Stomach cancer causes: Difference between revisions
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{{Stomach cancer}} | {{Stomach cancer}} | ||
{{CMG}}; {{AE}} {{MAD}} | {{CMG}}; {{AE}} {{OK}}, {{MAD}} | ||
== Overview == | == Overview == | ||
Causes of stomach cancer depend on the type of cancer. Adenocarcinomas are caused by [[genetic]] modulations due to [[chronic inflammation]] mainly by [[Helicobacter pylori|''H. pylori'']] infection. Diffuse gastric carcinomas do not have a [[precancerous]] lesion. [[Somatic]] [[mutations]] in the ''CDH1'' [[gene]] by hypermethylation, [[mutation]], and [[loss of heterozygosity]] are identified in 40 to 83 percent of sporadic diffuse-type gastric cancers. The [[E-cadherin]] [[gene]] (''CDH1'') encodes a [[Transmembrane protein|transmembrane cellular adhesion protein]]. | [[Causes]] of [[stomach cancer]] depend on the type of [[cancer]]. [[Adenocarcinomas]] are caused by [[genetic]] modulations due to [[chronic inflammation]] mainly by [[Helicobacter pylori|''H. pylori'']] infection. Diffuse [[Gastric carcinoma|gastric carcinomas]] do not have a [[precancerous]] lesion. [[Somatic]] [[mutations]] in the ''[[CDH1 (gene)|CDH1]]'' [[gene]] by hypermethylation, [[mutation]], and [[loss of heterozygosity]] are identified in 40 to 83 percent of sporadic diffuse-type [[Gastric cancer|gastric cancers]]. The [[E-cadherin]] [[gene]] (''CDH1'') encodes a [[Transmembrane protein|transmembrane cellular adhesion protein]]. | ||
== Stomach cancer causes == | == Stomach cancer causes == | ||
Causes of stomach cancer depend upon the type of cancer: | Causes of [[stomach cancer]] depend upon the type of [[cancer]]:<ref name="pmid27722154">{{cite journal |vauthors=Cheng XJ, Lin JC, Tu SP |title=Etiology and Prevention of Gastric Cancer |journal=Gastrointest Tumors |volume=3 |issue=1 |pages=25–36 |date=September 2016 |pmid=27722154 |pmc=5040890 |doi=10.1159/000443995 |url=}}</ref><ref name="pmid23639637">{{cite journal |vauthors=Correa P |title=Gastric cancer: overview |journal=Gastroenterol. Clin. North Am. |volume=42 |issue=2 |pages=211–7 |date=June 2013 |pmid=23639637 |pmc=3995345 |doi=10.1016/j.gtc.2013.01.002 |url=}}</ref><ref name="pmid15367571">{{cite journal |vauthors=Corley DA, Kubo A |title=Influence of site classification on cancer incidence rates: an analysis of gastric cardia carcinomas |journal=J. Natl. Cancer Inst. |volume=96 |issue=18 |pages=1383–7 |date=September 2004 |pmid=15367571 |doi=10.1093/jnci/djh265 |url=}}</ref><ref name="pmid16555931">{{cite journal |vauthors=Ramos-de la Medina A, More H, Medina-Franco H, Humar B, Gamboa A, Ortiz LJ, Donohue JH, Guilford P |title=Single nucleotide polymorphisms (SNPs) at CDH1 promoter region in familial gastric cancer |journal=Rev Esp Enferm Dig |volume=98 |issue=1 |pages=36–41 |date=January 2006 |pmid=16555931 |doi= |url=}}</ref> | ||
==== Adenocarcinoma ==== | ==== Adenocarcinoma ==== | ||
* Adenocarcinomas are caused by [[genetic]] modulations due to [[chronic inflammation]] mainly by H. pylori bacteria. | * [[Adenocarcinomas]] are caused by [[genetic]] modulations due to [[chronic inflammation]] mainly by [[H. pylori]] [[bacteria]].<ref name="pmid15367571">{{cite journal |vauthors=Corley DA, Kubo A |title=Influence of site classification on cancer incidence rates: an analysis of gastric cardia carcinomas |journal=J. Natl. Cancer Inst. |volume=96 |issue=18 |pages=1383–7 |date=September 2004 |pmid=15367571 |doi=10.1093/jnci/djh265 |url=}}</ref><ref name="pmid19798449">{{cite journal |vauthors=Ooi CH, Ivanova T, Wu J, Lee M, Tan IB, Tao J, Ward L, Koo JH, Gopalakrishnan V, Zhu Y, Cheng LL, Lee J, Rha SY, Chung HC, Ganesan K, So J, Soo KC, Lim D, Chan WH, Wong WK, Bowtell D, Yeoh KG, Grabsch H, Boussioutas A, Tan P |title=Oncogenic pathway combinations predict clinical prognosis in gastric cancer |journal=PLoS Genet. |volume=5 |issue=10 |pages=e1000676 |date=October 2009 |pmid=19798449 |pmc=2748685 |doi=10.1371/journal.pgen.1000676 |url=}}</ref> | ||
