The mGPS, PNI, and NLR were effective predictive indicators of postoperative complications. The PLR was the most useful prognostic indicator for pancreatic cancer patients after pancreaticoduodenectomy.
Tocotrienols (T3s) are members of the vitamin E family, have antioxidant properties, and are promising candidates for neuroprotection in the pathogenesis of neurodegenerative disorders such as Parkinson's disease (PD). However, whether their antioxidant capacities are required for their cytoprotective activity remains unclear. In this regard, the antioxidant-independent cytoprotective activity of T3s has received considerable attention. Here, we investigated the signaling pathways that are induced during T3-dependent cytoprotection of human neuroblastoma SH-SY5Y cells, as these cells are used to model certain elements of PD. T3s were cytoprotective against 1-methyl-4-phenylpyridinium ion (MPP(+)) and other PD-related toxicities. γT3 and δT3 treatments led to marked activation of the PI3K/Akt signaling pathway. Furthermore, we identified estrogen receptor (ER) β as an upstream mediator of PI3K/Akt signaling following γT3/δT3 stimulation. Highly purified γT3/δT3 bound to ERβ directly in vitro, and knockdown of ERβ in SH-SY5Y cells abrogated both γT3/δT3-dependent cytoprotection and Akt phosphorylation. Since membrane-bound ERβ was important for the signal-related cytoprotective effects of γT3/δT3, we investigated receptor-mediated caveola formation as a candidate for the early events of signal transduction. Knockdown of caveolin-1 and/or caveolin-2 prevented the cytoprotective effects of γT3/δT3, but did not affect Akt phosphorylation. This finding suggests that T3s and, in particular, γT3/δT3, exhibit not only antioxidant effects but also a receptor signal-mediated protective action following ERβ/PI3K/Akt signaling. Furthermore, receptor-mediated caveola formation is an important event during the early steps following T3 treatment.
Nicotine induces aberrant activation of aPKC via nAChR/PI3K signaling in PC cells, resulting in enhancement of cellular proliferation, migration and invasion.
Background: Sarcopenia is a prognostic factor in various cancers. However, the impact of sarcopenia in patients with recurrent pancreatic cancer remains unclear. This study evaluated the prognostic significance of sarcopenia in patients with recurrent pancreatic cancer. Methods: Seventy-four patients who developed postoperative recurrence of pancreatic cancer after undergoing pancreatectomies were enrolled. Sarcopenia in these patients was defined according to the psoas muscle index (PMI) measured via computed tomography at the third vertebra. Results: The mean PMIs at the time of recurrence were 4.47 ± 1.27 cm 2 /m 2 for men and 3.26 ± 0.70 cm 2 /m 2 for women. Of the 74 patients, 65 (87.8%) were diagnosed with sarcopenia with low PMI. The 2-year post-recurrence survival curve in the sarcopenia group was significantly worse than that in the non-sarcopenia group (P = 0.034). Multivariate analysis revealed that sarcopenia at the time of recurrence was an independent prognostic factor (P = 0.043) along with a high neutrophil-to-lymphocyte ratio (P = 0.004), early recurrence (P = 0.001), and chemotherapy after recurrence (P = 0.005) in patients with recurrent pancreatic cancer. Furthermore, the area under the curve (AUC) of the combination of sarcopenia and time to recurrence for predicting 2-year survival was 0.763, which was much higher than that of sarcopenia alone (AUC = 0.622). Conclusions: Sarcopenia is a useful prognostic factor in patients with recurrent pancreatic cancer. The combination of sarcopenia and time of recurrence may more accurately predict post-recurrence survival than can sarcopenia alone.
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