Gastric carcinoma is the fifth most common cancer and the third most cancer-related death globally.
Gastric adenocarcinoma is classified into two types: intestinal and diffuse, each with its morphologic appearance, etiology, and genetic profile.
Surgical resection with appropriate lymphadenectomy is the only possibly curative therapy option for people with stomach cancer.
Epidemiology
Globally, the incidence of gastric cancer has steadily decreased. Though, the rate has varied among areas such as Japan and China. The drop in gastric cancer may be attributable to the detection and treatment of viral causes and lifestyle changes of environmental and dietary risk factors. However, it remains widespread in places where fresh food storage and water quality are poor.
Most stomach cancers occur in underdeveloped nations, with males twice as likely as women and black men more than white men. Migration findings have identified the influence of lifestyle on the development of stomach cancer since the second and third generations born in the United States have decreased rates. White western civilizations with a better socioeconomic background have the lowest occurrence.
The histological patterns of stomach cancer have also changed epidemiologically, while the intestinal gastric type is gradually declining but remains more prevalent (70%). It is more common in men over the age of 50, and it is connected to environmental variables. On the other hand, the infiltrative or diffuse variety is about 30% but diagnosed at a younger age in both genders and has a poor prognosis.
Anatomy
Pathophysiology
According to Lauren’s histopathologic taxonomy, there are two primary histologic types of gastric carcinoma. The most common type is the intestinal type, characterized by its morphologic resemblance to adenocarcinomas of the gastrointestinal tract.
One hypothesis for the intestinal type of gastric cancer involves developing chronic gastritis caused by H. pylori, pernicious anemia, or high-salt diets to a loss of parietal cells, resulting in chronic atrophic gastritis.
Compensatory hypergastrinemia in atrophic gastritis causes persistent inflammation, which leads to intestinal metaplasia, dysplasia, and, eventually, cancer. The less prevalent diffuse-type gastric cancer is differentiated by a absence of intercellular adhesions, which disrupts glandular structure formation.
The lack of intercellular adhesions in individuals with a hereditary form of diffuse-type gastric cancer is caused by a germline mutation (HDGC) in the cellular adhesive protein E-cadherin. HDGC is a dominant characteristic with a significant penetrance, high invasiveness, a late presentation age of 38, and a poor outcome.
Asymptomatic CDH1 carriers may require preventive gastrectomy before 30, and women have a risk of developing breast cancer. There are no apparent precancerous lesions in the diffuse subtype.
Etiology
Nutritional variables such as high-salt preserved foods, consumption of N-nitroso compounds, smoking, a deficient vitamin A and C diet, ingesting significant amounts of barbecued or pickled foods, a lack of refrigerated goods, and unclean drinking water have all been related to an increased risk of stomach cancer.
Adenocarcinomas of the distal esophagus, proximal stomach, and junction are related with a higher risk of BMI, greater calorie consumption, gastroesophageal reflux, and smoking. Rubber production, tin mining, metal processing, and coal mining all enhance the danger.
Infection with H. pylori has a risk of 46-63%, whereas Epstein-Barr virus infection is estimated to be 5% to 10% globally. Radiation exposure and previous gastric surgery are also identified as risk factors.
Type A blood group has around 20% higher stomach cancer risk than other blood types is particularly related with the diffuse type. Pernicious anemia, an autoimmune chronic atrophic gastritis, increases the incidence of intestinal-type stomach cancer by up to sixfold.
Benign gastric ulcers, hypertrophic gastropathy, and gastric polyps is linked to an increased risk of stomach cancer. The majority of gastric carcinoma are spontaneous, although 5% to 10% of patients have a family history of the disease.
Genetics
Prognostic Factors
Gastric carcinoma prognosis correlates with tumor extent and includes nodal involvement and direct tumor spread outside the gastric wall. Localized gastric cancer can be cured in more than half of patients, although early-stage illness accounts for just 10-20% of all cases detected in the United States.
The overall 5-year survival rate for such individuals ranges from nearly zero for disseminated disease to approximately 50% for distal, localized illness. Localized carcinoma has a 5-year survival rate of 10-15% in people with proximal gastric cancer.
While therapy for individuals with diffused gastric cancer may result in symptomatic relief and lifespan prolongation, long-term remissions are unlikely.
