Stomach cancer risk factors: Difference between revisions

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{{CMG}}; {{AE}} {{PSD}} {{MAD}}
{{CMG}}; {{AE}} {{PSD}} {{MAD}}
{{Stomach cancer}}
{{Stomach cancer}}


==Overview==
==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 cells|epithelial cell]] damage. Risk factors for diffuse-type gastric cancer are salt and salt-preserved foods, [[Nitroso|nitroso compounds]], fruits and fibers, [[obesity]], smoking, [[Helicobacter pylori]], [[Non-steroidal anti-inflammatory drug|nonsteroidal antinflammatory]], Ebstien-Barr virus, gastric surgery, [[irradiation]], and familial predisposition.   
[[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|''Helicobacter pylori'']] infection, [[pernicious anemia]], a high salt diet, [[chronic inflammation]] results in [[Epithelial cells|epithelial cell]] damage. [[Risk factors]] for diffuse-type gastric cancer are salt and salt-preserved foods, [[Nitroso|nitroso compounds]], fruits and fibers, [[obesity]], smoking, [[Helicobacter pylori]], [[Non-steroidal anti-inflammatory drug|nonsteroidal antinflammatory]], [[Epstein Barr virus|Epstien-Barr virus]], [[gastric]] [[surgery]], [[irradiation]], and [[familial]] predisposition.   


==Risk Factors==
==Risk Factors==
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* [[Chronic inflammation]] results in [[Epithelial cells|epithelial cell]] damage. It is accompanied by a loss of [[Parietal cells|parietal cell]] [[mass]] and therefore a reduction in acid production and increase in gastric PH.
* [[Chronic inflammation]] results in [[Epithelial cells|epithelial cell]] damage. It is accompanied by a loss of [[Parietal cells|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.
* The increase in gastric pH permits colonization of [[bacteria]] capable of converting [[dietary]] [[nitrates]] to potent [[nitroso]] compounds.
==== '''Atrophic gastritis''' ====
==== '''Atrophic gastritis''' ====
* Atrophic gastritis is an autoimmune disorder that is characterized by atrophy of the glandular epithelium with loss of parietal and chief cells.  
* [[Atrophic gastritis]] is an [[autoimmune]] disorder that is characterized by [[atrophy]] of the [[Glandular tissue|glandular]] [[epithelium]] with loss of [[Parietal cell|parietal]] and [[chief cells]].  
* This causesn decrease in hydrochloric acid and a resultant increase in gastric pH.  
* 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.
* There is also loss of [[endocrine]] cells that secrete [[Transforming growth factor|transforming growth factors]] that help the stomach in [[Regeneration|regenerating]] damaged [[Tissue (biology)|tissue]].
'''Intestinal metaplasia and dysplasia'''
'''Intestinal metaplasia and dysplasia'''
* [[Metaplasia]] is the transformation of one differentiated cell type to another differentiated cell type.
* [[Metaplasia]] is the transformation of one [[Differentiation|differentiated]] [[cell]] type to another [[Differentiation|differentiated]] [[cell]] type.
* [[Dysplasia]] is an abnormality of development or an epithelial anomaly of growth and differentiation.
* [[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]].<ref name="pmid8463417">{{cite journal| author=Sobala GM, O'Connor HJ, Dewar EP, King RF, Axon AT, Dixon MF| title=Bile reflux and intestinal metaplasia in gastric mucosa. | journal=J Clin Pathol | year= 1993 | volume= 46 | issue= 3 | pages= 235-40 | pmid=8463417 | doi= | pmc=501177 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8463417  }}</ref>  
* It occurs as a result of [[Helicobacter pylori|''Helicobacter pylori'']] infection, [[bile]] reflux, or can be induced experimentally by [[irradiation]].<ref name="pmid8463417">{{cite journal| author=Sobala GM, O'Connor HJ, Dewar EP, King RF, Axon AT, Dixon MF| title=Bile reflux and intestinal metaplasia in gastric mucosa. | journal=J Clin Pathol | year= 1993 | volume= 46 | issue= 3 | pages= 235-40 | pmid=8463417 | doi= | pmc=501177 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8463417  }}</ref>  
* 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.<ref name="pmid7926493">{{cite journal| author=Rugge M, Farinati F, Baffa R, Sonego F, Di Mario F, Leandro G et al.| title=Gastric epithelial dysplasia in the natural history of gastric cancer: a multicenter prospective follow-up study. Interdisciplinary Group on Gastric Epithelial Dysplasia. | journal=Gastroenterology | year= 1994 | volume= 107 | issue= 5 | pages= 1288-96 | pmid=7926493 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7926493  }}</ref>
* 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.<ref name="pmid7926493">{{cite journal| author=Rugge M, Farinati F, Baffa R, Sonego F, Di Mario F, Leandro G et al.| title=Gastric epithelial dysplasia in the natural history of gastric cancer: a multicenter prospective follow-up study. Interdisciplinary Group on Gastric Epithelial Dysplasia. | journal=Gastroenterology | year= 1994 | volume= 107 | issue= 5 | pages= 1288-96 | pmid=7926493 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7926493  }}</ref>


