To evaluate the prevalence of sarcopenia in patients undergoing pancreatic surgery and to examine its impact on the surgical outcomes and survival of patients.Skeletal muscle index (SMI) was measured on preoperative CT. A patient was considered sarcopenic if SMI was <38.5 cm2/m2 for a female or <52.4 cm2/m2 for a male. Postoperative pancreatic fistula (POPF) and severe morbidity (Clavien≥3) were analyzed. Survival of patients with cancer was calculated using the Kaplan–Meier method.In total, 107 consecutive patients were included. Among them, 50 (47%) patients were sarcopenic and 65 (60%) were undernourished. The rates of severe morbidity and mortality were comparable between sarcopenic and nonsarcopenic groups. However, all POPF grade B or C and deaths occurred in the sarcopenic or nonsarcopenic overweight group (BMI > 25) with significantly lengthened hospital stays (P = .003). After pancreatectomy for cancer, 31 (40.2%) patients showed postoperative recurrence and 23 (29.9%) died after a median follow-up of 15 ± 13.5 months. Despite comparable histological types and stages, the median overall and disease-free survivals were lower in sarcopenic patients (16 months vs not reached, P = .02 and 11.1 months vs 22.5 months; P = .04, respectively). The multivariate analysis revealed that, sarcopenia trended to increase the risk of death (HR = 2.04, P = .07).Sarcopenia negatively impacted short- and long-term outcomes in patients undergoing pancreatectomy.

Growing body of evidence suggests that epithelial‐mesenchymal transition (EMT) is a critical process in tumor progression and chemoresistance in pancreatic cancer (PC). The aim of this study was to analyze the role of EMT‐like changes in acquisition of resistance to gemcitabine in pancreatic cells of the mesenchymal or epithelial phenotype. Therefore, chemoresistant BxPC‐3, Capan‐2, Panc‐1, and MiaPaca‐2 cells were selected by chronic exposure to increasing concentrations of gemcitabine. We show that gemcitabine‐resistant Panc‐1 and MiaPaca‐2 cells of mesenchymal‐like phenotype undergo further EMT‐like molecular changes mediated by ERK‐ZEB‐1 pathway, and that inhibition of ERK1/2 phosphorylation or ZEB‐1 expression resulted in a decrease in chemoresistance. Conversely, gemcitabine‐resistant BxPC‐3 and Capan‐2 cells of epithelial‐like phenotype did not show such typical EMT‐like molecular changes although the expression of the tight junction marker occludin could be found decreased. In pancreatic cancer patients, high ZEB‐1 expression was associated with tumor invasion and tumor budding. In addition, tumor budding was essentially observed in patients treated with neoadjuvant chemotherapy. These findings support the notion that gemcitabine treatment induces EMT‐like changes that sustain invasion and chemoresistance in PC cells.

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