As a common gastrointestinal tumor, the incidence of pancreatic cancer has been increasing in recent years. The disease shows multi-gene, multi-step complex evolution from occurrence to dissemination. Furthermore, pancreatic cancer has an insidious onset and an extremely poor prognosis, so it is difficult to obtain cinical specimens at different stages of the disease, and it is, therefore, difficult to observe tumorigenesis and tumor development in patients with pancreatic cancer. At present, no standard protocols stipulate clinical treatment of pancreatic cancer, and the benefit rate of new targeted therapies is low. For this reason, a well-established preclinical model of pancreatic cancer must be established to allow further exploration of the occurrence, development, invasion, and metastasis mechanism of pancreatic cancer, as well as to facilitate research into new therapeutic targets. A large number of animal models of pancreatic cancer are currently available, including a cancer cell line-based xenograft, a patient-derived xenograft, several mouse models (including transgenic mice), and organoid models. These models have their own characteristics, but they still cannot perfectly predict the clinical outcome of the new treatment. In this paper, we present the distinctive features of the currently popular pancreatic cancer models, and discuss their preparation methods, clinical relations, scientific purposes and limitations.

Introduction: Several studies have reported that intraductal papillary mucinous neoplasms (IPMNs) of the pancreas are associated with extra-pancreatic malignancies. However, there have been no population-based studies evaluating the risk of second primary cancers (SPCs) in patients with pancreatic IPMN. Methods: The Surveillance, Epidemiology, and End Results (SEER) database was used to identify and characterize data from patients with IPMN of the pancreas. The standard incidence ratio (SIR) of this cancer was calculated by estimating the relative risk (RR). A multivariate Cox regression model was used to estimate hazards ratios (HRs) of death and associated 95% CIs. Results: Of 2,850 patients with IPMN of the pancreas, 104 patients (3.65%) developed 118 SPCs. The SIR for all SPCs combined was 1.22 (95% confidence interval [CI] = 1.01–1.46; P < 0.05). There was an elevated risk of site-specific SPCs in the small intestine (SIR = 8.68; 95% CI = 2.36–22.22), pancreas (SIR = 2.66; 95% CI = 1.15–5.25), urinary bladder (SIR = 2.02; 95% CI = 1.05–3.54), and eye and orbit (SIR = 13.47; 95% CI = 1.63–48.67) in patients with pancreas IPMN. In age subgrouping, people aged younger than 50 years had an increased risk of all-site SPC with an SIR of 6.44 (95% CI = 2.78–12.68). Cox regression modeling showed that advanced disease stage and a short latency period carried a higher risk of death in IPMN patients with SPC. Conclusions: Patients diagnosed with pancreatic IPMNs were at higher risk than the general population for developing a second primary malignancy. Meanwhile, advanced historic stage and short latency period were associated with an elevated HR in IPMN patients who develop an SPC.

Pancreatic cancer, one of the most malignant gastrointestinal tumors, is prone to liver metastasis. However, due to the lack of appropriate and comprehensive diagnostic methods, it is difficult to accurately predict the survival outcomes. Therefore, there is a need to identify effective biomarkers, such as UDP-GlcNAc: βGal β-1,3-N-acetylglucosaminyltransferase 3 ( B3GNT3 ), that predict the survival outcome of patients with pancreatic cancer. In the present study, based on data from 171 cases of pancreatic cancer obtained from The Cancer Genome Atlas portal, the differential expression of mRNAs was screened by comparing cancerous tissues with adjacent tissues. Univariate Cox regression analysis demonstrated that B3GNT3 had prognostic capability and could be an independent prognostic factor for pancreatic adenocarcinoma (PAAD). Using the Tumor Immune Estimation Resource tool and Tumor-Immune System Interaction Database, a potential relationship between B3GNT3 expression and immune cell infiltration was identified in pancreatic carcinoma. Furthermore, 177 samples of pancreatic carcinoma were collected and the association of CD68 expression with B3GNT3 was assessed by immunohistochemical staining. B3GNT3 expression was associated with clinical outcomes in pancreatic carcinoma and related to infiltrating levels of immune cells, which indicated that B3GNT3 could be used as an immunotherapy target for PAAD.