=== '''Risk factors for diffuse-type gastric cancer:''' ===
=== '''Risk factors for diffuse-type gastric cancer:''' ===
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'''Nitroso compounds'''
'''Nitroso compounds'''
* [[Nitroso]] compounds are generated after consumption of [[nitrates]].<ref name="pmid9306073">{{cite journal| author=Tricker AR| title=N-nitroso compounds and man: sources of exposure, endogenous formation and occurrence in body fluids. | journal=Eur J Cancer Prev | year= 1997 | volume= 6 | issue= 3 | pages= 226-68 | pmid=9306073 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9306073  }}</ref>
* [[Nitroso]] compounds are generated after consumption of [[nitrates]].<ref name="pmid9306073">{{cite journal| author=Tricker AR| title=N-nitroso compounds and man: sources of exposure, endogenous formation and occurrence in body fluids. | journal=Eur J Cancer Prev | year= 1997 | volume= 6 | issue= 3 | pages= 226-68 | pmid=9306073 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9306073  }}</ref>
* Diets that are high in fried food and processed meat have been associated with an increased risk of gastric carcinoma.<ref name="pmid16882945">{{cite journal| author=Larsson SC, Orsini N, Wolk A| title=Processed meat consumption and stomach cancer risk: a meta-analysis. | journal=J Natl Cancer Inst | year= 2006 | volume= 98 | issue= 15 | pages= 1078-87 | pmid=16882945 | doi=10.1093/jnci/djj301 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16882945  }}</ref>  
* [[Diet (nutrition)|Diets]] that are high in fried food and processed meat have been associated with an increased risk of gastric carcinoma.<ref name="pmid16882945">{{cite journal| author=Larsson SC, Orsini N, Wolk A| title=Processed meat consumption and stomach cancer risk: a meta-analysis. | journal=J Natl Cancer Inst | year= 2006 | volume= 98 | issue= 15 | pages= 1078-87 | pmid=16882945 | doi=10.1093/jnci/djj301 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16882945  }}</ref>  
* A high [[PH]] environment increases [[bacterial]] growth in stomach that transform nitrate in [[Nitroso|nitrose]] compunds.<ref name="pmid8770466">{{cite journal| author=You WC, Zhang L, Yang CS, Chang YS, Issaq H, Fox SD et al.| title=Nitrite, N-nitroso compounds, and other analytes in physiological fluids in relation to precancerous gastric lesions. | journal=Cancer Epidemiol Biomarkers Prev | year= 1996 | volume= 5 | issue= 1 | pages= 47-52 | pmid=8770466 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8770466  }}</ref>  
* A high [[pH]] environment increases [[bacterial]] growth in stomach that transform nitrate in [[Nitroso|nitrose]] compunds.<ref name="pmid8770466">{{cite journal| author=You WC, Zhang L, Yang CS, Chang YS, Issaq H, Fox SD et al.| title=Nitrite, N-nitroso compounds, and other analytes in physiological fluids in relation to precancerous gastric lesions. | journal=Cancer Epidemiol Biomarkers Prev | year= 1996 | volume= 5 | issue= 1 | pages= 47-52 | pmid=8770466 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8770466  }}</ref>  
'''Fruits and fibers'''
'''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 [[Carcinogen|carcinogenic]] [[Nitroso|N-nitroso]] compounds inside the [[stomach]].<ref name="pmid12936950">{{cite journal| author=Riboli E, Norat T| title=Epidemiologic evidence of the protective effect of fruit and vegetables on cancer risk. | journal=Am J Clin Nutr | year= 2003 | volume= 78 | issue= 3 Suppl | pages= 559S-569S | pmid=12936950 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12936950  }}</ref>
