Helicobacter and gastric cancer disease mechanisms: host response and disease susceptibility

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dc.contributor.authorLi, Hanchen
dc.contributor.authorStoicov, Calin
dc.contributor.authorCai, Xun
dc.contributor.authorWang, Timothy C.
dc.contributor.authorHoughton, JeanMarie
dc.contributor.departmentDepartment of Medicine, Division of Gastroenterology
dc.contributor.studentCalin Stoicov
dc.date2022-08-11T08:09:00.000
dc.date.accessioned2022-08-23T16:15:11Z
dc.date.available2022-08-23T16:15:11Z
dc.date.issued2003-11-07
dc.date.submitted2008-10-22
dc.description.abstractHelicobacter infection is the single most common cause of gastric cancer worldwide. Although infection prevention and eradication of established infection offer the potential for cure, these strategies are neither feasible nor practical for widespread implementation. Patients most at risk need to be identified and targeted for treatment. For disease to occur, bacterial, environmental, and nutritional factors require a genetically susceptible host. Consequently, it is important to understand how the organism interacts with the host to cause disease. Only through an understanding of what places a patient at risk can we hope to identify susceptible patients early enough in disease to have an impact on their outcome. The immune response is the single most important determinant of disease. Single nucleotide polymorphisms within the promoter region of several critical proinflammatory genes dramatically increase the risk of Helicobacter-associated gastric cancer. Additionally, environmental and dietary factors may modulate the immune response or directly influence key apoptotic and proliferative signaling cascades to alter disease presentation. Lastly, concurrent disease states may have a dramatic impact on the host response to Helicobacter infection and influence disease. An understanding of the immune signaling pathways responsible for disease and the ways in which environmental risk factors influence these pathways will allow identification of populations that are most at risk and targeted prevention and treatment strategies.
dc.identifier.citationCurr Gastroenterol Rep. 2003 Dec;5(6):459-67. DOI 10.1007/s11894-003-0034-6
dc.identifier.contextkey654571
dc.identifier.doi10.1007/s11894-003-0034-6
dc.identifier.issn1522-8037 (Print)
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/679
dc.identifier.pmid14602053
dc.identifier.submissionpathgsbs_sp/679
dc.identifier.urihttps://hdl.handle.net/20.500.14038/34028
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14602053&dopt=Abstract">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1007/s11894-003-0034-6
dc.source.issue6
dc.source.journaltitleCurrent gastroenterology reports
dc.source.pages459-67
dc.source.volume5
dc.titleHelicobacter and gastric cancer disease mechanisms: host response and disease susceptibility
dc.typeJournal Article
dspace.entity.typePublication
html.description.abstract<p>Helicobacter infection is the single most common cause of gastric cancer worldwide. Although infection prevention and eradication of established infection offer the potential for cure, these strategies are neither feasible nor practical for widespread implementation. Patients most at risk need to be identified and targeted for treatment. For disease to occur, bacterial, environmental, and nutritional factors require a genetically susceptible host. Consequently, it is important to understand how the organism interacts with the host to cause disease. Only through an understanding of what places a patient at risk can we hope to identify susceptible patients early enough in disease to have an impact on their outcome. The immune response is the single most important determinant of disease. Single nucleotide polymorphisms within the promoter region of several critical proinflammatory genes dramatically increase the risk of Helicobacter-associated gastric cancer. Additionally, environmental and dietary factors may modulate the immune response or directly influence key apoptotic and proliferative signaling cascades to alter disease presentation. Lastly, concurrent disease states may have a dramatic impact on the host response to Helicobacter infection and influence disease. An understanding of the immune signaling pathways responsible for disease and the ways in which environmental risk factors influence these pathways will allow identification of populations that are most at risk and targeted prevention and treatment strategies.</p>
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