Pancreatic cancer

Description: Pancreatic carcinoma is a common pancreatic tumor. It is a malignant tumor with high malignancy and difficult diagnosis and treatment. About 90% of ductal adenocarcinomas originate from the glandular epithelium. Its morbidity and mortality have increased significantly in recent years. The 5-year survival rate is <1%, which is one of the worst malignant tumors. The early diagnosis rate of pancreatic cancer is not high, the operative mortality rate is high, and the cure rate is very low. The incidence of this disease is higher in men than in women. The ratio of male to female is 1.5~2:1. Male patients are far more common than premenopausal women. The incidence of postmenopausal women is similar to that of males. Causes: (1) Causes of the disease The cause of pancreatic cancer is not fully understood. Pancreatic cancer is associated with smoking, drinking, high-fat and high-protein diets, excessive coffee consumption, environmental pollution, and genetic factors; recent surveys have found that the incidence of pancreatic cancer in diabetic populations is significantly higher than in the general population; Patients with chronic pancreatitis have a certain relationship with the incidence of pancreatic cancer. It is found that the proportion of pancreatic cancer in patients with chronic pancreatitis is significantly increased; in addition, there are many factors related to the occurrence of this disease, such as occupation, environment, geography and so on. 1. Smoking animal experiments have shown that feeding animals with tobacco acid water can cause pancreatic cancer. A large sample survey showed that smokers have a 1.5 times higher chance of developing pancreatic cancer than non-smokers. The greater the amount of smoking, the more pancreatic cancer occurs. The higher the chance, the more pancreatic cancer occurs in a pack of 4 and 2 times higher than that of non-smokers. The above information indicates that smoking in some people can induce pancreatic cancer. 2. Inappropriate diet In recent years, some scholars have attributed the increase in pancreatic cancer to improper diet. Animal experiments have shown that animals fed a high protein, high fat diet can accelerate the regeneration of pancreatic ductal cells and increase the sensitivity to carcinogens. Domestic scholar Shen Kui and other clearly stated that the diet structure is closely related to the occurrence of pancreatic cancer, and many people eating meat are prone to this disease. Japanese scholars have pointed out that the increase in the incidence of pancreatic cancer in Japan in recent years is related to the Europeanization of Japanese diet. That is, eating high protein and high fat. Some scholars believe that there is more chance of developing pancreatic cancer in coffee, but it has not been further confirmed. 3. Diabetes and pancreatic cancer Patients with diabetes are prone to pancreatic cancer. However, recent studies have indicated that people with diabetes mellitus have twice as many pancreatic cancers as non-diabetic patients, and there is an increasing trend; others believe that it is 2 to 4 times the normal population, and even reported that the incidence rate can reach 12.4% of digestive system malignancies, but the true relationship between the two is not clear. 4. Chronic pancreatitis and pancreatic cancer As early as 1950, Mikal et al. noted the relationship between chronic pancreatitis and pancreatic cancer. In 1960, Panlino-Netto pointed out that only patients with chronic pancreatitis with pancreatic calcification existed concurrently with pancreatic cancer, 1977. White further pointed out that only 3 cases of pancreatic cancer were associated with primary calcified chronic pancreatitis, accounting for 2.2%. Chronic pancreatitis and diabetes may be related to the occurrence of pancreatic cancer. Chronic pancreatitis often coincides with pancreatic cancer. According to Mikal et al. (1950), 100 cases of autopsy were reported. 49% had chronic pancreatitis under the microscope and 84% had pancreatic interstitial fibrosis. Because pancreatic cancer can cause obstruction of the pancreatic duct, which leads to the occurrence of pancreatitis, it is difficult to determine the cause and effect. Some people think that chronic pancreatitis with old calcification has a carcinogenic effect on calcification. Panlino-Netto (1960) reported that only pancreatic calcification patients, pancreatitis and pancreatic cancer. However, in White (1977) cases of pancreatitis, there are primary calcification, only 3% with cancer, in addition to calcification in pancreatic cancer. As for the relationship between pancreatic cancer and diabetes, it is not very clear. About 5% to 20% of patients with pancreatic cancer have diabetes, and 80% of them have found diabetes and pancreatic cancer in the same year. A large number of cases have also shown that 5% to 19% of cancer patients with cancer occur in the pancreas, while only 4% of non-diabetic patients develop cancer in the pancreas, indicating that diabetic patients seem to be prone to pancreatic cancer. Sommers et al (1954) reported that 28% of patients with diabetes had pancreatic duct hyperplasia, while only 9% of the control group had pancreatic duct hyperplasia. It is envisaged that cancer can occur on the basis of pancreatic duct hyperplasia. Bell (1957) reported a total of 32,508 cases of autopsy of men over 40 years old. The incidence of pancreatic cancer in diabetic patients was more than double that of non-diabetics. But there is also some evidence that the incidence of pancreatic cancer is not significantly related to diabetes. According to Lemass (1960), patients with pancreatic cancer with diabetes do not have pathological changes in islet cells that are destroyed. The glucose metabolism of some patients with pancreatic cancer can be damaged to some extent, which may be due to the fact that the release of insulin is disturbed due to the absence of pathological changes in islet cells. Others believe that pancreatic cancer combined with diabetes is not specific. The incidence of diabetes in the general population is also 10%. 