Introduction to esophageal cancer

Description: Esophageal cancer is a common malignant tumor in humans, accounting for 2% of all malignant tumors, accounting for more than 90% of esophageal tumors. It ranks second only to gastric cancer in retrospective investigation of all malignant tumor deaths. It is estimated that about 200,000 people die of esophageal cancer every year in the world. China is a high-risk area for esophageal cancer, and it is one of the most common malignant tumors that are extremely harmful to people's lives and health. The age of onset is more than 40 years old, more men than women. However, in recent years, the number of people under the age of 40 has a growing trend. The occurrence of esophageal cancer is related to chronic nitrosamine stimulation, inflammation and trauma, genetic factors, and trace element content in drinking water, food and vegetables. But the exact reason is not clear and needs to be studied. Causes: (1) The cause of esophageal cancer has a high incidence area. This feature indicates that the area has its own conditions, such as the presence of strong carcinogens, cancer-promoting substances, lack of some anti-cancer factors and genetic susceptibility. However, the results of studies in various countries are very inconsistent, reflecting the diverse causes of esophageal cancer. Western scholars believe that smoking and drinking are the main reasons. In the high-incidence area of Lin County, China, because of poverty, residents drink alcohol for nearly one or two decades. At present, although the etiology of esophageal cancer is not fully understood, in recent years, the etiology of esophageal cancer has been explored in many ways. From nitrosamines, nutrients, trace elements, fungi and viruses, genetics and many other aspects, research and exploration at multiple levels have made significant progress. It is generally believed that the occurrence of esophageal cancer may be the result of a combination of various factors. The factors associated with the onset of esophageal cancer are as follows: 1. Living habits and chronic esophageal stimulation (1) Smoking and esophageal cancer: Western scholars believe that smoking may be esophagus The main cause of cancer. Epidemiological investigations have found that smoking in some high-risk areas of esophageal cancer is quite common. In some areas, residents do not smoke, and esophageal cancer is rare. For example, Paymaster reported that Indian Muslims, Christians, and Hindus who love sapphire leaf tobacco and chewing betel leaves have a high incidence of esophageal cancer, and esophageal cancer among the devotees without this hobby is rare. Therefore, it is believed that smoking may be the cause of the high incidence of upper esophageal cancer and mid-stage cancer. However, the previous epidemiological survey in China did not find that smoking is closely related to the occurrence of esophageal cancer. It seems that most of these studies have come from local high-incidence areas of esophageal cancer and are limited to the rural population. In recent years, Chinese scholars have conducted a large number of epidemiological investigations on high-incidence areas, low-incidence areas, and urban and rural esophageal cancers. Most of them still believe that smoking may also be a cancer-promoting factor in the development of esophageal cancer in China. Many studies have shown that tobacco is a carcinogen, and its harm to the human body is multi-effect. The carcinogen in tobacco may be swallowed to the esophagus with saliva or food or absorbed into the esophagus to cause cancer. It has been found that cigarette smoke and tar contain various carcinogens, such as polycyclic aromatic hydrocarbons such as benzo-α oxime, epoxides, lactones, peroxides and halogen ethers, and also contain various nitroso compounds such as arylene. Nitropyrrolidine, dimethyl nitrosamine, nitroso-nornicotine or nitroso-nicotine. In addition, there are a large number of alkanes and alkoxy radicals formed by the reaction of NO, NO2 and hydrocarbons in the smoke. These components can directly attack the fat, protein and nucleic acid components of the cells, causing cell damage and causing cancer. Several chemicals in tobacco were added to drinking water to feed Fisher rats for 30 weeks. As a result, 12/20 cases of esophageal tumors were found in rats with nitroso-nor-nicotine, and 3 of them were esophageal cancer, which further confirmed tobacco. Relationship with the occurrence of esophageal cancer. (2) Alcohol and esophageal cancer: the relationship between