* Consumption of fruits and dietary fibres is protective against gastric cancer due to high [[vitamin C]] content that reduce the formation of [[Carcinogen|carcinogenic]] [[Nitroso|N-nitroso]] compounds inside the [[stomach]].<ref name="pmid12936950">{{cite journal| author=Riboli E, Norat T| title=Epidemiologic evidence of the protective effect of fruit and vegetables on cancer risk. | journal=Am J Clin Nutr | year= 2003 | volume= 78 | issue= 3 Suppl | pages= 559S-569S | pmid=12936950 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12936950  }}</ref>
'''Obesity'''
'''Obesity'''
* Excess body weight is associated with an increased risk of gastric cancer.<ref name="pmid22898040">{{cite journal| author=Turati F, Tramacere I, La Vecchia C, Negri E| title=A meta-analysis of body mass index and esophageal and gastric cardia adenocarcinoma. | journal=Ann Oncol | year= 2013 | volume= 24 | issue= 3 | pages= 609-17 | pmid=22898040 | doi=10.1093/annonc/mds244 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22898040  }}</ref>
* Excess body weight is associated with an increased risk of gastric cancer.<ref name="pmid22898040">{{cite journal| author=Turati F, Tramacere I, La Vecchia C, Negri E| title=A meta-analysis of body mass index and esophageal and gastric cardia adenocarcinoma. | journal=Ann Oncol | year= 2013 | volume= 24 | issue= 3 | pages= 609-17 | pmid=22898040 | doi=10.1093/annonc/mds244 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22898040  }}</ref>
'''Smoking'''
'''Smoking'''
* Eighteen percent of gastric cancer cases were linked to smoking.<ref name="pmid14520702">{{cite journal| author=González CA, Pera G, Agudo A, Palli D, Krogh V, Vineis P et al.| title=Smoking and the risk of gastric cancer in the European Prospective Investigation Into Cancer and Nutrition (EPIC). | journal=Int J Cancer | year= 2003 | volume= 107 | issue= 4 | pages= 629-34 | pmid=14520702 | doi=10.1002/ijc.11426 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14520702  }}</ref>  
* Eighteen percent of gastric cancer cases were linked to [[smoking]].<ref name="pmid14520702">{{cite journal| author=González CA, Pera G, Agudo A, Palli D, Krogh V, Vineis P et al.| title=Smoking and the risk of gastric cancer in the European Prospective Investigation Into Cancer and Nutrition (EPIC). | journal=Int J Cancer | year= 2003 | volume= 107 | issue= 4 | pages= 629-34 | pmid=14520702 | doi=10.1002/ijc.11426 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14520702  }}</ref>  
'''Helicobacter pylori'''
'''Helicobacter pylori'''
* H. pylori infection has been associated with an increase in the risk with [[adenocarcinoma]], including both the [[intestinal]] and diffuse types.  
* ''[[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):'''
'''Nonsteroidal antinflammatory (NSAID):'''
* Regular use of NSAIDs has been inversely associated with the risk of distal gastric adenocarcinoma.<ref name="pmid195841322">{{cite journal| author=Epplein M, Nomura AM, Wilkens LR, Henderson BE, Kolonel LN| title=Nonsteroidal antiinflammatory drugs and risk of gastric adenocarcinoma: the multiethnic cohort study. | journal=Am J Epidemiol | year= 2009 | volume= 170 | issue= 4 | pages= 507-14 | pmid=19584132 | doi=10.1093/aje/kwp162 | pmc=2727180 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19584132  }}</ref>