5. Gene abnormal expression and pancreatic cancer are closely related to the occurrence of pancreatic cancer. The abnormal gene expression is closely related to the occurrence of pancreatic cancer. The relationship between the occurrence of various tumors and cellular genes is a hot spot for studying the causes of cancer. In each gene family, the mutation of the 12-site of the K-ras gene is closely related to the occurrence of pancreatic cancer, and the inactivation of the tumor suppressor gene P53 and the recently cloned MTS1 also has an effect. Since the occurrence of cancer is a multi-factor process, there may be activation and inactivation of various oncogenes or tumor suppressor genes, and it is not related to family inheritance. In 1991, Tada et al. detected 12 cases of patients with pancreatic cancer and 6 patients with chronic pancreatitis. The PCR test technique was used to detect the 12 codons of c-ki-ras in 12 pancreatic patients. The author further pointed out that the change in the codon at c-ki-ras 12 is mainly a mutation in the base. Tada et al. also suggested that c-ki-ras mutations differed from carcinogenic factors in animal experiments. Smokers can induce c-ki-ras 12-site mutations, while other carcinogens such as dimethyl Benzopyrene causes a mutation in the 61-site codon of the H-ras gene. Tada's clinical analysis of patients with pancreatic cancer concluded that the c-ki-ras gene mutation had no significant relationship with the degree of tumor differentiation, but was related to the size of the tumor, suggesting that the c-ki-ras gene mutation mainly promoted tumor progression. The Lemocene study found changes in the c-ki-ras gene in pancreatic ductal epithelial cells, suggesting that changes in the c-ki-ras gene cause pancreatic ductal epithelial cells to become cancerous, and then the cancer cells infiltrate outward. There are few studies on the occurrence and genetic alteration of pancreatic cancer, and many problems need further study. 6. Endocrine Disorders Pancreatic cancer may also be associated with endocrine, which is based on the incidence of men higher than that of women before menopause, and the incidence of women after menopause increases, similar to men. The incidence of women with a history of spontaneous abortion has also increased. 7. The role of bile For many years, it has been suggested that bile contains carcinogenic factors, because bile can flow back to the pancreatic duct, and pancreatic tissue is more sensitive to carcinogenic factors than bile duct, so pancreatic cancer is more common than cholangiocarcinoma. At the same time, in pancreatic cancer, the more common part of the pancreas in contact with bile, the higher the incidence of cancer, and the cancer originates from the catheter rather than the acinus, which also indicates that this view has a certain basis. (B) the pathogenesis 1. Primary pancreatic cancer can occur in any part of the pancreas, but the most common in the head of the pancreas. According to a large number of cases, the head of the pancreas is about twice as large as the tail of the pancreas, that is, the pancreatic head cancer accounts for 60% to 70%, and the pancreatic body tail cancer accounts for 25% to 30%. In a few cases, the cancer is scattered throughout. Gland, and it is difficult to determine its location. Bramhall et al found that 80% to 90% of the tumors in surgically treated pancreatic cancer are located in the head of the pancreas. According to recent data from the Pancreatic Cancer Professional Committee of the China Anti-Cancer Association, pancreatic head cancer accounts for 70.1%, pancreatic tail is 20.8%, and pancreatic cancer accounts for 9.1%. 2. Gross pathology The appearance of pancreatic cancer is not consistent. The general morphology of the pancreas in pancreatic cancer depends on the course of the disease and the size of the cancer. When the cancer is not large, the tumor block is deeply hidden in the pancreas and cannot be seen from the surface of the pancreas. There is only the feeling of irregular nodules at the time of percussion. When the cancer is enlarged, the shape of the pancreas changes, and there is a localized swelling of the tumor in the head or tail of the pancreas. The boundary between the tumor mass and the surrounding pancreatic tissue is not well understood. Pancreatic cancer on the cut surface is mostly gray or yellowish white irregular shape, and can also be yellowish white or grayish white. There are also bleeding spots or necrotic spots with brown or reddish brown. In the liquefied carcinoma, there are turbid brown-gray mucous fluids, some of which are small cystic cavity. The pancreas itself is often accompanied by increased fibrous tissue, which makes it firm in texture, and some have pancreatic atrophy in the pancreas. There may be localized fat necrosis, which may be due to cancer caused by pancreatic duct obstruction, pancreatic duct rupture, pancreatic juice spillover, causing local fat necrosis in the pancreas. The size of pancreatic cancer varies widely and is related