esophageal cancer and drinking. Foreign scholars have done a lot of epidemiological investigations. They found that many patients with esophageal cancer have a lot of drinking history, or most of them are brewers and staff related to wine merchants. Recently, British and Hong Kong scientists surveyed smoking and drinking in patients with esophageal cancer in Hong Kong. After thorough analysis, it was found that drinking alcohol may cause esophageal cancer more easily than smoking. Domestic scholar Zhang Yude et al investigated 1400 patients with esophageal cancer and found that the case group had a positive drinking history (average white wine more than 2 or more for 5 consecutive years), accounting for 26.9%, while the control group was 17%. However, Liu Boqi et al. conducted case-control on esophageal cancer patients in Yangzhong County of Jiangsu Province, Xinyuan County of Xinjiang, and Huai'an County of Jiangsu Province, and found that only Huai'an County, which has a large drinking capacity, is a positive result. It seems that the role of alcohol has a certain relationship with its duration and the amount of alcohol consumed. However, there is no report on the induction of esophageal cancer in animals by alcohol or alcoholic products. The more accepted view is that the wine itself may not be directly carcinogenic, but it has a cancer-promoting effect. Alcohol can act as a solvent for carcinogens, promote carcinogens to enter the esophagus, cause damage to the esophageal mucosa, and create conditions for the occurrence of esophageal cancer. Some studies at home and abroad have found that some wines may be contaminated with nitrosamines, polycyclic aromatic hydrocarbons, phenolic compounds, DDT, and the like. These contaminants may enhance the damage of alcohol to the esophageal mucosa. (3) Eating habits and esophageal cancer: After investigation of the incidence factors in high-incidence areas, it was found that patients with esophageal cancer had the habit of thick food, paste, eating too fast, and eating hot drinks. These factors damaged the esophageal epithelium and increased carcinogenicity. Sensitivity of matter. Most studies have shown that hot food is one of the pathogenesis factors of esophageal cancer. In China's high incidence of esophageal cancer, many residents and esophageal cancer patients have a good habit of eating hot. The researchers measured the temperature of the food in the bowl when the residents in the high-incidence area were eating, and found that it can be as high as 70-80 ° C and the highest is 80-88 ° C. It has been reported that mice fed with hot water at 75 °C can be found that epithelial cell degeneration, mucosal inflammation and cellular nucleic acid metabolism are affected, so long-term repeated thermal stimulation may promote the carcinogenesis of the esophagus. There are also reports that eating too fast, food is rough, eating and drinking, and drinking tea, and meals are not related to esophageal cancer. Kazakhs love to chew "Nas", which is very irritating and contains tobacco. In Japan, people who like to eat hot porridge have a higher incidence. Excessive long-term drinking of strong alcohol and a large number of smokers may be an important cause of esophageal cancer in European and American homes. (4) Chronic stimulation of esophagus: Some of the pathogenic factors mentioned above will cause irritation to the esophagus, and long-term repeated stimulation will further lead to esophageal mucosal lesions. Studies have found that certain esophageal lesions, such as esophageal achalasia, chronic esophagitis, benign esophageal stricture and esophageal leukoplakia, have a higher incidence of esophageal cancer, indicating chronic damage and inflammation caused by chronic irritation in the incidence of esophageal cancer It plays a role. 2. Nutritional factors and trace elements In recent years, Chinese scholars have done a lot of nutrition investigation and nutrition intervention experiments at some sites of esophageal cancer prevention and treatment. Among them, the Sino-US cooperation in the Linxian County of Henan Province, which has been in the past 14 years (the Chinese Academy of Medical Sciences and the National Cancer Institute NCI) research project, has achieved a series of phased results, which have been produced at home and abroad. Tremendous influence. The study found that nutritional deficiency is a common phenomenon in high-risk areas of esophageal cancer, vitamin A, C, E, riboflavin, niacin, animal protein, fat, fresh vegetables, fruit intake are low. Many