Stomach cancer risk factors: Difference between revisions

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==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|''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]] 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]], lack of fruits and fibers in diet, [[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==


=== '''Risk factors for intestinal type gastric cancer:''' ===
=== '''Risk factors for intestinal type gastric cancer:''' ===
* Chronic superficial gastritis caused by:
* Chronic superficial [[gastritis]] caused by:
* [[Helicobacter pylori|''Helicobacter pylori'']] infection
* [[Helicobacter pylori|''Helicobacter pylori'']] [[infection]]
* [[Pernicious anemia]]
* [[Pernicious anemia]]
* A high salt diet
* A high salt diet


* [[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 permits 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 tissue|glandular]] [[epithelium]] with loss of [[Parietal cell|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 causes a 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 factor|transforming growth factors]] that help the stomach in [[Regeneration|regenerating]] damaged [[Tissue (biology)|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 [[Differentiation|differentiated]] [[cell]] type to another [[Differentiation|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|''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:''' ===
'''Salt and salt-preserved foods'''
'''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.<ref name="pmid8671549">{{cite journal| author=Joossens JV, Hill MJ, Elliott P, Stamler R, Lesaffre E, Dyer A et al.| title=Dietary salt, nitrate and stomach cancer mortality in 24 countries. European Cancer Prevention (ECP) and the INTERSALT Cooperative Research Group. | journal=Int J Epidemiol | year= 1996 | volume= 25 | issue= 3 | pages= 494-504 | pmid=8671549 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8671549  }}</ref>
* A high intake of salt and salt-preserved foods such as salted fish and salted vegetables increases the risk of [[gastric cancer]].<ref name="pmid8671549">{{cite journal| author=Joossens JV, Hill MJ, Elliott P, Stamler R, Lesaffre E, Dyer A et al.| title=Dietary salt, nitrate and stomach cancer mortality in 24 countries. European Cancer Prevention (ECP) and the INTERSALT Cooperative Research Group. | journal=Int J Epidemiol | year= 1996 | volume= 25 | issue= 3 | pages= 494-504 | pmid=8671549 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8671549  }}</ref>
* Salt damages stomach [[Mucosal|mucosa]] and increases the susceptibility to [[carcinogenesis]].<ref name="pmid808633">{{cite journal| author=Tatematsu M, Takahashi M, Fukushima S, Hananouchi M, Shirai T| title=Effects in rats of sodium chloride on experimental gastric cancers induced by N-methyl-N-nitro-N-nitrosoguanidine or 4-nitroquinoline-1-oxide. | journal=J Natl Cancer Inst | year= 1975 | volume= 55 | issue= 1 | pages= 101-6 | pmid=808633 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=808633  }}</ref>  
* Salt damages [[stomach]] [[Mucosal|mucosa]] and increases the susceptibility to [[carcinogenesis]].<ref name="pmid808633">{{cite journal| author=Tatematsu M, Takahashi M, Fukushima S, Hananouchi M, Shirai T| title=Effects in rats of sodium chloride on experimental gastric cancers induced by N-methyl-N-nitro-N-nitrosoguanidine or 4-nitroquinoline-1-oxide. | journal=J Natl Cancer Inst | year= 1975 | volume= 55 | issue= 1 | pages= 101-6 | pmid=808633 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=808633  }}</ref>  
'''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>
* [[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>  
* [[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 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>
* 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'''
* ''[[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 [[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>
* 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>
'''Epstein Barr virus (EBV)'''
'''Epstein Barr virus (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>
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* [[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 groups|Blood group A]] individuals have an [[incidence]] ratio of 1.2 compared to [[Blood groups|blood group O]] individuals, which means that people with [[Blood groups|type A blood group]] have a slightly increased risk for the development of gastric cancer.<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 groups|Blood group A]] individuals have an [[incidence]] ratio of 1.2 compared to [[Blood groups|blood group O]] individuals, which means that people with [[Blood groups|type A blood group]] have a slightly increased risk for the development of [[gastric cancer]].<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>  
'''Familial predisposition'''
'''Familial predisposition'''
* Although most gastric cancers are sporadic, 10 percent of cases are [[familial]].  
* Although most [[Gastric cancer|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).  
* [[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)'''
'''Hereditary diffuse gastric cancer (HDGC)'''
* Clinical criteria for the [[diagnosis]] of HDGC has been described by the International Gastric Cancer Linkage Consortium.
* Clinical criteria for the [[diagnosis]] of HDGC has been described by the International [[Gastric Cancer]] Linkage Consortium.
* [[Germline mutation|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]].
* [[Germline mutation|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'' [[Carrier|mutation carriers]] is up to 70 percent in men and up to 56 percent in women.<ref name="pmid25979631">{{cite journal| author=van der Post RS, Vogelaar IP, Carneiro F, Guilford P, Huntsman D, Hoogerbrugge N et al.| title=Hereditary diffuse gastric cancer: updated clinical guidelines with an emphasis on germline CDH1 mutation carriers. | journal=J Med Genet | year= 2015 | volume= 52 | issue= 6 | pages= 361-74 | pmid=25979631 | doi=10.1136/jmedgenet-2015-103094 | pmc=4453626 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25979631  }}</ref>