* ''[[Ras oncogene|K-ras]]'' [[Mutations|mutations oncogenes]] are found in [[Invasive (medical)|invasive]] [[Cancer|cancers]] and | * ''[[Ras oncogene|K-ras]]'' [[Mutations|mutations oncogenes]] are found in [[Invasive (medical)|invasive]] [[Cancer|cancers]] and [[intestinal]] [[metaplasia]]. | ||
* [[Hepatocyte growth factor]] [[Receptor (biochemistry)|receptor]] c''-met'' [[oncogene]] is found in intestinal-type gastric cancers. | * [[Hepatocyte growth factor]] [[Receptor (biochemistry)|receptor]] c''-met'' [[oncogene]] is found in intestinal-type [[Gastric cancer|gastric cancers]]. | ||
* Almost 50% of gastric cancers have alterations in [[genes]] ''[[TP53 (gene)|TP53]],'' ''[[TP73L|TP73]]'', ''[[APC]]'', ''TFF'', ''[[DCC1|DCC]]'', ''LOH'', and ''[[FHIT]].'' | * Almost 50% of [[Gastric cancer|gastric cancers]] have alterations in [[genes]] ''[[TP53 (gene)|TP53]],'' ''[[TP73L|TP73]]'', ''[[APC]]'', ''TFF'', ''[[DCC1|DCC]]'', ''LOH'', and ''[[FHIT]].'' | ||
* Inactivation of [[P53 (protein)|p53]] in | * Inactivation of [[P53 (protein)|p53]] in [[gastric]] [[epithelial cells]] reduce their ability to undergo [[apoptosis]]. | ||
==== Diffuse gastric carcinoma ==== | ==== Diffuse gastric carcinoma ==== | ||
* Diffuse gastric carcinomas do not have a [[precancerous]] | * Diffuse [[Gastric carcinoma|gastric carcinomas]] do not have a [[precancerous]] [[lesion]]. | ||
* [[Somatic]] [[mutations]] in the ''CDH1'' [[gene]] by hypermethylation, [[mutation]], and [[loss of heterozygosity]] are identified in 40 to 83 percent of sporadic diffuse-type gastric cancers. The [[E-cadherin]] [[gene]] (''CDH1'') encodes a [[Transmembrane protein|transmembrane cellular adhesion protein]]. | * [[Somatic]] [[mutations]] in the ''CDH1'' [[gene]] by hypermethylation, [[mutation]], and [[loss of heterozygosity]] are identified in 40 to 83 percent of sporadic [[diffuse]]-type [[Gastric cancer|gastric cancers]]. The [[E-cadherin]] [[gene]] (''CDH1'') encodes a [[Transmembrane protein|transmembrane cellular adhesion protein]].<ref name="pmid14630673">{{cite journal |vauthors=Graziano F, Humar B, Guilford P |title=The role of the E-cadherin gene (CDH1) in diffuse gastric cancer susceptibility: from the laboratory to clinical practice |journal=Ann. Oncol. |volume=14 |issue=12 |pages=1705–13 |date=December 2003 |pmid=14630673 |doi= |url=}}</ref><ref name="pmid16555931">{{cite journal |vauthors=Ramos-de la Medina A, More H, Medina-Franco H, Humar B, Gamboa A, Ortiz LJ, Donohue JH, Guilford P |title=Single nucleotide polymorphisms (SNPs) at CDH1 promoter region in familial gastric cancer |journal=Rev Esp Enferm Dig |volume=98 |issue=1 |pages=36–41 |date=January 2006 |pmid=16555931 |doi= |url=}}</ref> | ||
* Prostate [[stem cell]] [[antigen]] [[gene]] is also involved in regulating | * [[Prostate]] [[stem cell]] [[antigen]] [[gene]] is also involved in regulating [[gastric]] [[Epithelium|epithelial cell]] [[proliferation]]. Its [[Cytoplasm|cytoplasmic]] tail interacts with [[Catenin|catenins]] making the [[Cell adhesion molecule|adhesion]]. | ||
==References== | ==References== | ||
Latest revision as of 15:47, 16 January 2019
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omer Kamal, M.D.[2], Mohammed Abdelwahed M.D[3]
Overview
Causes of stomach cancer depend on the type of cancer. Adenocarcinomas are caused by genetic modulations due to chronic inflammation mainly by H. pylori infection. Diffuse gastric carcinomas do not have a precancerous lesion. Somatic mutations in the CDH1 gene by hypermethylation, mutation, and loss of heterozygosity are identified in 40 to 83 percent of sporadic diffuse-type gastric cancers. The E-cadherin gene (CDH1) encodes a transmembrane cellular adhesion protein.
