Stomach cancer risk factors: Difference between revisions
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==Risk Factors== | ==Risk Factors== | ||
* | |||
* | === '''Risk factors for intestinal type gastric cancer:''' === | ||
* | * Chronic superficial gastritis caused by: | ||
* | * Helicobacter pylori infection | ||
* | * Pernicious anemia | ||
* | * A high salt diet | ||
* | |||
*[[ | * Chronic inflammation results in epithelial cell damage. It is accompanied by a loss of parietal cell mass and therefore a reduction in acid production and increase in gastric PH. | ||
* | The increase in gastric pH would permit colonization of bacteria capable of converting dietary nitrates to potent nitroso compounds. | ||
* | |||
*[[ | ==== '''Atrophic gastritis''' ==== | ||
* | * Atrophic gastritis is an autoimmune disorder that is characterized by atrophy of the glandular epithelium with loss of parietal and chief cells. | ||
*[[Familial | * This causesn decrease in hydrochloric acid and a resultant increase in gastric pH. | ||
* There is also loss of endocrine cells that secrete transforming growth factors that help the stomach in regenerating damaged tissue. | |||
'''Intestinal metaplasia and dysplasia''' | |||
Metaplasia is | |||
Dysplasia is | |||
* .It occurs as a result of Helicobacter pylori infection, bile reflux, or can be induced experimentally by irradiation [4,5]. | |||
* It was estimated that approximately 1 in 39 patients with intestinal metaplasia and 1 in 19 with dysplasia would develop gastric cancer within 20 years. [11] [10]. | |||
=== '''Risk factors for diffuse-type gastric cancer:''' === | |||
'''Salt and salt-preserved foods''' | |||
* A high intake of salt and salt-preserved foods such as salted fish and salted vegetables increases the risk of gastric cancer. [12-17] [18]. | |||
* Salt damages stomach mucosa and increases the susceptibility to carcinogenesis. [19-21]. | |||
'''Nitroso compounds''' | |||
* Nitroso compounds are generated after consumption of nitrates. [23] | |||
* Diets that are high in fried food and processed meat have been associated with an increased risk of gastric carcinoma. [15,26,27] [28]. | |||
* A high pH environment increases bacterial growth in stomach that transform nitrate in nitrose compunds. [24]. [25]. | |||
'''Fruits and fibers''' | |||
* Consumption of fruits and dietry fibres is protective against gastric cancer due to high vitamin C content that reduce the formation of carcinogenic N-nitroso compounds inside the stomach [36]. [37]. [12]. [30-33]. 35 | |||
'''Obesity''' | |||
* Excess body weight is associated with an increased risk of gastric cancer [40-42]. [40]. | |||
'''Smoking''' | |||
* Eighteen percent of gastric cancer cases were linked to smoking. 44]. | |||
'''Helicobacter pylori''' | |||
* H. pylori infection has been associated with an increase in the risk with adenocarcinoma, including both the intestinal and diffuse types [49]. | |||
'''Nonsteroidal antinflammatory (NSAID):''' | |||
Regular use of NSAIDs has been inversely associated with the risk of distal gastric adenocarcinoma [54,55] | |||
'''EBV''' | |||
* Ten percent of gastric cancers worldwide are associated with EBV [57,58]. | |||
* It isrelated to DNA methylation of genetic alleles that protect against multiple cancers. Methylation of these alleles inhibit the expression of these alleles [59-64]. | |||
'''Gastric surgery''' | |||
* There is an increased risk of gastric cancer after gastric surgery [78-81]: | |||
* Gastrojejunostomy (Billroth II procedure) carries a higher risk than the Billroth I.[79,81-83] due to regurgitation of alkaline bile and pancreatic juice. | |||
'''Irradiation''' | |||
* An elevated risk of gastric cancer has been reported in adult survivors of testicular cancer and Hodgkin lymphoma, and in childhood cancer survivors who received abdominal radiotherapy [84]. | |||
'''Blood group''' | |||
* Blood group A individuals have shows a 20 percent excess of gastric cancer than other groups. [90-92]. | |||
'''Familial predisposition''' | |||
* Although most gastric cancers are sporadic, 10 percent of cases. | |||
Truly hereditary (familial) gastric cancer accounts for 1 to 3 percent of the global burden of gastric cancer and comprises at least three major syndromes: | |||