* The cumulative risk for [[gastric cancer]] by the age of 80 years for ''CDH1'' [[Carrier|mutation carriers]] is up to 70 percent in men and up to 56 percent in women.<ref name="pmid25979631">{{cite journal| author=van der Post RS, Vogelaar IP, Carneiro F, Guilford P, Huntsman D, Hoogerbrugge N et al.| title=Hereditary diffuse gastric cancer: updated clinical guidelines with an emphasis on germline CDH1 mutation carriers. | journal=J Med Genet | year= 2015 | volume= 52 | issue= 6 | pages= 361-74 | pmid=25979631 | doi=10.1136/jmedgenet-2015-103094 | pmc=4453626 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25979631  }}</ref>
* Promoter [[Methylation|hypermethylation]], [[mutation]], and [[loss of heterozygosity]] play key roles in the development of HDGC.  
* Promoter [[Methylation|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 end result is loss of [[expression]]/reduced [[expression]] of the [[cell adhesion molecule]] [[E-cadherin]].
* The risk of gastric cancer in [[Asymptomatic carrier|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.<ref name="pmid22723466">{{cite journal |vauthors=Onitilo AA, Aryal G, Engel JM |title=Hereditary diffuse gastric cancer: a family diagnosis and treatment |journal=Clin Med Res |volume=11 |issue=1 |pages=36–41 |year=2013 |pmid=22723466 |pmc=3573088 |doi=10.3121/cmr.2012.1071 |url=}}</ref>
* The risk of [[gastric cancer]] in [[Asymptomatic carrier|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]].<ref name="pmid22723466">{{cite journal |vauthors=Onitilo AA, Aryal G, Engel JM |title=Hereditary diffuse gastric cancer: a family diagnosis and treatment |journal=Clin Med Res |volume=11 |issue=1 |pages=36–41 |year=2013 |pmid=22723466 |pmc=3573088 |doi=10.3121/cmr.2012.1071 |url=}}</ref>
* Women in these affected families are also at high risk of developing [[breast cancer]], predominantly [[lobular]].
* 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 ''[[CDH11|CDH1]]'' [[mutation]] carriers is approximately 42 percent, and like the gastric cancers, the increased relative risk starts early.<ref name="pmid21813476">{{cite journal| author=Worthley DL, Phillips KD, Wayte N, Schrader KA, Healey S, Kaurah P et al.| title=Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS): a new autosomal dominant syndrome. | journal=Gut | year= 2012 | volume= 61 | issue= 5 | pages= 774-9 | pmid=21813476 | doi=10.1136/gutjnl-2011-300348 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21813476  }}</ref>
* The cumulative risk of [[breast cancer]] at the age of 80 years for ''[[CDH11|CDH1]]'' [[mutation]] carriers is approximately 42 percent, and like the [[Gastric cancer|gastric cancers]], the increased relative risk starts early.<ref name="pmid21813476">{{cite journal| author=Worthley DL, Phillips KD, Wayte N, Schrader KA, Healey S, Kaurah P et al.| title=Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS): a new autosomal dominant syndrome. | journal=Gut | year= 2012 | volume= 61 | issue= 5 | pages= 774-9 | pmid=21813476 | doi=10.1136/gutjnl-2011-300348 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21813476  }}</ref>
'''Gastric adenocarcinoma proximal polyposis of the stomach (GAPPS)'''
'''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 [[Colon polyps|colorectal polyposis]] or other hereditary gastrointestinal (GI) cancer syndrome.  
* 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 [[Colon polyps|colorectal polyposis]] or other hereditary gastrointestinal (GI) [[cancer]] syndrome.  
* It exhibits [[incomplete penetrance]].  
* It exhibits [[incomplete penetrance]].  
'''Familial intestinal gastric cancer (FIGC)'''
'''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.  
* FIGC should be considered a potential [[diagnosis]] when [[histopathological]] reports denote intestinal-type [[Gastric cancer|gastric cancers]] that segregate within families without [[gastric]] [[polyposis]].  
* An [[autosomal dominant inheritance]] pattern has been noted in many such families.<ref name="pmid10593993">{{cite journal| author=Caldas C, Carneiro F, Lynch HT, Yokota J, Wiesner GL, Powell SM et al.| title=Familial gastric cancer: overview and guidelines for management. | journal=J Med Genet | year= 1999 | volume= 36 | issue= 12 | pages= 873-80 | pmid=10593993 | doi= | pmc=1734270 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10593993  }}</ref>  
* An [[autosomal dominant inheritance]] pattern has been noted in many such families.<ref name="pmid10593993">{{cite journal| author=Caldas C, Carneiro F, Lynch HT, Yokota J, Wiesner GL, Powell SM et al.| title=Familial gastric cancer: overview and guidelines for management. | journal=J Med Genet | year= 1999 | volume= 36 | issue= 12 | pages= 873-80 | pmid=10593993 | doi= | pmc=1734270 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10593993  }}</ref>  
'''Other hereditary cancer syndromes''':
'''Other hereditary cancer syndromes''':

Revision as of 15:59, 16 January 2019


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, 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:

Atrophic gastritis

Intestinal metaplasia and dysplasia

Risk factors for diffuse-type gastric cancer:

Salt and salt-preserved foods

Nitroso compounds

Fruits and fibers

Obesity

Smoking

Helicobacter pylori

Nonsteroidal antinflammatory (NSAID):

Epstein Barr virus (EBV)

Gastric surgery

Irradiation

Blood group

Familial predisposition

Hereditary diffuse gastric cancer (HDGC)

Gastric adenocarcinoma proximal polyposis of the stomach (GAPPS)

Familial intestinal gastric cancer (FIGC)

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. ↑ 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.
  19. ↑ 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.
  20. ↑ 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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