Objective Several studies have suggested that an elevated neutrophil–lymphocyte ratio (NLR) is associated with a poorer prognosis in patients with pancreatic cancer (PC). The correlations between the NLR and immunohistochemical (IHC) analysis with regard to the prognosis of patients with PC remain to be elucidated. By using IHC findings, we determined the value of the NLR as a prognostic factor in patients with PC. Material and methods We collected the clinico-pathological data of 28 consecutive patients who underwent surgical resection for PC between January 2008 and December 2012 at The Jikei University Kashiwa Hospital. We investigated whether the NLR and IHC results were related and ensured the consistency of the prognosis of patients with PC. Results The Kaplan–Meier curves for the disease-free survival (DFS) and the overall survival (OS) revealed that an NLR ≥ 5 is an implicit factor for decreased DFS and OS in patients with PC (p = 0.003, p < 0.001, log-rank test). The density of CD163⁺macrophages and CD66b⁺neutrophils was significantly higher in the high NLR group; on the contrary, the density of CD20⁺lymphocytes was significantly higher in the low NLR group. Moreover, a Mann–Whitney U test showed that the NLR was significantly correlated with a high density of CD20⁺lymphocytes (p = 0.031) and CD163⁺macrophages (p = 0.023), while the NLR was not significantly correlated with CD66b⁺neutrophils (p = 0.397). Conclusions Our results demonstrated the validity of the NLR by IHC analyses and we determined that a higher value of NLR is a trustworthy prognostic factor for patients with PC.

Despite extensive research in the pathogenesis, early detection, and therapeutic approaches of pancreatic ductal adenocarcinoma (PDAC), it remains a devastating and incurable disease. As the global incidence and prevalence of PDAC continue to rise, there is a pressing need to place strong emphasis on its prevention. Although it is widely recognized that cigarette smoking, a potentially modifiable risk factor, has been linked to PDAC development, its contribution to prognosis is still uncertain. Moreover, the mechanistic pathways of PDAC progression secondary to smoking are various and lack a summative narration. Herein, we update and summarize the direct and indirect roles cigarette smoking plays on PDAC development, review literature to conclude the impact cigarette smoking has on prognosis, and postulate a comprehensive mechanism for cigarette smoking–induced PDAC.

Although many diagnostic and therapeutic modalities for pancreatic cancer have been proposed, an urgent need for improved therapeutic strategies remains. Oligonucleotide therapeutics, such as those based on antisense RNAs, small interfering RNA (siRNA), microRNA (miRNA), aptamers, and decoys, are promising agents against pancreatic cancer, because they can identify a specific mRNA fragment of a given sequence or protein, and interfere with gene expression as molecular-targeted agents. Within the past 25 years, the diversity and feasibility of these drugs as diagnostic or therapeutic tools have dramatically increased. Several clinical and preclinical studies of oligonucleotides have been conducted for patients with pancreatic cancer. To support the discovery of effective diagnostic or therapeutic options using oligonucleotide-based strategies, in the absence of satisfactory therapies for long-term survival and the increasing trend of diseases, we summarize the current clinical trials of oligonucleotide therapeutics for pancreatic cancer patients, with underlying preclinical and scientific data, and focus on the possibility of oligonucleotides for targeting pancreatic cancer in clinical implications.

Patients with pancreatic ductal adenocarcinoma (PDA) typically succumb to mortality early, even following surgical resection. Therefore, prognostic factors associated with early mortality are required to improve the survival of patients with PDA following surgical resection. Carbohydrate sulfotransferase 15 (CHST15) is responsible for the biosynthesis of sulfated chondroitin sulfate E (CS-E), which serves a pivotal function in cancer progression by cleaving CD44. CHST15 and CD44 expression in PDA tissue were assessed as a prognostic factor in patients with PDA following surgical resection. A total of 36 consecutive patients with PDA were enrolled following surgical resection between January 2008 and December 2014. The intensities of CHST15 and CD44 expression were analyzed by immunohistochemical staining. The recurrence period was significantly earlier in the strong CHST15 expression group compared with the negative-to-moderate CHST15 expression group. Overall survival (OS) was also significantly decreased in the strong CHST15 expression group compared with the negative-to-moderate CHST15 expression group. Multivariate analysis also indicated significant associations between CHST15 overexpression and disease-free survival (DFS) and OS. However, expression of CD44 in PDA tissue was not associated with DFS or OS. The present study has demonstrated for the first time that high CHST15 expression in PDA tissue may represent a potential predictive marker of DFS and OS in patients with PDA following surgical resection.

The incidence of metabolic syndrome with fatty liver is spreading on a worldwide scale. Correspondingly, the number of patients with the hepatic phenotype of metabolic syndrome, non-alcoholic fatty liver disease (NAFLD), and in its advanced states, non-alcoholic steatohepatitis (NASH), and the subsequent hepatocellular carcinoma (HCC) derived from NASH (NASH-HCC) is increasing remarkably. A large-scale epidemiological study revealed that obesity can be a risk factor of such cancers as HCC. Moreover, despite the ongoing trends of declining cancer incidence and mortality for most cancer types, HCC has experienced a markedly increased rate of both. Considering the differences in liver-related mortality among NAFLD patients, NASH, and NASH-HCC should be included in the objectives of initiatives to manage NAFLD patients and their progression to the advanced stages. Unfortunately, research has yet to make a crucial drug discovery for the effective treatment of NASH and NASH-HCC, although it is urgently needed. The latest widespread concept of the "multiple parallel hits hypothesis," whereby multiple factors contribute concurrently to disease pathogenesis has led to advances in the elucidation of hepatic and systemic molecular mechanisms driving NASH and the subsequent NASH-HCC progression; the results are not only extensive but promising for therapeutics. Here, we have summarized the myriad landmark discoveries of recent research into the pathogenic processes underlying NASH-HCC development and with the greatest possibility for a new generation of pharmaceutical products for interference and treatment.