hereditary diffuse gastric cancer (HDGC), | |||
gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS), | |||
and familial intestinal gastric cancer (FIGC). | |||
'''Hereditary diffuse gastric cancer''' | |||
clinical criteria for HDGC as described by the International Gastric Cancer Linkage Consortium (IGCLC). | |||
Germline truncating mutations in the ''CDH1'' gene, which encodes the cell adhesion protein E-cadherin, have been identified | |||
HDGC is inherited as an autosomal dominant trait with high penetrance. | |||
The cumulative risk for gastric cancer by age 80 for ''CDH1'' mutation carriers is up to 70 percent in men and up to 56 percent in women [94]. | |||
promoter hypermethylation, mutation, and loss of heterozygosity. The end result is loss of expression of the cell adhesion molecule E-cadherin. | |||
The risk of gastric cancer in asymptomatic carriers of a pathogenetic ''CDH1 ''mutation who belong to families with highly penetrant hereditary diffuse gastric cancer is sufficiently high to warrant prophylactic gastrectomy. | |||
Women in these affected families are also at high risk of developing breast cancer, predominantly lobular. The cumulative risk of breast cancer to age 80 for ''CDH1'' mutation carriers is approximately 42 percent, and like the gastric cancers, the increased relative risk starts early (before age 30) [94]. | |||
'''GAPPS''' | |||
GAPPS was characterized by the autosomal dominant transmission of fundic gland polyposis | |||
that are restricted to the proximal stomach, with no evidence of duodenal or colorectal polyposis or other hereditary gastrointestinal (GI) cancer syndrome [95,96]. | |||
It is characterized by incomplete penetrance. | |||
'''Familial intestinal gastric cancer''' | |||
FIGC should be considered a potential diagnosis when histopathological reports denote intestinal-type gastric cancers that segregate within families without gastric polyposis. | |||
An autosomal dominant inheritance pattern has been noted in many such families [97]. | |||
'''Other hereditary cancer syndromes''': | |||
* Lynch syndrome (hereditary nonpolyposis colorectal cancer), | |||
* Familial adenomatous polyposis (FAP) | |||
* Li-Fraumeni syndrome | |||
* Peutz Jeghers syndrome | |||
* juvenile polyposis | |||
* Hereditary breast and ovarian cancer syndrome | |||
* Cowden's syndrome | |||
==References== | ==References== | ||
Revision as of 14:48, 3 November 2017
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Parminder Dhingra, M.D. [2]
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Overview
Common risk factors in the development of stomach cancer are helicobacter pylori infection, cigarette smoking, family history of stomach cancer, and a diet high in salted smoked or preserved foods.
Risk Factors
Risk factors for intestinal type gastric cancer:
- Chronic superficial gastritis caused by:
- Helicobacter pylori infection
- Pernicious anemia
- A high salt diet
- Chronic inflammation results in epithelial cell damage. It is accompanied by a loss of parietal cell mass and therefore a reduction in acid production and increase in gastric PH.
The increase in gastric pH would permit colonization of bacteria capable of converting dietary nitrates to potent nitroso compounds.
Atrophic gastritis
- Atrophic gastritis is an autoimmune disorder that is characterized by atrophy of the glandular epithelium with loss of parietal and chief cells.
- This causesn decrease in hydrochloric acid and a resultant increase in gastric pH.
- There is also loss of endocrine cells that secrete transforming growth factors that help the stomach in regenerating damaged tissue.
Intestinal metaplasia and dysplasia
Metaplasia is
Dysplasia is
- .It occurs as a result of Helicobacter pylori infection, bile reflux, or can be induced experimentally by irradiation [4,5].
- It was estimated that approximately 1 in 39 patients with intestinal metaplasia and 1 in 19 with dysplasia would develop gastric cancer within 20 years. [11] [10].
Risk factors for diffuse-type gastric cancer:
Salt and salt-preserved foods
- A high intake of salt and salt-preserved foods such as salted fish and salted vegetables increases the risk of gastric cancer. [12-17] [18].