Stomach cancer causes
Causes of stomach cancer depend upon the type of cancer:[1][2][3][4]
Adenocarcinoma
- Adenocarcinomas are caused by genetic modulations due to chronic inflammation mainly by H. pylori bacteria.[3][5]
- K-ras mutations oncogenes are found in invasive cancers and intestinal metaplasia.
- Hepatocyte growth factor receptor c-met oncogene is found in intestinal-type gastric cancers.
- Almost 50% of gastric cancers have alterations in genes TP53, TP73, APC, TFF, DCC, LOH, and FHIT.
- Inactivation of p53 in gastric epithelial cells reduce their ability to undergo apoptosis.
Diffuse gastric carcinoma
- Diffuse gastric carcinomas do not have a precancerous lesion.
- Somatic mutations in the CDH1 gene by hypermethylation, mutation, and loss of heterozygosity are identified in 40 to 83 percent of sporadic diffuse-type gastric cancers. The E-cadherin gene (CDH1) encodes a transmembrane cellular adhesion protein.[6][4]
- Prostate stem cell antigen gene is also involved in regulating gastric epithelial cell proliferation. Its cytoplasmic tail interacts with catenins making the adhesion.
References
- ↑ Cheng XJ, Lin JC, Tu SP (September 2016). "Etiology and Prevention of Gastric Cancer". Gastrointest Tumors. 3 (1): 25–36. doi:10.1159/000443995. PMC 5040890. PMID 27722154.
- ↑ Correa P (June 2013). "Gastric cancer: overview". Gastroenterol. Clin. North Am. 42 (2): 211–7. doi:10.1016/j.gtc.2013.01.002. PMC 3995345. PMID 23639637.
- ↑ 3.0 3.1 Corley DA, Kubo A (September 2004). "Influence of site classification on cancer incidence rates: an analysis of gastric cardia carcinomas". J. Natl. Cancer Inst. 96 (18): 1383–7. doi:10.1093/jnci/djh265. PMID 15367571.
- ↑ 4.0 4.1 Ramos-de la Medina A, More H, Medina-Franco H, Humar B, Gamboa A, Ortiz LJ, Donohue JH, Guilford P (January 2006). "Single nucleotide polymorphisms (SNPs) at CDH1 promoter region in familial gastric cancer". Rev Esp Enferm Dig. 98 (1): 36–41. PMID 16555931.
- ↑ Ooi CH, Ivanova T, Wu J, Lee M, Tan IB, Tao J, Ward L, Koo JH, Gopalakrishnan V, Zhu Y, Cheng LL, Lee J, Rha SY, Chung HC, Ganesan K, So J, Soo KC, Lim D, Chan WH, Wong WK, Bowtell D, Yeoh KG, Grabsch H, Boussioutas A, Tan P (October 2009). "Oncogenic pathway combinations predict clinical prognosis in gastric cancer". PLoS Genet. 5 (10): e1000676. doi:10.1371/journal.pgen.1000676. PMC 2748685. PMID 19798449.
- ↑ Graziano F, Humar B, Guilford P (December 2003). "The role of the E-cadherin gene (CDH1) in diffuse gastric cancer susceptibility: from the laboratory to clinical practice". Ann. Oncol. 14 (12): 1705–13. PMID 14630673.