reports indicate that the lack of meat, eggs, vegetables and fruits can increase the risk of esophageal cancer. Chinese and American scholars have found that supplementing a diet rich in high protein, vitamins and minerals can protect the body and prevent esophageal cancer. Tests have shown that fresh vegetables, fruits, tea, and vitamins have anti-mutation effects, and the relative lack of risk factors should be considered as esophageal cancer. Recently, some scholars have found that feeding corn with pure corn feed can significantly increase the carcinogenic rate of methylphenylnitrosamine, suggesting that nutrient deficiency can increase the sensitivity of esophageal epithelial cells to nitrosamine carcinogens. Some animal experiments have also confirmed that the lack of vitamins A, C, E, and riboflavin can promote esophageal lesions and enhance the role of carcinogens in the esophagus. In-depth analysis found that vitamin C can block the synthesis of carcinogenic N-nitroso compounds, riboflavin deficiency can significantly increase the induction rate of methylbenzylnitrosamine in rat esophageal cancer, and shorten its latency. This further reveals the mechanism by which vitamins fight cancer. Lin County's research results show that supplementation of riboflavin and niacin compound nutrients to high-incidence areas may reduce the incidence of esophageal cancer. Therefore, supplementing vitamins in high-incidence areas may be an effective preventive measure. The relationship between trace elements and tumors has attracted more and more attention. The investigation confirmed that the content of trace elements such as molybdenum, selenium, cobalt, manganese, iron, nickel and zinc in water and soil in high-incidence areas of esophageal cancer is low. The lack of molybdenum has received more attention and is considered to be a factor in the pathogenesis of esophageal cancer. Molybdenum is low in nature and unevenly distributed. The serum molybdenum test in some high-incidence areas showed an average of 2.2-2.9 ng/ml, which was significantly lower than the mean value of serum molybdenum (4.8-5.9 ng/ml) in non-high-incidence areas. Molybdenum is a component of plant nitrite reductase. Molybdenum deficiency can accumulate nitrite in the environment and crops, while application of molybdenum fertilizer can increase the content of molybdenum in food, reduce the content of nitrite, and the intake of molybdenum is insufficient. It can affect the activity and physiological functions of some enzymes, which may be one of the causes of the increased incidence of esophageal cancer. Some investigations have shown that selenium is absent in high-risk areas of esophageal cancer. Selenium has a protective effect on cell membrane peroxidation through the action of glutathione peroxidase, enhancing the body's immune response and resistance to cancer occurrence and growth. Although organic selenium deficiency may not directly cause esophageal cancer, it may increase the susceptibility to carcinogens. Studies on human and environmental zinc deficiency in high-incidence areas have been reported, and zinc deficiency can lead to decreased immunity. Animal experiments show that cadmium has a role in inducing cancer in the esophagus and anterior stomach of mice, suggesting that cadmium may be a risk factor for esophageal cancer. In Lin County, patients with esophageal epithelial hyperplasia supplemented with multi-vitamin mineral compound nutrient solution, found that the epithelial hyperplasia can be reversed, the cancer rate is significantly lower than the control group, indicating that the secondary prevention of drug-blocking esophageal cancer has achieved preliminary good results. 3. Nitrosamine compounds Nitrosamines are recognized as a strong carcinogen. More than a dozen nitrosamines have been shown to induce esophageal cancer in animals, including methylbenzylnitrosamine (NMBAR), sarcosine ethyl nitrosamine (NSAR), nitrosopyrrolidine (NPyr), and Nitroso piperidine (NPip), N-3-methylbutyl-N-1-methylacetonyl nitrosamine (NAMBNA), and the like. Nitrosamines and their precursors are widely distributed in the environment and enter the body through drinking water and food. Its precursor is nitrosated in the stomach to produce nitrosamines. In recent years, it has been found that the nitrate content in the drinking water of Henan Linxian County, Hebei Cixian County, Shexian County, Guangdong Shantou, Shanxi Qufu and Yangcheng in the high incidence areas of esophageal cancer is significantly higher than that in the low-incidence