Increased consumption of salt
High nitrate consumption
Diet low in vitamin A and C
Ill-prepared foods (smoked, salted)
Extremely hot food
Unhealthy drinking water
Rubber workers in coal mine workers
Helicobacter pylori infection
Epstein-Barr virus infection
Passed before the operation for stomach ulcers, stomach
Genetic Factors of Gastric Cancer
A blood group
Hereditary colon cancer
Adenomatous polyps of the stomach
Chronic atrophic gastritis
The 2-6 fold increased risk of stomach cancer in some studies have reported that Hp infection. Increase in the incidence of gastric cancer with Hp infection mechanism is not fully understood. However, the incidence of Hp infection, atrophic gastritis and chronic low-acidic environment which also seems to increase the incidence of metaplasia and dysplasia. Research has over 10 years of Hp infection in gastric cancer was seen in 5% of people reported positive.
c) Postgastrectomy: the rest of the stomach mucosa after partial gastrectomy and atrophic gastritis develops rapidly in areas close to the stoma with intestinal metaplasia, and was found to be more frequent.
d) Pernicious anemia: Pernicious anemia in people of increased frequency of carcinoma, atrophic gastritis and intestinal metaplasia are frequent in the corpus and fundus is connected. Studies in 2% of gastric carcinoma patients were found to be pernicious anemininde
e) Gender: Stomach cancer in males than in females in almost all countries are 1.2-2.5 times higher. The rate of intestinal type 2 / 1, while the diffuse type is equal to the ratio of male to female. Male dominance is high or low incidence of gastric cancer has been observed in all countries.
f) Menetrier disease (hyperplastic gastropathy): Menetrier disease, epithelial hyperplasia, depending on the stomach surface and gastric foveola pililerinin giant looks to gain, excessive mucus secretion, and hypochlorhydria is characterized by hypoalbuminemia developing gastropathy.
I) intestinal metaplasia: the frequency of intestinal metaplasia, gastric carcinoma, such as the frequency increases in direct proportion with age. This type of change, according to type of diffuse intestinal type carcinomas are more frequent and widespread. Classifications of intestinal metaplasia metaplastic epithelium usually is made according to the type of mucin produced by cells in cell morphology and complete (type I) and incomplete (type II) is divided into two main groups. Type II, type IIa and type IIb are divided into two sub-groups. Type IIa cells secrete mucin. Type IIb is a more differentiated cells, and secrete mainly sulfomusin. Most of this type IIb metaplasia was observed to be associated with cancer.
h) adenoma polyps of the stomach: stomach adenomas in other epithelial polyps (non-neoplastic) are rare compared to. Two centimeters higher than the frequency of large-scale adenomas and carcinomas. Precursor lesions for adenomas and carcinomas, as well as can be seen frequently in conjunction with stomach carcinoma. For this reason, the stomach removed, and the accompanying adenoma detected whether a lesion should be investigated further.
I) Gastric epithelial dysplasia: a precancerous condition of gastric dysplasia (35). Depending on the structure distortion and low-grade and high grade nuclear atypical divided into two. Tubular structures is limited to changes in dysplasia, invasive cancer called basal membrane is exceeded. Low-grade dysplasia, 15% of high-grade dysplasia progresses 0-. For this reason, low-grade dysplasia, repeated biopsies should be followed. High grade dysplasia is much more serious condition, 0-15% back, 14-and 58% will continue in the same way, 25-80% of the cancer becomes invasive. Polyps, or ulcers associated with high-grade dysplasia is likely to invasive cancer at diagnosis. Endoscopic treatment of high grade dysplasia resection or gastrectomy
I) p53 and genetic factors: studies in the early diagnosis of stomach cancer in the stomach lesions and carcinomas, p53 gene mutations in a high degree of atypia was reported high rates encountered. Accumulation of this protein, low-grade carcinomas 43%, 68% of those with high-grade shown. Moreover, p53 mutation has also been used to determine the patient's prognosis at the same time. P53 mutation has been reported that a high proportion of poor prognosis cancers detected. In other words, both the detection of p53 and prognosis in early gastric cancer as a marker in determining the best
Oncogenes, tumor suppressor effect of mutations in the genes, the E-cadherin, 4, 5q, 9p, 18q, and 20q, and tumor suppressor genes on chromosomes, chromosomes, such as loss of heterozygosity (LOH) and the formation of DNA replication errors (especially the simple repetitive sequences), as mentioned above, p53 mutation, somatic mutation of p16, APC (adenomatosis polyposis coli), EGF, TGF, c-erb-B2 overexpression of growth factors such as the stomach is thought to be the roles STUDIES.