Stomach Cancer Research Paper

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Updated: May 16, 2022
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Category: Apoptosis
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Gastric cancer is one of the most common cancers in the world (1). In the United States, 22220 new gastric cancer patients are diagnosed each year, of which up to 10990 are expected to die (2). Among the cancer deaths up to the 1980s, gastric cancer ranked second after lung cancer and the incidence decreased in the last decade (3). One reason for this decline was the identification of H.pylori infection and some dietary and environmental risk factors (4). In this period of time, the decline rate in China, especially in some regions, was less dramatic.

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Especially in women and young age group, the rate of decline was less (5). Between 1977 and 2006, this rate declined in the United States, except for the 29-39 year old white race (6). An interesting hypothesis was the proliferation of refrigerators (7). As a result, fresh food and vegetable consumption increased the chance of using antioxidant resources (8).

In recent years, due to the increased incidence of cancer in young population, gastric cancer will continue to play an important role in future deaths due to gastric cancer and cancer (9). The incidence of gastric cancer varies according to different geographical regions. North America and Africa regions have low rates, while East Asia, Eastern Europe and South America have the highest proportion .Over 70 percent of stomach cancers occur in developing countries. Stomach cancer is more common in men than women in both developed and developing countriesA decrease in mortality rates was found in the southern regions in the same region from north to south (10). This indicates an increased risk of stomach cancer in high geographic latitudes.

According to the Lauren classification there are two different types of stomach cancer being diffuse and intestinal. Diffuse or infiltrative type has a worse prognosis. In parallel with the overall decline in the incidence of gastric cancer, there has been a worldwide decline in intestinal gastric cancer rates over the past decade. In contrast, diffuse type decline was slower. As a result, the diffuse type constitutes approximately 30 percent of gastric cancer in some recently reported series (11). Despite the decline in general gastric cancer, there has been an increase in the incidence of cardia type cancer in the stomach. A secondary increase in the incidence of Barrett’s esophagus in proximal type gastric cancer has been identified (12). Turkey and the East in the incidence of gastric cancer is located in a transition zone between the West (13).

Referring to statistical data of the Ministry of 2012 annual cancer incidence rates in women of stomach cancer seen in Turkey, 8.6 / 100,000 with 7th rank; in men, it was found in the 5th rank with an incidence rate of 21.6 / 100.000 (14). Although the effects of some factors on prognosis are almost always observed in studies on prognosis of gastric cancer, some factors show differences between different studies.

Gastric cancer is a disease in which human beings have been captured since ancient times and is well The first possible case of gastric cancer is found in the Ebers inscriptions written in 1860 BC. Ibn-i Sina also mentioned gastric cancer (980-1037). Avenzoar (1070-1162) reported autopsy findings of a patient with gastric cancer. Morgagni gave detailed information about stomach cancers for the first time in 1761. In 1839, G.L Bayle’s book on stomach tumors was published.

Cuneo (1900) mentioned the importance of lymphatic drainage for gastric cancer for the first time. Pean performed the first gastric resection in 1879 in a patient with gastric cancer. In 1881, Theodor Billroth performed a successful pylor resection in a cancer patient and survived for 4 months. Connor died in 1884 in a patient with gastric cancer who required total gastrectomy. Schlatter performed his first successful total gastrectomy in 1897 and he survived for 14 months (15,16). The principles of diagnosis and treatment of gastric cancer have shown great improvements to date

In 1925, M. Kemal Oke published a case of gastrectomy for pylorus tumor (17). In 1930, 1937, 1941, 1951, Dr. Bahattin Toker, Dr.Cafer Kankat, Dr.Kaz?m ?.Gürkan, and Dr.Bedii Gorbon made new expansions in gastric surgery (18,19,20,21).

In the 1950s, a stapler device was developed in the Soviet Union. In 1951, Allen found that most of the gastric cancer relapses developed by the residual tissue remaining in the remainder of the vein and concluded that the upper limit should be examined histopathologically (22).

In 1967 the TNM classification was accepted by the International Association for Fight Against Cancer (UICC). With the development of technology in the last 2 decades of the 20th century, new applications were introduced. With the development of technology in the last 2 decades of the 20th century, new applications were introduced. In 1984, the Japanese gastroenterologist Tada T1N0 performed the first endoscopic mucosal resection of gastric cancer (23).

Recently, laparoscopic procedures have been marked by surgical treatment of gastric cancer. With the Da Vinci laparoscopy, which is the end point of robotic surgery, it has become possible to perform all maneuvers of the human arm with the same perfection. While the fundus and corpus acid contain salivary glands, the antrum contains alkaline secreting glands, gastrin releasing G cells, and endocrine cells. Although the pylorus is not a visible visual appearance, it is felt as a palpable muscular hoop. When viewed from the outside, the acidic part of the stomach and the other parts are distinguished by incisura angularis.