area. According to the investigation, seven volatile nitrosamines were detected in the environment of Linxian County, a high incidence area of esophageal cancer. The high positive rate was dimethyl nitrosamine (64%), dipropyl nitrosamine (30%) and diethyl. Nitrosamine (24%). It was also detected that the cornmeal contained non-volatile sarcosine nitrosamine and the radish strip contained proline nitrosamine. The content of nitrite and nitrate in the contaminated food in Lin County is high. Secondary and tertiary amines are also widely distributed in food and the environment. Under acidic conditions in the stomach, amines and nitrites are easily combined to produce nitrosamines. It is reported that people with high incidence of esophageal cancer have moldy foods, which contain more nitrosamines and precursors. Mold can not only reduce nitrate to nitrite, but also decompose food protein to increase secondary amine content, thereby promoting the synthesis of nitrosamines. Lu Shixin reported for the first time in the world that residents with different esophageal cancer mortality rates consumed different amounts of nitrosamines from the diet. The intake of nitrosamines in the diet was: Lin County (高发)>济源(中高发)>禹县(low hair). The results showed that the amount of nitrosamine intake from the diet was positively correlated with the incidence of esophageal cancer. The total nitrosamine content in the gastric juice of Linxian County was found to be 24.93 ppb in male gastric juice, 20.51 ppb in females and 18% in females, which is the ratio of male to female in the incidence of esophageal cancer in Lin County. Match. The content of nitrosamines in the gastric juice of Linxian County was significantly positively correlated with the lesions of the esophageal epithelium, normal mild hyperplasia, severe hyperplasia and carcinogenesis. Animal experiments have shown that nitrosamines can induce esophageal cancer in animals, and blocking the nitrosation of amines can prevent the occurrence of esophageal cancer. A new nitroso compound, nitrosoisoproline, found in the urine of Linxian County can cause malignant transformation of NIH3T3 cells and inoculate fibrosarcoma in nude mice. In recent years, Lu Shixin et al. used NMBzA found in the environment of Linxian County to co-culture with human fetal esophageal epithelium for three weeks. The epithelium was transplanted into the mesentery of BALB/C nude mice, and NMBzA was used to continue feeding the nude mice. Cancer, no tumor in the control group of nude mice. The presence of the AIu sequence in the DNA extracted from the NMBzA-induced tumor tissue demonstrated that the induced tumor was derived from human tissue. These results demonstrate for the first time that nitrosamines can induce human esophageal epithelial squamous cell carcinoma, providing direct evidence for the etiology of nitrosamines in esophageal cancer in Lin County. Sauerkraut is a traditional food in China's high-incidence areas of esophageal cancer, Linxian County, Shanxi Yangcheng, Sichuan Yanting, and Jiangsu Yangzhong. In addition to some contaminated fungi, it also found trace amounts of benzo-α and nitrosamines. Contains a nitroso compound called Roussin Red Methyl Ester. About 55% of the sauerkraut in Lin County contains this compound, and the content is between 1 and 5 ppm. Experiments have shown that Roussin red methyl ester can cause malignant transformation of C3H/10T1/2 cells activated by 3-methylcholane. After application of mouse skin, the epidermis can be thickened and the number of sebaceous glands can be reduced. This compound may be present. A carcinogen in sauerkraut. A number of epidemiological surveys have shown that sauerkraut is one of the high-risk areas of both fungi and nitrosamines. 4. The role of fungi and viruses (1) The role of fungi: Studies have shown that the incidence of high incidence of esophageal cancer in China is related to fungal esophagitis and fungal contamination of food. Through repeated epidemiological investigations in Linxian, Yangcheng, Cixian, Yanting, Nanbromo and Xinjiang areas in Gaofa District, it was found that certain fungi and their metabolites in food, sauerkraut and mildew food are important for esophageal cancer. Risk factors. For example, the carcinogenic effects of aflatoxin B1 have been recognized. Linxian food is often contaminated by Fusarium oxysporum, Alternaria alternata, Penicillium arcuate, Geotrichum candidum, and Aspergillus flavus. These fungi not only reduce nitrate to nitrite, but also break down proteins, increase the amine content in food, and