Pancreatic cancer is related to heredity, which can be confirmed by the following two points: first, the process of pancreatic tumor formation is accompanied by the accumulation of dominant mutations, and second, individuals who inherit gene mutations have a higher risk of pancreatic cancer. There are four types of genes involved in the occurrence of pancreatic cancer: oncogenes, tumor suppressor genes, genome maintenance genes, and tissue maintenance genes. Among gene mutations, some are inherited from the family, called germline mutations, and the other part is acquired mutations, which cause tumors in tissues and will not be inherited to offspring, called somatic mutations. The first reports of familial pancreatic cancer were case reports of multiple family members developing pancreatic cancer. For example, in 1973, MacDermott and Kramer reported that four siblings in a family had pancreatic cancer one after another. In 1982, Dat and Sontag reported a case of pancreatic cancer in a brother. These reports not only include multiple people in the same generation of the family suffering from the disease, but also multiple members of several generations in some families suffering from pancreatic cancer. Ehrenthal et al. reported a family with three generations suffering from pancreatic cancer. Lynch may be the first to cite a large number of familial pancreatic cancer cases and assume that there is an autosomal dominant inheritance mode in some families. However, to date, the view that pancreatic cancer is familial has not been widely recognized. Some epidemiologists have conducted research on the familial incidence of pancreatic cancer. These studies have shown that the incidence of people with a family history of pancreatic cancer is 3-13 times higher than that of sporadic cases, and pancreatic cancer tends to cluster in some families. Genetic syndromes associated with an increased risk of pancreatic cancer include familial atypical multiple nevi, malignant melanoma, breast cancer, hereditary non-polyposis colorectal cancer, familial pancreatitis, Peatz-Jeghers syndrome, etc. Patients with these syndromes have the same mutated genes as pancreatic cancer. Although it is clear that family members with a high incidence of pancreatic cancer have an increased risk of pancreatic cancer, it is not clear how to deal with it. Preventive surgery is an option, but total pancreatectomy can lead to diabetes and significant postoperative complications. A more reasonable countermeasure is to screen at-risk family members to detect early, potentially treatable pancreatic cancer. Unfortunately, existing serum markers, such as Ca199, are not sensitive and specific enough for screening. Some experts recommend the use of laparoscopic ultrasound combined with abdominal CT scans for screening of high-risk family members. With the progress of molecular biology and the increase in people's understanding of pancreatic cancer genetics, molecular genetic screening may be used for early detection of pancreatic cancer in the near future. |
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