Gastric Cancer as Preventable Disease
Gastric cancer, 1 of the 5 most common causes of cancer death, is associated with a 5-year overall survival rate less than 30%. A minority of cancers occurs as part of syndromic diseases; more than 90% of adenocarcinomas are considered as the ultimate consequence of a longstanding mucosal inflammati...
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| Published in | Clinical gastroenterology and hepatology Vol. 15; no. 12; pp. 1833 - 1843 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.12.2017
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1542-3565 1542-7714 1542-7714 |
| DOI | 10.1016/j.cgh.2017.05.023 |
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| Abstract | Gastric cancer, 1 of the 5 most common causes of cancer death, is associated with a 5-year overall survival rate less than 30%. A minority of cancers occurs as part of syndromic diseases; more than 90% of adenocarcinomas are considered as the ultimate consequence of a longstanding mucosal inflammation. Helicobacter pylori infection is the leading etiology of non–self-limiting gastritis, which may result in atrophy of the gastric mucosa and impaired acid secretion. Gastric atrophy establishes a field of cancerization prone to further molecular and phenotypic changes, possibly resulting in cancer growth. This well-understood natural history provides the clinicopathologic rationale for primary and secondary cancer prevention strategies. A large body of evidence demonstrates that combined primary (H pylori eradication) and secondary (mainly endoscopy) prevention efforts may prevent or limit the progression of gastric oncogenesis. This approach, which is tailored to different country-specific gastric cancer incidence, socioeconomic, and cultural factors, requires that the complementary competences of gastroenterologists, oncologists, and pathologists be amalgamated into a common strategy of health policy. |
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| AbstractList | Gastric cancer, 1 of the 5 most common causes of cancer death, is associated with a 5-year overall survival rate less than 30%. A minority of cancers occurs as part of syndromic diseases; more than 90% of adenocarcinomas are considered as the ultimate consequence of a longstanding mucosal inflammation. Helicobacter pylori infection is the leading etiology of non–self-limiting gastritis, which may result in atrophy of the gastric mucosa and impaired acid secretion. Gastric atrophy establishes a field of cancerization prone to further molecular and phenotypic changes, possibly resulting in cancer growth. This well-understood natural history provides the clinicopathologic rationale for primary and secondary cancer prevention strategies. A large body of evidence demonstrates that combined primary (H pylori eradication) and secondary (mainly endoscopy) prevention efforts may prevent or limit the progression of gastric oncogenesis. This approach, which is tailored to different country-specific gastric cancer incidence, socioeconomic, and cultural factors, requires that the complementary competences of gastroenterologists, oncologists, and pathologists be amalgamated into a common strategy of health policy. Gastric cancer, 1 of the 5 most common causes of cancer death, is associated with a 5-year overall survival rate less than 30%. A minority of cancers occurs as part of syndromic diseases; more than 90% of adenocarcinomas are considered as the ultimate consequence of a longstanding mucosal inflammation. Helicobacter pylori infection is the leading etiology of non-self-limiting gastritis, which may result in atrophy of the gastric mucosa and impaired acid secretion. Gastric atrophy establishes a field of cancerization prone to further molecular and phenotypic changes, possibly resulting in cancer growth. This well-understood natural history provides the clinicopathologic rationale for primary and secondary cancer prevention strategies. A large body of evidence demonstrates that combined primary (H pylori eradication) and secondary (mainly endoscopy) prevention efforts may prevent or limit the progression of gastric oncogenesis. This approach, which is tailored to different country-specific gastric cancer incidence, socioeconomic, and cultural factors, requires that the complementary competences of gastroenterologists, oncologists, and pathologists be amalgamated into a common strategy of health policy.Gastric cancer, 1 of the 5 most common causes of cancer death, is associated with a 5-year overall survival rate less than 30%. A minority of cancers occurs as part of syndromic diseases; more than 90% of adenocarcinomas are considered as the ultimate consequence of a longstanding mucosal inflammation. Helicobacter pylori infection is the leading etiology of non-self-limiting gastritis, which may result in atrophy of the gastric mucosa and impaired acid secretion. Gastric atrophy establishes a field of cancerization prone to further molecular and phenotypic changes, possibly resulting in cancer growth. This well-understood natural history provides the clinicopathologic rationale for primary and secondary cancer prevention strategies. A large body of evidence demonstrates that combined primary (H pylori eradication) and secondary (mainly endoscopy) prevention efforts may prevent or limit the progression of gastric oncogenesis. This approach, which is tailored to different country-specific gastric cancer incidence, socioeconomic, and cultural factors, requires that the complementary competences of gastroenterologists, oncologists, and pathologists be amalgamated into a common strategy of health policy. |
| Author | Hunt, Richard H. Sugano, Kentaro El-Serag, Hashem B. El-Omar, Emad M. Fassan, Matteo Kuipers, Ernst J. Di Mario, Francesco Graham, David Y. Rugge, Massimo Genta, Robert M. Malfertheiner, Peter |
| Author_xml | – sequence: 1 givenname: Massimo surname: Rugge fullname: Rugge, Massimo email: massimo.rugge@unipd.it organization: Department of Medicine (DIMED), University of Padua, Padua, Italy – sequence: 2 givenname: Robert M. surname: Genta fullname: Genta, Robert M. organization: Miraca Life Sciences Research Institute, Irving, and Departments of Pathology and Medicine, Baylor College of Medicine, Houston, Texas – sequence: 3 givenname: Francesco surname: Di Mario fullname: Di Mario, Francesco organization: Department of Clinical and Experimental Medicine, University of Parma, Parma, Italy – sequence: 4 givenname: Emad M. surname: El-Omar fullname: El-Omar, Emad M. organization: St George and Sutherland Clinical School, University of New South Wales, Sydney, Australia – sequence: 5 givenname: Hashem B. surname: El-Serag fullname: El-Serag, Hashem B. organization: Department of Medicine, Michael E. DeBakey VA Medical Center, Baylor College of Medicine, Houston, Texas – sequence: 6 givenname: Matteo surname: Fassan fullname: Fassan, Matteo organization: Department of Medicine (DIMED), University of Padua, Padua, Italy – sequence: 7 givenname: Richard H. surname: Hunt fullname: Hunt, Richard H. organization: Division of Gastroenterology, Department of Medicine and Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Canada – sequence: 8 givenname: Ernst J. surname: Kuipers fullname: Kuipers, Ernst J. organization: Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands – sequence: 9 givenname: Peter surname: Malfertheiner fullname: Malfertheiner, Peter organization: Department of Gastroenterology, University of Magdeburg, Magdeburg, Germany – sequence: 10 givenname: Kentaro surname: Sugano fullname: Sugano, Kentaro organization: Department of Medicine, Jichi Medical University, Tochigi, Japan – sequence: 11 givenname: David Y. surname: Graham fullname: Graham, David Y. organization: Department of Medicine, Michael E. DeBakey VA Medical Center, Baylor College of Medicine, Houston, Texas |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28532700$$D View this record in MEDLINE/PubMed |
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| Title | Gastric Cancer as Preventable Disease |
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