Stomach cancer risk factors
Jump to navigation
Jump to search
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omer Kamal, M.D.[2], Parminder Dhingra, M.D. [3], Mohammed Abdelwahed M.D[4]
|
Stomach cancer Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Stomach cancer risk factors On the Web |
|
American Roentgen Ray Society Images of Stomach cancer risk factors |
|
Risk calculators and risk factors for Stomach cancer risk factors |
Overview
Risk factors vary according to the type of gastric cancer. Common risk factors for intestinal-type of stomach cancer are chronic superficial gastritis caused by Helicobacter pylori infection, pernicious anemia, a high salt diet, chronic inflammation results in epithelial cell damage. Risk factors for diffuse-type gastric cancer are salt and salt-preserved foods, nitroso compounds, lack of fruits and fibers in diet, obesity, smoking, Helicobacter pylori, nonsteroidal antinflammatory, Epstien-Barr virus, gastric surgery, irradiation, and familial predisposition.
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 permits 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 causes a 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 the transformation of one differentiated cell type to another differentiated cell type.
- Dysplasia is an abnormality of development or an epithelial anomaly of growth and differentiation.
- It occurs as a result of Helicobacter pylori infection, bile reflux, or can be induced experimentally by irradiation.[1]
- 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.[2]
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.[3]
- Salt damages stomach mucosa and increases the susceptibility to carcinogenesis.[4]
Nitroso compounds
- Nitroso compounds are generated after consumption of nitrates.[5]
- Diets that are high in fried food and processed meat have been associated with an increased risk of gastric carcinoma.[6]
- A high pH environment increases bacterial growth in stomach that transform nitrate in nitrose compunds.[7]
Fruits and fibers
- Consumption of fruits and dietary fibres is protective against gastric cancer due to high vitamin C content that reduce the formation of carcinogenic N-nitroso compounds inside the stomach.[8]
Obesity
- Excess body weight is associated with an increased risk of gastric cancer.[9]
Smoking
- Eighteen percent of gastric cancer cases were linked to smoking.[10]
Helicobacter pylori
- H. pylori infection has been associated with an increase in the risk with adenocarcinoma, including both the intestinal and diffuse types.
Nonsteroidal antinflammatory (NSAID):
- Regular use of NSAIDs has been inversely associated with the risk of distal gastric adenocarcinoma.[11]
Epstein Barr virus (EBV)
- Ten percent of gastric cancers worldwide are associated with EBV.[12]
- It is related to DNA methylation of genetic alleles that protect against multiple cancers. Methylation of these alleles inhibit the expression of these alleles.[13]
Gastric surgery
- There is an increased risk of gastric cancer after gastric surgery.[14]
- Gastrojejunostomy (Billroth II procedure) carries a higher risk than the Billroth I 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.[15]
Blood group
- Blood group A individuals have an incidence ratio of 1.2 compared to blood group O individuals, which means that people with type A blood group have a slightly increased risk for the development of gastric cancer.[16]
Familial predisposition
- Although most gastric cancers are sporadic, 10 percent of cases are familial.
- Familial gastric cancer accounts for 1 to 3 percent of the global burden of gastric cancer and includes hereditary diffuse gastric cancer (HDGC), gastric adenocarcinoma, proximal polyposis of the stomach (GAPPS), and familial intestinal gastric cancer (FIGC).
Hereditary diffuse gastric cancer (HDGC)
- Clinical criteria for the diagnosis of HDGC has been described by the International Gastric Cancer Linkage Consortium.
- Germline mutations in the CDH1 gene, which encodes the cell adhesion protein E-cadherin, have been identified HDGC is inherited in an autosomal dominant fashion with high penetrance.
- The cumulative risk for gastric cancer by the age of 80 years for CDH1 mutation carriers is up to 70 percent in men and up to 56 percent in women.[17]
- Promoter hypermethylation, mutation, and loss of heterozygosity play key roles in the development of HDGC.
- The end result is loss of expression/reduced expression of the cell adhesion molecule E-cadherin.
- The risk of gastric cancer in asymptomatic carriers of a pathogeneic CDH1 mutation who belong to families with high penetrance hereditary diffuse gastric cancer is sufficiently high to warrant prophylactic gastrectomy.[18]
- Women in these affected families are also at high risk of developing breast cancer, predominantly lobular.
- The cumulative risk of breast cancer at the age of 80 years for CDH1 mutation carriers is approximately 42 percent, and like the gastric cancers, the increased relative risk starts early.[19]
Gastric adenocarcinoma proximal polyposis of the stomach (GAPPS)
- GAPPS is characterized by an autosomal dominant transmission of fundic gland polyposis that is restricted to the proximal stomach, with no evidence of duodenal or colorectal polyposis or other hereditary gastrointestinal (GI) cancer syndrome.
- It exhibits incomplete penetrance.
Familial intestinal gastric cancer (FIGC)
- 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.[20]
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
- ↑ Sobala GM, O'Connor HJ, Dewar EP, King RF, Axon AT, Dixon MF (1993). "Bile reflux and intestinal metaplasia in gastric mucosa". J Clin Pathol. 46 (3): 235–40. PMC 501177. PMID 8463417.
- ↑ Rugge M, Farinati F, Baffa R, Sonego F, Di Mario F, Leandro G; et al. (1994). "Gastric epithelial dysplasia in the natural history of gastric cancer: a multicenter prospective follow-up study. Interdisciplinary Group on Gastric Epithelial Dysplasia". Gastroenterology. 107 (5): 1288–96. PMID 7926493.