Continue the therapy until disease progression or unacceptable toxicity occurs
If the 1st infusion is tolerable, then go with subsequent infusions given over 30 minutes
200-1000 mg/m² per day intravenously for 24 hours as a part of a platinum-based regimen)
Frequency and duration of every cycle differs on the basis of dose and regimen
In combination with tegafur and oteracil:
Take a dose of 40 mg/m2 as per body surface area two times daily for one week pre-operatively and for 15 days after operation starting on day 15 after operation
Gastric carcinoma is the fifth most common cancer and the third most cancer-related death globally.
Gastric adenocarcinoma is classified into two types: intestinal and diffuse, each with its morphologic appearance, etiology, and genetic profile.
Surgical resection with appropriate lymphadenectomy is the only possibly curative therapy option for people with stomach cancer.
Globally, the incidence of gastric cancer has steadily decreased. Though, the rate has varied among areas such as Japan and China. The drop in gastric cancer may be attributable to the detection and treatment of viral causes and lifestyle changes of environmental and dietary risk factors. However, it remains widespread in places where fresh food storage and water quality are poor.
Most stomach cancers occur in underdeveloped nations, with males twice as likely as women and black men more than white men. Migration findings have identified the influence of lifestyle on the development of stomach cancer since the second and third generations born in the United States have decreased rates. White western civilizations with a better socioeconomic background have the lowest occurrence.
The histological patterns of stomach cancer have also changed epidemiologically, while the intestinal gastric type is gradually declining but remains more prevalent (70%). It is more common in men over the age of 50, and it is connected to environmental variables. On the other hand, the infiltrative or diffuse variety is about 30% but diagnosed at a younger age in both genders and has a poor prognosis.
According to Lauren’s histopathologic taxonomy, there are two primary histologic types of gastric carcinoma. The most common type is the intestinal type, characterized by its morphologic resemblance to adenocarcinomas of the gastrointestinal tract.
One hypothesis for the intestinal type of gastric cancer involves developing chronic gastritis caused by H. pylori, pernicious anemia, or high-salt diets to a loss of parietal cells, resulting in chronic atrophic gastritis.
Compensatory hypergastrinemia in atrophic gastritis causes persistent inflammation, which leads to intestinal metaplasia, dysplasia, and, eventually, cancer. The less prevalent diffuse-type gastric cancer is differentiated by a absence of intercellular adhesions, which disrupts glandular structure formation.
The lack of intercellular adhesions in individuals with a hereditary form of diffuse-type gastric cancer is caused by a germline mutation (HDGC) in the cellular adhesive protein E-cadherin. HDGC is a dominant characteristic with a significant penetrance, high invasiveness, a late presentation age of 38, and a poor outcome.
Asymptomatic CDH1 carriers may require preventive gastrectomy before 30, and women have a risk of developing breast cancer. There are no apparent precancerous lesions in the diffuse subtype.
Nutritional variables such as high-salt preserved foods, consumption of N-nitroso compounds, smoking, a deficient vitamin A and C diet, ingesting significant amounts of barbecued or pickled foods, a lack of refrigerated goods, and unclean drinking water have all been related to an increased risk of stomach cancer.
Adenocarcinomas of the distal esophagus, proximal stomach, and junction are related with a higher risk of BMI, greater calorie consumption, gastroesophageal reflux, and smoking. Rubber production, tin mining, metal processing, and coal mining all enhance the danger.
Infection with H. pylori has a risk of 46-63%, whereas Epstein-Barr virus infection is estimated to be 5% to 10% globally. Radiation exposure and previous gastric surgery are also identified as risk factors.
Type A blood group has around 20% higher stomach cancer risk than other blood types is particularly related with the diffuse type. Pernicious anemia, an autoimmune chronic atrophic gastritis, increases the incidence of intestinal-type stomach cancer by up to sixfold.
Benign gastric ulcers, hypertrophic gastropathy, and gastric polyps is linked to an increased risk of stomach cancer. The majority of gastric carcinoma are spontaneous, although 5% to 10% of patients have a family history of the disease.
Gastric carcinoma prognosis correlates with tumor extent and includes nodal involvement and direct tumor spread outside the gastric wall. Localized gastric cancer can be cured in more than half of patients, although early-stage illness accounts for just 10-20% of all cases detected in the United States.
The overall 5-year survival rate for such individuals ranges from nearly zero for disseminated disease to approximately 50% for distal, localized illness. Localized carcinoma has a 5-year survival rate of 10-15% in people with proximal gastric cancer.
While therapy for individuals with diffused gastric cancer may result in symptomatic relief and lifespan prolongation, long-term remissions are unlikely.