promote the synthesis of nitrosamines. The carcinogenic effect of moldy food has been confirmed by animal experiments. Moldy corneal surface (including Fusarium oxysporum) induced rat esophageal papilloma, gastric papilloma and esophageal cancer, and can cause epithelial hyperplasia and papilloma-like changes in the esophagus and anterior stomach of mice. The content and species of Fusarium oxysporum detected in the grain of Linxian County were significantly higher than those in the low-incidence areas of esophageal and cardiac cancer at home and abroad, and positively correlated with the incidence of esophageal and cardiac cancer. The mycotoxins that have been isolated and identified from Fusarium include Fusarium oxysporum, deoxynivalenol, 3-acetyl sphaerothecinol, 15-acetyl fulvicin, T- 2 toxins and zearalenone. Among them, Fusarium oxysporum and Deoxynivalenol have the highest content in moldy corn. The two kinds of toxins with high toxin content can be induced to produce esophageal, anterior stomach and glandular gastric hypertrophic changes in 20% proportion, suggesting that these two toxins have potential carcinogenic effects. It is further proved that Fusarium may be one of the main carcinogenic fungi in high-incidence areas. Alternaria alternata is also a fungus that has been studied in recent years. The contamination rate of Alternaria alternata in five high-incidence counties of Henan esophageal cancer (6.53%) was higher than that of three low-incidence counties (3.9%). The main mycotoxin contained in it is inter-associated with sporopolol monomethyl ether (AME) and alginol (AOH). The mutagenicity and tumorigenicity of Alternaria alternata are mainly related to these two toxins. The study found that AME and AOH have mutagenic effects on TA102 and E.Coli test bacteria, which can induce DNA single-strand breaks in USD and ZBS cells and rat hepatocytes of human amniotic membrane FL cells. AME can interfere with the transcriptional activity of rRNA, damage human lymphocyte DNA, induce V79 cell mutation, and transform NIH/3T3 cells. The transformed cells can grow on soft agar. The inoculated BALB/C nude mice have tumorigenicity. AME and AOH can promote lipid peroxidation and inhibit the activity of superoxide dismutase (SOD), which is associated with cell carcinogenesis. The cultured human embryonic esophageal epithelium was treated with AME or AOH in vitro for a short period of time, and DNA was extracted therefrom, and the DNA was transfected into NIH-3T3 cells, and the cells were malignantly transformed. Transformed cells can grow on soft agar and are tumorigenic. In recent years, it has also been demonstrated that A- or AOH-treated human embryonic esophageal epithelium has C-Ha-ras mutation and amplification, and activation and amplification of C-myc gene. AME and AOH induced human embryonic esophageal epithelial hyperplasia, which also successfully induced esophageal squamous cell carcinoma. The above results indicate that Alternaria alternata plays an important role in the etiology of human esophageal cancer. Some studies have shown that the micronucleus rate of red blood cells in mouse bone marrow induced by extract of Penicillium arcuticus is significantly different from that of the solvent control group (P<0.01), showing a significant dose-effect correlation. Mutagenesis experiments suggest that the metabolic extract of Penicillium arcuatus can directly damage genetic DNA. Bacillus subtilis DNA recombination test, UDs test, DSL test showed that Penicillium chrysogenum could produce mutagenic substances. The above results suggest that mold is one of the factors in the pathogenesis of esophageal cancer. (2) The role of the virus: The role of the virus in the pathogenesis of esophageal cancer has also attracted the attention of scholars at home and abroad. The viruses currently studied are mainly human papillomavirus (HPV) and Epstein Barr Virous (EBV). 