Endoscopically, GE is observed as the transition site between the smooth and light pink epithelium of the esophagus and the pink pleated epithelium of the stomach. It can be easily distinguished at the boundary between the acid-releasing corpus portion and the non-acidic release antrum. When the anthal rugas are parallel to the long axis of the organ, rhizomes in the corpus are oblique. The pylorus is easily viewed as a flat circle.

With age, the non-acidic secretion of anthum may shift upwards. Thus, the acid-secreting portion of the stomach can regress up to 30%. Thus, the ability of the stomach to release acid decreases. Loss of the oxzic mucosa may result from chronic gastritis (24, 25). An increase in gastrin-releasing mucosa may lead to a decrease in the protective epithelium of the stomach and thus to the formation of ulcers (26).

More than one reason is involved in the etiology of gastric cancer. While H.pylori infection contributes to the development of cancer in the majority of cases, dietary characteristics, lifestyle, obesity, smoking, genetic and environmental characteristics also play a role in the development of gastric cancer (35). H. pylori chronic active gastritis and atrophic gastritis can lead to early steps in the series of carcinogenesis. In addition, a number of studies have shown a clear association between H. pylori infection and gastric adenocarcinoma (36).

Epidemiological studies show a strong correlation between H. pylori seropositivity and gastric cancer. For example, 17 populations of 13 different countries (11 European countries, the United States of America and Japan) compared the H.pylori-infected population to the uninfected population in the EUROGAST study found that the rate of gastric cancer was six times higher in H. pylori-infected populations (37).

In a large prospective study dealing with H. pylori and cancer risk, 1526 Japanese patients were included. Patients underwent endoscopic biopsy.1246 patients had H. pylori infection. In a mean follow-up of 7.8 years, 36 patients with H. pylori developed gastric cancer (2.9 percent). Non-infected people did not develop gastric cancer (39). Various hypotheses have been proposed to explain the role of H. pylori in carcinogenesis, although the exact mechanism is not fully understood.

Some polymorphisms of IL-1 beta and other cytoki In a study, we compared the IL-1 beta polymorphisms of 393 patients with 430 gastric cancer. In a study, we compared the IL-1 beta polymorphisms of 393 patients with 430 gastric cancer. Two specific polymorphisms (IL-1B-31T and IL-1RN 2) were associated with low acid secretion and gastric atrophy. In 38% of H. pylori-related gastric cancer cases, these alleles were found to be present. IL-1 beta is regulated by the presence of H. pylori, a potent inhibitor of gastric acid secretion (40). In this respect, it was thought to be a risk factor for precancerous lesions in patients infected with H.pylori with gene polymorphism (41).

Another hypothesis is shown in vitro. H. pylori infection leads to the interaction of CD11a / CD18- and CD11b / CD18 with intercellular adhesion molecule-1 (ICAM-1). Nitric oxide synthase is produced and forms reactive oxygen metabolites such as nitric oxide, superoxide, hydroxyl ions DNA damage. This mutation leads to malignancy (42). H. pylori and immune response lead to apoptosis, proliferation, differentiation and autophagy. Two important processes in carcinogenesis include apoptosis (programmed cell death) and hyperproliferation (43).

Following severe DNA damage, apoptosis occurs as a protective mechanism to prevent mutated DNA proliferation. Atrophic gastritis with destruction and destruction of glands, may be the result of apoptosis. The mechanism caused by H. pylori apoptosis is still unclear. A study of the organism leads to apoptosis by both direct and indirect mechanisms. In the latter case, H. pylori is induced by pro-inflammatory stimuli (eg, tumor necrosis factor alpha), making the epithelial cells susceptible to apoptosis (44).

In general, H. pylori is thought to induce multiple-step carcinogenesis and progressively cause chronic atrophic gastritis and dysplastic changes. However, the presence of gastric cancer in only a small number of people infected with H. pylori suggests that other carcinogenic factors are necessary for cancer development. Microsatellite instability and genetic changes (p53 and APC / ß-Catenin) play a role in the later stages of the pathogenetic process beginning with H. pylori.. H. pylori, gastric epithelial DNA mutation, increased free oxygen radicals, interleukin levels change, decreased cytoprotective substances and changes in the microenvironment of the stomach in many steps, such as epithelial dysplasia leads to the role (45).

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Stomach Cancer Research Paper. (2021, Apr 03). Retrieved from