Continue the therapy until disease progression or unacceptable toxicity occurs
If the 1st infusion is tolerable, then go with subsequent infusions given over 30 minutes
200-1000 mg/m² per day intravenously for 24 hours as a part of a platinum-based regimen)
Frequency and duration of every cycle differs on the basis of dose and regimen
In combination with tegafur and oteracil:
Take a dose of 40 mg/m2 as per body surface area two times daily for one week pre-operatively and for 15 days after operation starting on day 15 after operation
Gastric carcinoma is the fifth most common cancer and the third most cancer-related death globally.
Gastric adenocarcinoma is classified into two types: intestinal and diffuse, each with its morphologic appearance, etiology, and genetic profile.
Surgical resection with appropriate lymphadenectomy is the only possibly curative therapy option for people with stomach cancer.
Globally, the incidence of gastric cancer has steadily decreased. Though, the rate has varied among areas such as Japan and China. The drop in gastric cancer may be attributable to the detection and treatment of viral causes and lifestyle changes of environmental and dietary risk factors. However, it remains widespread in places where fresh food storage and water quality are poor.
Most stomach cancers occur in underdeveloped nations, with males twice as likely as women and black men more than white men. Migration findings have identified the influence of lifestyle on the development of stomach cancer since the second and third generations born in the United States have decreased rates. White western civilizations with a better socioeconomic background have the lowest occurrence.
The histological patterns of stomach cancer have also changed epidemiologically, while the intestinal gastric type is gradually declining but remains more prevalent (70%). It is more common in men over the age of 50, and it is connected to environmental variables. On the other hand, the infiltrative or diffuse variety is about 30% but diagnosed at a younger age in both genders and has a poor prognosis.
According to Lauren’s histopathologic taxonomy, there are two primary histologic types of gastric carcinoma. The most common type is the intestinal type, characterized by its morphologic resemblance to adenocarcinomas of the gastrointestinal tract.
One hypothesis for the intestinal type of gastric cancer involves developing chronic gastritis caused by H. pylori, pernicious anemia, or high-salt diets to a loss of parietal cells, resulting in chronic atrophic gastritis.
Compensatory hypergastrinemia in atrophic gastritis causes persistent inflammation, which leads to intestinal metaplasia, dysplasia, and, eventually, cancer. The less prevalent diffuse-type gastric cancer is differentiated by a absence of intercellular adhesions, which disrupts glandular structure formation.
The lack of intercellular adhesions in individuals with a hereditary form of diffuse-type gastric cancer is caused by a germline mutation (HDGC) in the cellular adhesive protein E-cadherin. HDGC is a dominant characteristic with a significant penetrance, high invasiveness, a late presentation age of 38, and a poor outcome.
Asymptomatic CDH1 carriers may require preventive gastrectomy before 30, and women have a risk of developing breast cancer. There are no apparent precancerous lesions in the diffuse subtype.
Nutritional variables such as high-salt preserved foods, consumption of N-nitroso compounds, smoking, a deficient vitamin A and C diet, ingesting significant amounts of barbecued or pickled foods, a lack of refrigerated goods, and unclean drinking water have all been related to an increased risk of stomach cancer.
Adenocarcinomas of the distal esophagus, proximal stomach, and junction are related with a higher risk of BMI, greater calorie consumption, gastroesophageal reflux, and smoking. Rubber production, tin mining, metal processing, and coal mining all enhance the danger.
Infection with H. pylori has a risk of 46-63%, whereas Epstein-Barr virus infection is estimated to be 5% to 10% globally. Radiation exposure and previous gastric surgery are also identified as risk factors.
Type A blood group has around 20% higher stomach cancer risk than other blood types is particularly related with the diffuse type. Pernicious anemia, an autoimmune chronic atrophic gastritis, increases the incidence of intestinal-type stomach cancer by up to sixfold.
Benign gastric ulcers, hypertrophic gastropathy, and gastric polyps is linked to an increased risk of stomach cancer. The majority of gastric carcinoma are spontaneous, although 5% to 10% of patients have a family history of the disease.
Gastric carcinoma prognosis correlates with tumor extent and includes nodal involvement and direct tumor spread outside the gastric wall. Localized gastric cancer can be cured in more than half of patients, although early-stage illness accounts for just 10-20% of all cases detected in the United States.
The overall 5-year survival rate for such individuals ranges from nearly zero for disseminated disease to approximately 50% for distal, localized illness. Localized carcinoma has a 5-year survival rate of 10-15% in people with proximal gastric cancer.
While therapy for individuals with diffused gastric cancer may result in symptomatic relief and lifespan prolongation, long-term remissions are unlikely.
https://www.ncbi.nlm.nih.gov/books/NBK459142/
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