Family inheritance of esophageal cancer

There is a familial clustering phenomenon in the incidence of esophageal cancer. Although this may be related to the family's common living environment, the chromosome aberration rate in families with a high incidence of esophageal cancer is higher than that in families with a low incidence, suggesting that genetic factors play a certain role in the incidence of esophageal cancer. There is more and more evidence related to cancer and genetics, including both population and family levels and cellular and molecular levels, all of which believe that the separation ratio of cancer is less than 0-25. The inheritance of esophageal cancer is the same as this, and both belong to polygenic inheritance, that is, multiple genes with small effects (microgenes) under the action of certain environmental factors, produce a large total effect and cause cancer. Esophageal cancer can also be regarded as a total effect that occurs when a certain "threshold" is reached under the action of multiple micro-effect susceptibility genes.

Molecular biological markers such as p53, EGFR, c-erbB, int-2, and hst-1 have important auxiliary value for the early diagnosis, prognosis, and treatment selection of esophageal cancer. Someone used the HPV18E6E7 gene to establish the immortalized esophageal epithelial cell line SHEE, supporting the view that HPV18 may be related to the cause of esophageal cancer and further clarifying the cause and pathogenesis of esophageal cancer.

It is generally believed that esophageal epithelial dysplasia and Barrett's esophagus are precancerous lesions of esophageal cancer, which evolve into carcinoma in situ after the stage of epithelial dysplasia. According to pathological observation, the incidence rate can reach 30%.

The most common site of esophageal cancer is the middle segment, accounting for about 50%, followed by the lower segment, and the least in the upper segment, accounting for 30% and 20% respectively. Esophageal cancer is divided into three stages: early, middle and late. The size of early esophageal cancer lesions is less than 3 cm, and the depth of infiltration is limited to the mucosa or submucosa. The size of mid-stage lesions is 3 to 5 cm, and the muscle layer has been invaded or there is local lymph node metastasis. The size of late-stage cancer is more than 5 cm, and there is distant metastasis. According to the gross pathological morphology, early esophageal cancer can be divided into latent type, erosive type, plaque type and papillary type, among which plaque type is the most common, and this type of cancer cells is well differentiated. Mid- and late-stage esophageal cancer is divided into medullary type, mushroom type, ulcerative type, constriction type, intracavitary type and undetermined type. The medullary type has the highest degree of malignancy and accounts for more than 1/2 of mid- and late-stage esophageal cancer. In pathological histology, esophageal cancer is divided into squamous cell carcinoma, adenocarcinoma, undifferentiated carcinoma and carcinosarcoma. Squamous cell carcinoma is the most common, accounting for about 90% of esophageal cancer.