Approximately 30% of pancreatic cancer patients harbor targetable mutations. However, there has been no therapy targeting these molecules clinically. Nucleic acid medicines show high specificity and can target RNAs. Nucleic acid medicine is expected to be the next-generation treatment next to small molecules and antibodies. There are several kinds of nucleic acid drugs, including antisense oligonucleotides, small interfering RNAs, microRNAs, aptamers, decoys, and CpG oligodeoxynucleotides. In this review, we provide an update on current research of nucleic acid-based therapies. Despite the challenging obstacles, we hope that nucleic acid drugs will have a significant impact on the treatment of pancreatic cancer. The combination of genetic diagnosis using next generation sequencing and targeted therapy may provide effective precision medicine for pancreatic cancer patients.

Lung cancer remains the leading cause of cancer-related deaths, with an estimated 1.76 million deaths reported in 2018. Numerous studies have focused on the prevention and treatment of lung cancer using rodent models. Various chemicals, including tobacco-derived agents induce lung cancer and pre-cancerous lesions in rodents. In recent years, transgenic engineered rodents, in particular, those generated with a focus on the well-known gene mutations in human lung cancer (KRAS, EGFR, and p53 mutations) have been widely studied. Animal studies have revealed that chronic inflammation significantly enhances lung carcinogenesis, and inhibition of inflammation suppresses cancer progression. Moreover, the reduction in tumor size by suppression of inflammation in animal experiments suggests that chronic inflammation influences the promotion of tumorigenesis. Here, we review rodent lung tumor models induced by various chemical carcinogens, including tobacco-related carcinogens, and transgenics, and discuss the roles of chronic inflammation in lung carcinogenesis.

In order to establish an appropriate bioassay for detection of lung damage after fine particle inhalation, sequential histopathological changes were here examined after intratracheal instillation of quartz (DQ-12, 4 mg/rat), as a typical lung toxic agent, in F344 male rats. A total of 50, 10-week-old animals, were separated into two groups. Twenty five were exposed to the material suspended in saline (0.2 ml) using a specially designed aerolizer and subgroups were sacrificed 1, 3, 7, 14, and 28 days thereafter. The remaining 25 rats were exposed by intratracheal instillation to saline (0.2 ml) as a control group and were sacrificed on the same days. Both groups received intraperitoneal injections of BrdU before sacrifice, and both groups underwent assessment of lung histopathology with immunohistochemical demonstrations of BrdU, iNOS and MMP-3 as end-point markers. The results suggest that Days 1 and 28 after intratracheal instillation of test fine particles are the most appropriate for detection of acute and subacute inflammatory changes, respectively. Furthermore, BrdU on Day 1 and iNOS on Day 28 proved to be suitable end-point markers for this purpose. Although instillation and inhalation models are different, the present instillation model can be used for detection of acute or subacute lung toxicity due to inhaled fine particles.