- Salt damages stomach mucosa and increases the susceptibility to carcinogenesis. [19-21].
Nitroso compounds
- Nitroso compounds are generated after consumption of nitrates. [23]
- Diets that are high in fried food and processed meat have been associated with an increased risk of gastric carcinoma. [15,26,27] [28].
- A high pH environment increases bacterial growth in stomach that transform nitrate in nitrose compunds. [24]. [25].
Fruits and fibers
- Consumption of fruits and dietry fibres is protective against gastric cancer due to high vitamin C content that reduce the formation of carcinogenic N-nitroso compounds inside the stomach [36]. [37]. [12]. [30-33]. 35
Obesity
- Excess body weight is associated with an increased risk of gastric cancer [40-42]. [40].
Smoking
- Eighteen percent of gastric cancer cases were linked to smoking. 44].
Helicobacter pylori
- H. pylori infection has been associated with an increase in the risk with adenocarcinoma, including both the intestinal and diffuse types [49].
Nonsteroidal antinflammatory (NSAID):
Regular use of NSAIDs has been inversely associated with the risk of distal gastric adenocarcinoma [54,55]
EBV
- Ten percent of gastric cancers worldwide are associated with EBV [57,58].
- It isrelated to DNA methylation of genetic alleles that protect against multiple cancers. Methylation of these alleles inhibit the expression of these alleles [59-64].
Gastric surgery
- There is an increased risk of gastric cancer after gastric surgery [78-81]:
- Gastrojejunostomy (Billroth II procedure) carries a higher risk than the Billroth I.[79,81-83] due to regurgitation of alkaline bile and pancreatic juice.
Irradiation
- An elevated risk of gastric cancer has been reported in adult survivors of testicular cancer and Hodgkin lymphoma, and in childhood cancer survivors who received abdominal radiotherapy [84].
Blood group
- Blood group A individuals have shows a 20 percent excess of gastric cancer than other groups. [90-92].
Familial predisposition
- Although most gastric cancers are sporadic, 10 percent of cases.
Truly hereditary (familial) gastric cancer accounts for 1 to 3 percent of the global burden of gastric cancer and comprises at least three major syndromes:
hereditary diffuse gastric cancer (HDGC),
gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS),
and familial intestinal gastric cancer (FIGC).
Hereditary diffuse gastric cancer
clinical criteria for HDGC as described by the International Gastric Cancer Linkage Consortium (IGCLC).
Germline truncating mutations in the CDH1 gene, which encodes the cell adhesion protein E-cadherin, have been identified
HDGC is inherited as an autosomal dominant trait with high penetrance.
The cumulative risk for gastric cancer by age 80 for CDH1 mutation carriers is up to 70 percent in men and up to 56 percent in women [94].
promoter hypermethylation, mutation, and loss of heterozygosity. The end result is loss of expression of the cell adhesion molecule E-cadherin.
The risk of gastric cancer in asymptomatic carriers of a pathogenetic CDH1 mutation who belong to families with highly penetrant hereditary diffuse gastric cancer is sufficiently high to warrant prophylactic gastrectomy.
Women in these affected families are also at high risk of developing breast cancer, predominantly lobular. The cumulative risk of breast cancer to age 80 for CDH1 mutation carriers is approximately 42 percent, and like the gastric cancers, the increased relative risk starts early (before age 30) [94].
GAPPS
GAPPS was characterized by the autosomal dominant transmission of fundic gland polyposis
that are restricted to the proximal stomach, with no evidence of duodenal or colorectal polyposis or other hereditary gastrointestinal (GI) cancer syndrome [95,96].
It is characterized by incomplete penetrance.
Familial intestinal gastric cancer
FIGC should be considered a potential diagnosis when histopathological reports denote intestinal-type gastric cancers that segregate within families without gastric polyposis.
An autosomal dominant inheritance pattern has been noted in many such families [97].
Other hereditary cancer syndromes:
- Lynch syndrome (hereditary nonpolyposis colorectal cancer),
- Familial adenomatous polyposis (FAP)
- Li-Fraumeni syndrome
- Peutz Jeghers syndrome
- juvenile polyposis
- Hereditary breast and ovarian cancer syndrome
- Cowden's syndrome