. Five patients, two males and three females, whose median age was 64 years, had sustained stercoral perforation of the sigmoid colon. Chronic constipation was the common symptom among these patients. Three patients underwent a Hartmannos procedure and another two were treated with segmental colectomy with anastomosis and diverting colostomy. There was one surgical mortality and the other patients had an uneventful hospital stay. Timely intervention to prevent and/or treat any associated sepsis along with extensive peritoneal lavage and surgical intervention to remove diseased colonic tissue at the primary stercoral ulceration site coupled with aggressive therapy for peritonitis are key treatment modalities in salvaging patients presenting with stercoral perforation of the colon.

BackgroundStromal cell-derived factor-1 (SDF-1) (CXC chemokine ligand-12)/CXC chemokine receptor 4 (CXCR4) is involved in the carcinogenesis of human gastric cancer, where it stimulates angiogenesis and favors metastasis of tumor cells to distant organs. In addition, resistin is suggested to be an important link between obesity and the development of gastric cancer. Resistin has identified as an important player in inflammatory responses, and emerged as a mediator in inflammation-associated cancer. A limited number of studies have investigated the association of resistin and SDF-1 with gastric cancer. Herein, we investigated the molecular mechanisms by which resistin influences the expression of SDF-1 in gastric carcinoma cells.ResultsHuman gastric cancer cell lines were exposed to doses of resistin; SDF-1 expression and secretion levels were then determined. Real-time polymerase chain reaction and western blotting analyses were performed to clarify molecular changes. Inhibition of Toll-like receptor 4 (TLR4) by a competitive antagonist inhibited resistin-induced SDF-1 expression. Pharmacological inhibitors and small interfering RNA (siRNA) demonstrated that activation of the p38 mitogen-activated protein kinase (MAPK) pathway is critical for resistin-induced SDF-1 expression mediated by TLR4. The promoter activity and transcription factor enzyme-linked immunosorbent assay revealed that resistin induced expression of SDF-1 mediated by NF-κB in gastric cancer cells. Inhibition of p38 MARK activation blocked the SDF-1-induced expression and the SDF-1 promoter activity in the cancer gastric cells. Chromatin immunoprecipitation assay revealed that inhibition of p38 MARK activation also blocked the resistin-increased NF-κB-DNA-binding activity.ConclusionsResistin-induced SDF-1 upregulation by activation of TLR4, p38 MARK and NF-κB may explain a new role of resistin in the link of obesity and gastric cancer.