The pancreas was for a long time a mystery, hidden deep behind the peritoneum. The ancient Greeks named it pancreas around 100 B.C., meaning “all flesh”. It is also recorded in Chinese medical texts, and is referred to as “pancreas” in the Book of Difficult Questions, and as “kidney fat” in the “Compendium of Materia Medica” by Li Shizhen in the Ming Dynasty. However, for nearly a thousand years, its true function was not recognized until the last century, when its function was gradually discovered and its related diseases were recognized with the development of related technology. In 1679, Morgagni first described pancreatic cancer, and subsequent studies over the centuries have recognized that pancreatic cancer is a progressive disease caused by multiple genetic variants stimulated by multiple factors. Chronic pancreatitis, diabetes, smoking, obesity and physical inactivity, and associated genetic alterations are now recognized as risk factors for pancreatic cancer. The relationship between chronic pancreatitis and pancreatic cancer was discussed as early as 1913 by John B. Deaver, but was not confirmed until controlled studies with large samples began in the 1980s. The interest in diabetes and pancreatic cancer was reported in the literature in the 1940s, and from 2005 to the present, 26 Meta-analyses on the relationship between diabetes and related treatments and pancreatic cancer have been conducted by PubMed search (mostly after 1975), which shows that it has been one of the hot spots that have been paid attention to. Most scholars now believe that long-term diabetes is a high-risk factor for pancreatic cancer, while new-onset diabetes may be an early symptom of pancreatic cancer. The discovery of mutated genes associated with pancreatic cancer is one of the major breakthroughs in the field of pancreatic cancer research. 1980s, literature in Science, Cell and other journals reported that K-ras mutations are very frequent in pancreatic cancer. K-ras mutations occur in approximately 90% of pancreatic cancers and 40%-90% of precancerous pancreatic cancers (including 90% of pancreatic intraepithelial neoplasia, 40%-60% of pancreatic intraductal papillary mucinous tumors). The construction of animal models allows a more in-depth study of the role of genetic mutations in pancreatic carcinogenesis. The genetically engineered mouse, established in 2003, was a milestone. In this model, the K-ras (G12D) mutant was introduced into the endogenous K-ras gene by cre-Lox technology, and pancreatic tissue-specific expression was achieved by Pdxl promoter guidance. This mouse model developed pancreatic intraepithelial neoplasia with partial progression to cancer. The introduction of mutations such as Tp53 deletion and TGF-βII receptor further accelerated the development of pancreatic cancer. Recent large-scale high-throughput sequencing of pancreatic cancer-related genes suggests that pancreatic cancer-related genetic alterations mainly occur in about 63 genes in 12 pathways, while the development of pancreatic cancer requires up to 10-30 years of accumulation of genetic alterations. The treatment of pancreatic cancer has developed into a multidisciplinary and comprehensive treatment model including surgery, chemotherapy and radiotherapy in the last hundred years. 1941, Whipple established the stage I pancreaticoduodenectomy which is a milestone in the history of pancreatic surgery. After decades of development, pancreaticoduodenectomy has become the standard treatment for early stage pancreatic cancer with high survival rate and few complications. Gemcitabine is an effective agent for adjuvant and advanced chemotherapy of pancreatic cancer, and recent clinical trials suggest that the four-drug combination regimen FOLFIRINOX (5-fluorouracil, calcium tetrahydrofolate, irinotecan, oxaliplatin) and albumin-bound paclitaxel combined with gemcitabine regimen can improve the survival of patients with advanced pancreatic cancer. Targeted therapies are also a hot topic of current research, but most have not yielded effective results, with only studies showing a slight improvement in survival with erlotinib. Despite the great progress in the treatment of pancreatic cancer, the overall survival rate is still low, mainly because most patients with pancreatic cancer are already at an advanced stage when they are diagnosed. Therefore, early diagnosis of pancreatic cancer has been a hot topic of research. Imaging techniques such as CT and MRI have played an important role in the diagnosis of pancreatic cancer, while the application of ultrasound endoscopy and endoscopic retrograde cholangiopancreatography has not only further improved the diagnosis rate of pancreatic cancer, but also provided a basis for cytological or histological diagnosis. However, it is still difficult to diagnose smaller pancreatic tumors, as well as the relatively expensive cost of the above tests is not conducive to screening, so it has a limited role in early diagnosis. CA19-9 is a monoclonal antibody prepared from colon cancer cell antigen, which has been widely used in pancreatic cancer diagnosis and efficacy detection, but it cannot be used for early diagnosis and screening alone due to the limitation of specificity and sensitivity. In recent years, the combination of new onset diabetes as an early symptom of pancreatic cancer, various novel tumor markers in circulating blood such as antibodies to related antigens (mucin-1 recognized by PAM4, soluble iC3b, REG4, phosphorylated protein p-ER1/2, CEACAM1, APRIL, DJ-1 and LAMC2), micro RNA, circulating tumor cells, etc., provides new hope for early diagnosis of pancreatic cancer. hope. In 2013, the International Pancreatic Cancer Screening proposed a screening strategy for pancreatic cancer, which is mainly based on people with genetic background, while the screening strategy for the general population remains to be explored.