1HPV: The relationship between human papillomavirus infection and cervical cancer has been recognized. In recent years, studies have found that the esophagus is also a good site for HPV infection. HPV infection of esophagus is reported to be mainly type 6, type 16, and type 18. Currently, some studies suggest that HPV type 16 is associated with esophageal squamous cell carcinoma, and HPV type 18 is associated with adenocarcinoma. There are many studies on HPV16 in China. The detection of HPV16 DNA in esophageal cancer and adjacent tissues showed that the detection rates of HPV16 DNA in cancer and adjacent tissues were 60% and 51.95%, respectively. It is suggested that HPV16 infection is a common phenomenon of esophageal cancer, which may be related to the occurrence of esophageal cancer. HPV in vitro experiments have shown that it has a role in causing cell transformation, but the mechanism of action of HPV is still unclear. Some scholars believe that HPV DNA can be integrated into the DNA of esophageal cancer tissues, which may cause gene abnormalities to participate in tumor development. Some scholars believe that HPV may cause the occurrence of esophageal cancer by reducing local lymphocytes, destroying the local immune surveillance system, and synergistically with other carcinogenic factors. However, Lu Shixin and others failed to detect HPV DNA in esophageal cancer and adjacent tissues in Linxian County by means of molecular hybridization and polymerase chain reaction. It seems that the relationship between HPV and esophageal cancer needs further study. 2EB virus: relationship between EBV and cancer In the past, the literature mainly focused on nasopharyngeal carcinoma. Reports on the relationship with esophageal cancer are rare. Foreign Mori et al found that the positive rate of Epstein-Barr virus in esophageal cancer was 3.3%. Domestic Wu Mingyao found that the positive rate of esophageal cancer: EBVLMP-1 (potential membrane protein 1) was 6.3%. EBV-positive cells show morphological changes such as cytoplasmic loosening and vacuolar degeneration, which may be related to the response of EBV-infected cancer cells. Regarding the pathogenicity of EBV positive rate and EBV, there are generally two hypotheses: A.EBV infection occurs after canceration, and the EBV test of mucosal epithelial cells in this patient is often negative; B.EBV infection occurs before canceration, and It plays a role in the formation of cancer. Because of the low positive rate of cases found so far, the link between EBV and esophageal cancer remains to be further studied. 5. Genetic factors A large number of studies have shown that cancer is the result of long-term repeated effects of various environmental factors on individuals with different genetic qualities. The proportion of family history of cancer in patients with esophageal cancer has been significantly higher than that of the control group, suggesting that there is a genetic predisposition to esophageal cancer, and genetic factors may be an important risk factor for the onset. With the development of molecular biology and molecular genetics, there is a lot of evidence that the malignant transformation of normal cells involves changes in the structure and regulation of genetic material. What is inherited from the previous generation is not the tumor itself, but the susceptibility to cancer. . The nature of this tumor susceptibility may be caused by abnormal DNA structure or replication, transcription, and expression errors in the patient, or may be related to the activation or inactivation of carcinogens, the loss or loss of enzyme activity required for harmlessness, or may be congenital or acquired. Sex chromosome aberrations or the result of certain immune genetic defects. It has been observed that the chromosomal aberration rate of high-risk family members is significantly higher than that of the control group. Experiments have shown that lymphocytes of high-incidence family members are more susceptible to sister chromosome exchange (SCE), and possible endemic fragile sites have been found on their chromosomes, such as 1p13-p36 and 4q21-q31, which may be involved in esophageal cancer. Some important synergies. Studies have found that family susceptibility to esophageal cancer is associated with familial immunodeficiency, esophageal cancer patients with family history of cancer and their relatives, some immune functions are significantly lower than the control group without cancer family, and patients and their relatives have more Similar immunodeficiency defects. Whether this immune dysfunction is caused by genetic or environmental factors remains to be further studied. 