* Regular use of [[Non-steroidal anti-inflammatory drug|NSAIDs]] has been inversely associated with the risk of distal gastric adenocarcinoma.<ref name="pmid195841322">{{cite journal| author=Epplein M, Nomura AM, Wilkens LR, Henderson BE, Kolonel LN| title=Nonsteroidal antiinflammatory drugs and risk of gastric adenocarcinoma: the multiethnic cohort study. | journal=Am J Epidemiol | year= 2009 | volume= 170 | issue= 4 | pages= 507-14 | pmid=19584132 | doi=10.1093/aje/kwp162 | pmc=2727180 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19584132  }}</ref>
'''EBV'''
'''EBV'''
* Ten percent of gastric cancers worldwide are associated with [[Epstein Barr virus|EBV.]]<ref name="pmid19603026">{{cite journal| author=Boysen T, Mohammadi M, Melbye M, Hamilton-Dutoit S, Vainer B, Hansen AV et al.| title=EBV-associated gastric carcinoma in high- and low-incidence areas for nasopharyngeal carcinoma. | journal=Br J Cancer | year= 2009 | volume= 101 | issue= 3 | pages= 530-3 | pmid=19603026 | doi=10.1038/sj.bjc.6605168 | pmc=2720225 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19603026  }}</ref>
* Ten percent of gastric cancers worldwide are associated with [[Epstein Barr virus|EBV.]]<ref name="pmid19603026">{{cite journal| author=Boysen T, Mohammadi M, Melbye M, Hamilton-Dutoit S, Vainer B, Hansen AV et al.| title=EBV-associated gastric carcinoma in high- and low-incidence areas for nasopharyngeal carcinoma. | journal=Br J Cancer | year= 2009 | volume= 101 | issue= 3 | pages= 530-3 | pmid=19603026 | doi=10.1038/sj.bjc.6605168 | pmc=2720225 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19603026  }}</ref>
* It is related to [[DNA methylation]] of genetic alleles that protect against multiple cancers. [[Methylation]] of these alleles inhibit the expression of these [[alleles]].<ref name="pmid153520402">{{cite journal| author=Sakuma K, Chong JM, Sudo M, Ushiku T, Inoue Y, Shibahara J et al.| title=High-density methylation of p14ARF and p16INK4A in Epstein-Barr virus-associated gastric carcinoma. | journal=Int J Cancer | year= 2004 | volume= 112 | issue= 2 | pages= 273-8 | pmid=15352040 | doi=10.1002/ijc.20420 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15352040  }}</ref>  
* It is related to [[DNA methylation]] of [[genetic]] [[alleles]] that protect against multiple cancers. [[Methylation]] of these [[alleles]] inhibit the expression of these [[alleles]].<ref name="pmid153520402">{{cite journal| author=Sakuma K, Chong JM, Sudo M, Ushiku T, Inoue Y, Shibahara J et al.| title=High-density methylation of p14ARF and p16INK4A in Epstein-Barr virus-associated gastric carcinoma. | journal=Int J Cancer | year= 2004 | volume= 112 | issue= 2 | pages= 273-8 | pmid=15352040 | doi=10.1002/ijc.20420 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15352040  }}</ref>  
'''Gastric surgery'''
'''Gastric surgery'''
* There is an increased risk of gastric cancer after gastric surgery.<ref name="pmid25320511">{{cite journal| author=Takeno S, Hashimoto T, Maki K, Shibata R, Shiwaku H, Yamana I et al.| title=Gastric cancer arising from the remnant stomach after distal gastrectomy: a review. | journal=World J Gastroenterol | year= 2014 | volume= 20 | issue= 38 | pages= 13734-40 | pmid=25320511 | doi=10.3748/wjg.v20.i38.13734 | pmc=4194557 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25320511  }}</ref>
* There is an increased risk of gastric cancer after [[gastric]] [[surgery]].<ref name="pmid25320511">{{cite journal| author=Takeno S, Hashimoto T, Maki K, Shibata R, Shiwaku H, Yamana I et al.| title=Gastric cancer arising from the remnant stomach after distal gastrectomy: a review. | journal=World J Gastroenterol | year= 2014 | volume= 20 | issue= 38 | pages= 13734-40 | pmid=25320511 | doi=10.3748/wjg.v20.i38.13734 | pmc=4194557 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25320511  }}</ref>