to the length of the disease. Generally, the diameter of the mass is often above 5cm. Most of the cancers located in the head of the pancreas are extremely hard. There is no obvious boundary between the cancerous tissue and the normal glandular tissue. Sometimes this hard cancer can infiltrate the peripancreatic tissue extensively, and the pancreatic adhesion can not be recognized in a group of cancerous tissues; but sometimes cancer The tissue can also be located in the center of the pancreas and looks the same as the normal pancreas, with only the head of the pancreas being particularly hard. There are also many fibrous tissue hyperplasia and significant reduction of glandular tissue on the cut surface, which is difficult to distinguish from chronic pancreatitis. Pancreatic cancer can be derived from the pancreatic duct, acinar or islet. Usually pancreatic cancer is derived from pancreatic duct epithelium, accounting for about 85% of the total cases, less from acinar and islet; the former occurs mainly in the head of the pancreas, while the latter is often in the pancreas or tail. 3. Histological changes The microscopic findings of pancreatic cancer mainly depend on the degree of differentiation of adenocarcinoma tissues. The well-differentiated people form a more mature tubular tissue of the pancreatic gland. The cells are mainly high cubes, similar in size, rich in cytoplasm, and nuclear. Similar, mostly at the bottom, showing a polarization distribution. Poorly differentiated people can form various forms or even form a glandular tubular structure, and become solid strip-like, nested, flaky, cluster-like diffuse infiltration. The cells vary in size and shape, and can be spherical, round, or polygonal. The boundaries are not clear, the positions of the nuclei are different, and the nuclei are deeply stained and have no nucleoli. The pancreatic duct-like structure of pancreatic cancer is irregularly arranged, and its epithelial cells are arranged in a stratified manner, and the positions of the nucleus are different (Fig. 1). When the pancreatic duct epithelium proliferates and has a papillary projection, it is a papillary structure called papillary pancreatic cancer. Occasionally, there is a goblet cell metaplasia, and squamous cell metaplasia can also be seen. Under electron microscopy, Mucinogen granules but no zymogen granules were seen, all from larger pancreatic duct epithelial cells. When squamous cell degeneration is obvious, it is called adenosquamous cell carcinoma or adenocanthoma. Microscopic examination showed focal hemorrhage, necrosis and steatosis of varying degrees, called cystic adenocarcinoma. If accompanied by pancreatic duct obstruction, pancreatic acinar atrophy, with papillary hyperplasia. 4. Pathological stage of pancreatic cancer The vast majority (>80%) of pancreatic cancer originates from ductal epithelial cells, and the majority of adenocarcinomas of pancreatic ductal epithelial cells from the pancreas are predominant. A small number of small pancreatic ductal epithelial cells can be derived from the pancreas. Pancreatic cancer from large, medium and small pancreatic ducts, collectively referred to as hard cancer, due to its hard texture. Pancreatic cancer originating from pancreatic vesicle cells is rare, and the cancerous tumor is soft and scented. (1) Recommended criteria for the Japanese Pancreatic Disease Association (Table 1): The Japanese Pancreatic Disease Association recommends the standard T1 to T4, that is, T1 tumor diameter ≤ 2.0 cm, T2: 2.1 to 4.0 cm; T3: 4.1 to 6.0 cm; T4 > 6.0 cm. N shows lymph node involvement; N0 is no lymph node involvement; N1 is involved in lymph nodes around the pancreas; N2 has secondary lymph node involvement; N3 has near-stage third-grade lymph node metastasis. S shows pancreatic capsule involvement: S0 means that the pancreatic capsule is not invaded, S1 refers to the pancreatic capsule infiltration, S2 means that the pancreatic capsule is infiltrated, and S3 refers to the infiltration of the surrounding organs of the pancreas. Rp showed post-peritoneal involvement: Rp0 showed no post-peritoneal involvement, Rp1 suspected retroperitoneal involvement, Rp2 must have retroperitoneal involvement, and Rp3 showed severe retroperitoneal invasion. V shows the peri-pancreatic vascular involvement, mainly refers to the portal vein, superior mesenteric vein, and splenic vein involvement: V0 means no vascular involvement, V1 suspected vascular involvement, V2 must have vascular involvement, and V3 blood vessels are seriously violated. The Japanese Pancreatic Cancer Association divided the lymph nodes around the pancreas into 18 groups, 3 stations (Fig. 2, Table 2). (2) TNM staging: The pathological staging of pancreatic cancer contributes to the selection of treatment options and prognosis evaluation. Commonly used are TNM staging, the following is the latest revision of the 2002 International Anticancer Association (UICC) and the Japanese Pancreatic Disease Association (JPS). The American Cancer Alliance (AJCC) staging standard is roughly the same as the UICC standard. The sixth edition of the UICC staging (2002) (Table 3). 1T stage: Tx: primary tumor can not be determined To: no primary tumor evidence Tis: carcinoma in situ (including Pan In III) T1: tumor is confined to the pancreas ≤ 2cm T2: tumor is confined to the pancreas > 2cm T3: tumor has pancreatic Infiltration, but not invading the peritoneal trunk and superior mesenteric artery T4: Tumor invasion of the celiac trunk and superior mesenteric artery (can not remove the primary lesion) 2N staging: Read more...