6. Study on esophageal oncogenes (1) Oncogenes: Studies on the DNA of esophageal cancer tissues and paracancerous epithelial tissues revealed that most C-mye, EGFR gene amplification or expression enhancement. From esophageal specimens obtained from high-risk areas of esophageal cancer in China, Italy, and France, 32% of cases had cyclin D gene amplification, and 63% of cases had cyclin D mRNA overexpression. Other expression enhancements include Int-1, HER-1 genes, etc. The high expression and over-amplification of these oncogenes may be related to the occurrence of esophageal cancer. (2) Tumor suppressor gene: There are abnormalities in the structure of Rb gene in about 1/3 of esophageal cancer and adjacent tissues, such as partial or partial loss of the fragment. About 10% to 70% of esophageal cancers have p53 gene mutations, and most of the mutations are in exons 5-9, and the detection rate of p53 gene loss is 43% to 52%. The loss rates of APC and MCC genes in esophageal cancer were 50% and 58%, respectively. The loss rate of adenocarcinoma appeared to be higher than that of squamous cell carcinoma, and the loss rate of DCC gene was 33%. The homozygous loss rate of p16 gene is 16.7%. The above suggests that the inactivation of tumor suppressor gene may also be an important link in the pathogenesis of esophageal cancer. (3) Candidate tumor suppressor genes: Recently, Lu Shixin applied mRNA differential PCR display technology to identify four human esophageal cancer-related gene cDNA fragments, named ECRG1 to ECRG4, which were cloned and identified to confirm that ECRG1 and ECRG2 may be new esophagus. Cancer-associated candidate tumor suppressor genes, which may be involved in the development of esophageal cancer. NMBzA and genetic abnormalities: Studying the relationship between environmental carcinogens and oncogene activation and tumor suppressor gene inactivation, NMBzA can lead to amplification or high expression of oncogenes C-myc, Int-2 and EGFR, and can lead to tumor suppressor genes. Mutation or deletion of Rb, APC and MCC. These suggest that the chemical carcinogen NMBzA can activate the proto-oncogene or inactivate the tumor suppressor gene during the initiation phase of carcinogenesis, which may be the cause of cancer rather than the result. In recent years, the application of methylbenzylnitrosamine (MBNA) found in the environment of Linxian County to human fetal esophageal epithelium for 3 weeks, the epithelium was transplanted into the mesentery of BALB/C nude mice, and the MBNA of nude mice was continued. Results Squamous cell carcinoma occurred in the mesentery, no tumor in the esophagus, and no tumor in the control group. The DNA of the induced tumor is hybridized with the human specific repeat sequence, Alu sequence, and the Alu sequence is found in the induced tumor, which proves that the tumor originates from human tissues. The experiment confirmed for the first time that nitrosamine can induce human esophageal epithelial squamous cell carcinoma and provide direct evidence for the cause of nitrosamine in esophageal cancer in Lin County. The above data suggest that the occurrence of esophageal cancer is the result of multiple factors, multiple stages and multiple oncogenes. (B) the pathogenesis 1. Distribution of tumor sites Clinically, the esophagus is usually divided into three segments: upper, middle and lower. From the entrance of the esophagus to the upper edge of the upper aortic arch, the lower segment from the lower edge of the lower pulmonary vein to the lower part of the portal. In 1987, the International Union Against Cancer (UICC) proposed a new segmentation criteria for esophageal cancer: the upper edge of the esophagus to the upper edge of the sternum is the cervical segment, and the lower part is the thoracic segment. The thoracic esophagus is divided into three sections: upper, middle and lower. From the upper edge of the sternal stem to the plane of the tracheal bifurcation, the upper part of the chest is the upper part of the tracheal bifurcation plane to the entrance of the iliac crest (the junction of the esophagus and the esophagus), and the lower part (including the anatomical ventral esophagus) (Fig. 1). According to past statistics, although there are certain regional differences in the occurrence of esophageal cancer, reports in most countries are still relatively consistent. The most common sites for esophageal cancer are 50% of the middle and third segments; followed by the lower third. Segment, accounting for 30%; the upper 1/3 segment is less, about 20%. According to the Henan Linxian People's Hospital, the distribution of 633 cases of esophageal cancer was determined by the combination of esophageal cytology and X-ray. The upper, middle and lower segments were 11.7%, 63.4% and 24.9%, respectively. 2. Pathological types (1) Gross type: Esophageal cancer can be divided into early and middle stages. Early esophageal cancer refers to carcinoma in situ (intraepithelial neoplasia) and early invasive carcinoma. The latter cancer tissue invades the submucosa but has not yet invaded the muscle layer. Read more...