* [[Gastrojejunostomy]] (Billroth II procedure) carries a higher risk than the Billroth I due to regurgitation of [[alkaline]] [[bile]] and [[pancreatic juice]].
* [[Gastrojejunostomy]] (Billroth II procedure) carries a higher risk than the Billroth I due to regurgitation of [[alkaline]] [[bile]] and [[pancreatic juice]].
'''Irradiation'''
'''Irradiation'''
* An elevated risk of gastric cancer has been reported in adult survivors of [[testicular cancer]] and [[Hodgkin's lymphoma|Hodgkin lymphoma,]] and in childhood cancer survivors who received [[abdominal]] [[radiotherapy]].<ref name="pmid22665813">{{cite journal| author=Henderson TO, Oeffinger KC, Whitton J, Leisenring W, Neglia J, Meadows A et al.| title=Secondary gastrointestinal cancer in childhood cancer survivors: a cohort study. | journal=Ann Intern Med | year= 2012 | volume= 156 | issue= 11 | pages= 757-66, W-260 | pmid=22665813 | doi=10.7326/0003-4819-156-11-201206050-00002 | pmc=3554254 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22665813  }}</ref>   
* An elevated risk of gastric cancer has been reported in adult survivors of [[testicular cancer]] and [[Hodgkin's lymphoma|Hodgkin lymphoma,]] and in childhood [[cancer]] survivors who received [[abdominal]] [[radiotherapy]].<ref name="pmid22665813">{{cite journal| author=Henderson TO, Oeffinger KC, Whitton J, Leisenring W, Neglia J, Meadows A et al.| title=Secondary gastrointestinal cancer in childhood cancer survivors: a cohort study. | journal=Ann Intern Med | year= 2012 | volume= 156 | issue= 11 | pages= 757-66, W-260 | pmid=22665813 | doi=10.7326/0003-4819-156-11-201206050-00002 | pmc=3554254 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22665813  }}</ref>   
'''Blood group'''
'''Blood group'''
* Blood group A individuals have shows a 20 percent excess of gastric cancer than other groups.<ref name="pmid20937632">{{cite journal| author=Edgren G, Hjalgrim H, Rostgaard K, Norda R, Wikman A, Melbye M et al.| title=Risk of gastric cancer and peptic ulcers in relation to ABO blood type: a cohort study. | journal=Am J Epidemiol | year= 2010 | volume= 172 | issue= 11 | pages= 1280-5 | pmid=20937632 | doi=10.1093/aje/kwq299 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20937632  }}</ref>  
* Blood group A individuals have shows a 20 percent excess of gastric cancer than other groups.<ref name="pmid20937632">{{cite journal| author=Edgren G, Hjalgrim H, Rostgaard K, Norda R, Wikman A, Melbye M et al.| title=Risk of gastric cancer and peptic ulcers in relation to ABO blood type: a cohort study. | journal=Am J Epidemiol | year= 2010 | volume= 172 | issue= 11 | pages= 1280-5 | pmid=20937632 | doi=10.1093/aje/kwq299 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20937632  }}</ref>  

Revision as of 00:38, 20 December 2017


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Parminder Dhingra, M.D. [2] Mohammed Abdelwahed M.D[3]

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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, fruits and fibers, obesity, smoking, Helicobacter pylori, nonsteroidal antinflammatory, Epstien-Barr virus, gastric surgery, irradiation, and familial predisposition.

Risk Factors

Risk factors for intestinal type gastric cancer:

Atrophic gastritis

Intestinal metaplasia and dysplasia

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

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

Nonsteroidal antinflammatory (NSAID):

  • Regular use of NSAIDs has been inversely associated with the risk of distal gastric adenocarcinoma.[11]

EBV

Gastric surgery

Irradiation

Blood group

  • Blood group A individuals have shows a 20 percent excess of gastric cancer than other groups.[16]

Familial predisposition

  • Although most gastric cancers are sporadic, 10 percent of cases.
  • 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.
  • Germline 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.[17]
  • 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.[18]

GAPPS

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.[19]

Other hereditary cancer syndromes:

References

  1. ↑ 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.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ 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.
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ 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.
  12. ↑ 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.
  13. ↑ 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.
  14. ↑ 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.
  15. ↑ 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.
  16. ↑ 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.
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ 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.

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