Intraabdominal sporadic desmoid tumors and inflammation: an updated literature review and presentation and insights on pathogenesis of synchronous sporadic mesenteric desmoid tumors occurring after surgery for necrotizing pancreatitis.

Sporadic intra-abdominal desmoid tumors are rare and known to potentially occur after trauma including previous surgery, although knowledge of the underlying pathogenetic mechanism is still limited. We reviewed the recent literature on sporadic intraabdominal desmoids and inflammation as we investigated the mutational and epigenetic makeup of a case of multiple synchronous mesenterial desmoids occurring after necrotizing pancreatitis. A 62-year-old man had four mesenteric masses up to 4.8 cm diameter detected on CT eighteen months after laparotomy for peripancreatic collections from necrotizing pancreatitis. All tumors were excised and diagnosed as mesenteric desmoids. DNA from peripheral blood was tested for a multigene panel. The tumour DNA was screened for three most frequent ß-catenin gene mutations T41A, S45F and S45P. Expression levels of miR-21-3p and miR-197-3-p were compared between the desmoid tumors and other wild-type sporadic desmoids. The T41A CTNNB1 mutation was present in all four desmoid tumors. miR-21-3p and miR-197-3p were respectively upregulated and down-regulated in the mutated sporadic mesenteric desmoids, with respect to wild-type lesions. The patient is free from recurrence 34 months post-surgery. The literature review did not show similar studies. To our knowledge, this is the first study to interrogate genetic and epigenetic signature of multiple intraabdominal desmoids to investigate potential association with abdominal inflammation following surgery for necrotizing pancreatitis. We found mutational and epigenetic features that hint at potential activation of inflammation pathways within the desmoid tumor.

Lack of prognostic role of pre- and postoperative peritoneal cytology and cytokeratin PCR-expression on local recurrence after curative anterior resection for mid-low rectal cancer.

Local recurrence continues to be a major problem in rectal cancer. After cancer removal, detection of viable cancer cells could be useful to identify patients at risk for local recurrence. Thus, aim of the study was the detection of residual peritoneal cancer cells with a possible prognostic role for local recurrence. Twenty-nine patients were operated (R0) for low (extraperitoneal) rectal cancer, without neoadjuvant radiochemotherapy. Before and immediately after cancer removal, a peritoneal lavage was done to evaluate by RT-PCR the cytokeratin 20 mRNA on isolated cells and in order to detect cancer cells by the Thin-prep test. After a median follow-up of 39 months, 5 patients died (17%), one for non-cancer-related disease, two (7%) for local recurrence and peritoneal carcinosis, and two for distant metastases. Preoperative cytology with Thin-prep test was positive in 4 patients (14%), while postoperative peritoneal cytology was positive only in 1 patient, different from the previous. No patient developed local or distal recurrence and all were disease-free at the end of the follow-up. RT-PCR analysis was positive on the peritoneal lavage after cancer removal in 11 patients. One died for unrelated cause and no one developed local recurrences. Local recurrence occurred in only 1 of the 2 patients with positive RT-PCR analysis on the first lavage and negative on the second lavage. Our study demonstrates a not important prognostic role of Thin-prep test and RT-PCR of cytokeratin 20 mRNA on the detection of patients at risk for local recurrence after curative resection of rectal cancer.