Pancreatic cancer is the 12th most common malignancy in the world and the 7th leading cause of cancer death, with a 5-year survival rate of only 10%. The global burden of pancreatic cancer has doubled over the past 25 years, and it now ranks among the top 10 cancer deaths in more than 130 countries. Therefore, there is an urgent need to investigate the molecular functions of its related genes in order to develop effective targeted drugs.

Target Genes Delivered In Vivo in Pancreatic Cancer

Most pancreatic cancers originate from pancreatic intraepithelial neoplasia (PanIN), and then gradually acquire gene mutations and develop into pancreatic cancer. The more common gene mutations include KRAS, TP53, P16/CDKN2A and SMAD4 mutations. Among them, the mutation rate of KRAS gene is as high as 90%, which is the earliest and most common genetic event known to pancreatic cancer. In recent years, many advances have been made in targeting KRAS. TP53 has been widely studied as a well-known "tumor suppressor gene". About 80% of pancreatic cancer patients have TP53 inactivating mutations, among which the R273H site mutation is the most common. About 50% of pancreatic cancers have SMAD4-inactivating mutations, and these patients have a low rate of lymph node metastasis and a good response to neoadjuvant chemotherapy. In addition to the above common driver genes, DNA mismatch repair (MMR) genes are also involved in the development of pancreatic cancer, such as ataxia-telangiectasia-mutated (ATM) genes and the KLF4 mutation in intraductal papillary mucinous tumors. In addition, there are genes related to tumor metabolism, such as lactate dehydrogenase A (LDHA), PI3K/AKT signal transduction pathway, and methylthioadenosine phosphorylase (MTAP).

Figure 1. Stages of pancreatic cancer evolution. (Makohon-Moore A, et al.; 2016)

In addition to the above genes, there are interesting pancreatic cancer-related genes that need to be explored and studied. Therefore, there is a need for an in vivo transfection system that can precisely target pancreatic cancer tissue and be taken up by tumor cells to function in vivo. The system can help researchers overcome various challenges encountered during in vivo transfection:

• Relevant molecular function studies can only be carried out in vitro, lacking important in vivo data
• Using in vitro transfection system for in vivo transfection, the transfection efficiency is very low;
• The in vivo transfection system used is not specific to pancreatic cancer tissues and cells, and is toxic to the body;
• The in vivo transfection system used cannot penetrate the pancreatic cancer tissue into the tumor tissue;
• The nucleic acid load of the in vivo transfection system is low, and it is difficult to achieve the expected effect;
• Etc…

Our Advantage:

• We can provide an in vivo transfection system for pancreatic cancer tissues and cells to achieve efficient transfection
• Our system can target multiple targets at the same time, improving targeting accuracy
• The in vivo transfection system has low toxicity to the body and is safe to use
• In vivo transfection system vectors can protect nucleic acids from degradation during in vivo delivery
• Persistent knockout effect in experimental animals after a single injection
• The system load is high, and the transfection needs of different doses can be completed
• Professional design and service team to provide you with reliable service and technical support
• Timely feedback of technical reports

CD BioSciences specializes in developing transfection systems and customizing transfection reagents for gene transfection using our core technologies. With our high-quality products and services, your transfection results can be greatly improved. If you can't find a perfect in vivo transfection system, you can contact us. We can provide one-to-one personal customization service.

Reference

1. SIEGEL R L, et al.; Cancer statistics, 2021.CA Cancer J Clin. 2021, 71(1): 7-33.
2. HAYASHI A, et al.; The pancreatic cancer genome revisited. Nat Rev Gastroenterol Hepatol. 2021, 18(7): 469-481.
3. SIMANSHU D K, et al.; RAS proteins and their regulators in human disease. Cell. 2017,170(1):17-33.
4. GUPTA V K, et al.; Hypoxia-driven oncometabolite L-2HG maintains stemness-differentiation balance and facilitates immune evasion in pancreatic cancer. Cancer Res. 2021, 81(15): 4001-4013.
5. Makohon-Moore A, et al.; Pancreatic cancer biology and genetics from an evolutionary perspective. Nat Rev Cancer. 2016, 16(9):553-65.

* For research use only. Not for use in clinical diagnosis or treatment of humans or animals.