Medical genetic factors of esophageal cancer

The mechanism of tumorigenesis is one of the most important topics in oncology research. In recent years, the discovery of oncogenes has become a major breakthrough in basic tumor research. Research on esophageal cancer also focuses on the role of genetic factors and related genes in the occurrence process.

1. Genetic factors of esophageal cancer

Clinical investigations and studies have found that the incidence of esophageal cancer has a clear family clustering phenomenon. In areas of high incidence of esophageal cancer in my country, about 1/4 to 1/2 of patients have a positive family history, with the highest rate in the paternal line, followed by the maternal line, and the lowest in the collateral line. The chromosome aberration rate of peripheral blood lymphocytes in families with high incidence of esophageal cancer is higher, which may be a genetic factor that determines the susceptibility to esophageal cancer in high-incidence areas. Clinical investigations and studies have also found that residents in areas with high incidence of esophageal cancer still maintain a high level of morbidity and mortality when they move to other areas, suggesting that esophageal cancer has a certain relationship with genetics.

2. Genes associated with esophageal cancer

The occurrence of esophageal cancer is caused by multiple factors such as environment and heredity. Its molecular biological basis is gene mutation. The related genes include proto-oncogenes and tumor suppressor genes. Proto-oncogenes, also known as cell tumor suppressor genes, refer to DNA sequences homologous to viral oncogenes in normal cells of vertebrates and humans. Tumor suppressor genes, also known as anti-cancer genes, refer to a class of DNA fragments in the nuclear genome that can inhibit cell growth and promote cell differentiation. Molecular biological studies have confirmed that the onset of esophageal cancer is related to the activation of proto-oncogenes such as H-ras, C-myc, and hsl-1, and the inactivation of tumor suppressor genes such as Rb and p53.