- ↑ Joossens JV, Hill MJ, Elliott P, Stamler R, Lesaffre E, Dyer A; et al. (1996). "Dietary salt, nitrate and stomach cancer mortality in 24 countries. European Cancer Prevention (ECP) and the INTERSALT Cooperative Research Group". Int J Epidemiol. 25 (3): 494–504. PMID 8671549.
- ↑ Tatematsu M, Takahashi M, Fukushima S, Hananouchi M, Shirai T (1975). "Effects in rats of sodium chloride on experimental gastric cancers induced by N-methyl-N-nitro-N-nitrosoguanidine or 4-nitroquinoline-1-oxide". J Natl Cancer Inst. 55 (1): 101–6. PMID 808633.
- ↑ Tricker AR (1997). "N-nitroso compounds and man: sources of exposure, endogenous formation and occurrence in body fluids". Eur J Cancer Prev. 6 (3): 226–68. PMID 9306073.
- ↑ Larsson SC, Orsini N, Wolk A (2006). "Processed meat consumption and stomach cancer risk: a meta-analysis". J Natl Cancer Inst. 98 (15): 1078–87. doi:10.1093/jnci/djj301. PMID 16882945.
- ↑ You WC, Zhang L, Yang CS, Chang YS, Issaq H, Fox SD; et al. (1996). "Nitrite, N-nitroso compounds, and other analytes in physiological fluids in relation to precancerous gastric lesions". Cancer Epidemiol Biomarkers Prev. 5 (1): 47–52. PMID 8770466.
- ↑ Riboli E, Norat T (2003). "Epidemiologic evidence of the protective effect of fruit and vegetables on cancer risk". Am J Clin Nutr. 78 (3 Suppl): 559S–569S. PMID 12936950.
- ↑ Turati F, Tramacere I, La Vecchia C, Negri E (2013). "A meta-analysis of body mass index and esophageal and gastric cardia adenocarcinoma". Ann Oncol. 24 (3): 609–17. doi:10.1093/annonc/mds244. PMID 22898040.
- ↑ González CA, Pera G, Agudo A, Palli D, Krogh V, Vineis P; et al. (2003). "Smoking and the risk of gastric cancer in the European Prospective Investigation Into Cancer and Nutrition (EPIC)". Int J Cancer. 107 (4): 629–34. doi:10.1002/ijc.11426. PMID 14520702.
- ↑ Epplein M, Nomura AM, Wilkens LR, Henderson BE, Kolonel LN (2009). "Nonsteroidal antiinflammatory drugs and risk of gastric adenocarcinoma: the multiethnic cohort study". Am J Epidemiol. 170 (4): 507–14. doi:10.1093/aje/kwp162. PMC 2727180. PMID 19584132.
- ↑ Boysen T, Mohammadi M, Melbye M, Hamilton-Dutoit S, Vainer B, Hansen AV; et al. (2009). "EBV-associated gastric carcinoma in high- and low-incidence areas for nasopharyngeal carcinoma". Br J Cancer. 101 (3): 530–3. doi:10.1038/sj.bjc.6605168. PMC 2720225. PMID 19603026.
- ↑ Sakuma K, Chong JM, Sudo M, Ushiku T, Inoue Y, Shibahara J; et al. (2004). "High-density methylation of p14ARF and p16INK4A in Epstein-Barr virus-associated gastric carcinoma". Int J Cancer. 112 (2): 273–8. doi:10.1002/ijc.20420. PMID 15352040.
- ↑ Takeno S, Hashimoto T, Maki K, Shibata R, Shiwaku H, Yamana I; et al. (2014). "Gastric cancer arising from the remnant stomach after distal gastrectomy: a review". World J Gastroenterol. 20 (38): 13734–40. doi:10.3748/wjg.v20.i38.13734. PMC 4194557. PMID 25320511.
- ↑ Henderson TO, Oeffinger KC, Whitton J, Leisenring W, Neglia J, Meadows A; et al. (2012). "Secondary gastrointestinal cancer in childhood cancer survivors: a cohort study". Ann Intern Med. 156 (11): 757–66, W-260. doi:10.7326/0003-4819-156-11-201206050-00002. PMC 3554254. PMID 22665813.
- ↑ Edgren G, Hjalgrim H, Rostgaard K, Norda R, Wikman A, Melbye M; et al. (2010). "Risk of gastric cancer and peptic ulcers in relation to ABO blood type: a cohort study". Am J Epidemiol. 172 (11): 1280–5. doi:10.1093/aje/kwq299. PMID 20937632.
- ↑ van der Post RS, Vogelaar IP, Carneiro F, Guilford P, Huntsman D, Hoogerbrugge N; et al. (2015). "Hereditary diffuse gastric cancer: updated clinical guidelines with an emphasis on germline CDH1 mutation carriers". J Med Genet. 52 (6): 361–74. doi:10.1136/jmedgenet-2015-103094. PMC 4453626. PMID 25979631.
- ↑ Onitilo AA, Aryal G, Engel JM (2013). "Hereditary diffuse gastric cancer: a family diagnosis and treatment". Clin Med Res. 11 (1): 36–41. doi:10.3121/cmr.2012.1071. PMC 3573088. PMID 22723466.
- ↑ Worthley DL, Phillips KD, Wayte N, Schrader KA, Healey S, Kaurah P; et al. (2012). "Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS): a new autosomal dominant syndrome". Gut. 61 (5): 774–9. doi:10.1136/gutjnl-2011-300348. PMID 21813476.
- ↑ Caldas C, Carneiro F, Lynch HT, Yokota J, Wiesner GL, Powell SM; et al. (1999). "Familial gastric cancer: overview and guidelines for management". J Med Genet. 36 (12): 873–80. PMC 1734270. PMID 10593993.