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Precision Medicine Approaches to Prevent Gastric Cancer

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Gastric cancer remains one of the most common causes of cancer-related death worldwide, although the incidence is declining gradually. The primary risk factor for gastric cancer is Helicobacter pylori infection. The Kyoto global consensus report recommends eradication of H. pylori in all infected patients. However, because it is difficult to stratify the risk of carcinogenesis among patients with a history of H. pylori infection, annual endoscopic surveillance is performed for everyone after eradication. This review summarizes the current approaches used to screen for novel molecules that could assist in the diagnosis of gastric cancer and reduce mortality. Most well-studied molecules are tissue protein biomarkers expressed by the gastric epithelium and associated with metaplasia-dysplasia-carcinoma sequences. Other strategies focus on the origin of cancer stem cell-related markers, such as CD44, and immune reaction-related markers, such as matrix metallopeptidases. Noninvasive methods such as blood-based approaches are more attractive. Serum pepsinogen levels predict the severity of gastric mucosal atrophy before H. pylori eradication, whereas plasma ghrelin levels are associated with atrophy even after eradication. Cell-free DNAs and RNAs are attractive tools for the early detection of cancer. These ideas could lead to the development of more personalized strategies for cancer prevention based on cuttingedge technologies.

Abstract

Gastric cancer remains one of the most common causes of cancer-related death worldwide, although the incidence is declining gradually. The primary risk factor for gastric cancer is Helicobacter pylori infection. The Kyoto global consensus report recommends eradication of H. pylori in all infected patients. However, because it is difficult to stratify the risk of carcinogenesis among patients with a history of H. pylori infection, annual endoscopic surveillance is performed for everyone after eradication. This review summarizes the current approaches used to screen for novel molecules that could assist in the diagnosis of gastric cancer and reduce mortality. Most well-studied molecules are tissue protein biomarkers expressed by the gastric epithelium and associated with metaplasia-dysplasia-carcinoma sequences. Other strategies focus on the origin of cancer stem cell-related markers, such as CD44, and immune reaction-related markers, such as matrix metallopeptidases. Noninvasive methods such as blood-based approaches are more attractive. Serum pepsinogen levels predict the severity of gastric mucosal atrophy before H. pylori eradication, whereas plasma ghrelin levels are associated with atrophy even after eradication. Cell-free DNAs and RNAs are attractive tools for the early detection of cancer. These ideas could lead to the development of more personalized strategies for cancer prevention based on cuttingedge technologies.

참고문헌 (100)

  1. Ferlay J, "Estimating the global cancer incidence and mortality in 2018 : GLOBOCAN sources and methods", Int J Cancer, 144, pp.1941~1953 (2019)
  2. Helicobacter, "Gastric cancer and Helicobacter pylori : a combined analysis of 12case control studies nested within prospective cohorts", Gut, 49, pp.347~353 (2001)
  3. Zhang X, "Endoscopic screening in Asian countries is associated with reduced gastric cancer mortality : a meta-analysis and systematic review", Gastroenterology, 155, pp.347~354 (2018)
  4. Suzuki H, "Gastric cancer : evidence boosts Helicobacter pylori eradication", Nat Rev Gastroenterol Hepatol, 15, pp.458~460 (2018)
  5. Choi IJ, "Helicobacter pylori therapy for the prevention of metachronous gastric cancer", N Engl J Med, 378, pp.1085~1095 (2018)
  6. Fukase K, "Effect of eradication of Helicobacter pylori on incidence of metachronous gastric carcinoma after endoscopic resection of early gastric cancer : an open-label, randomised controlled trial", Lancet, 372, pp.392~397 (2008)
  7. Ma JL, "Fifteen-year effects of Helicobacter pylori, garlic, and vitamin treatments on gastric cancer incidence and mortality", J Natl Cancer Inst, 104, pp.488~492 (2012)
  8. Mera RM, "Dynamics of Helicobacter pylori infection as a determinant of progression of gastric precancerous lesions : 16-year follow-up of an eradication trial", Gut, 67, pp.1239~1246 (2018)
  9. Sugano K, "Kyoto global consensus report on Helicobacter pylori gastritis", Gut, 64, pp.1353~1367 (2015)
  10. Suzuki H, "Helicobacter pylori : Helicobacter pylori gastritis : a novel distinct disease entity", Nat Rev Gastroenterol Hepatol, 12, pp.556~557 (2015)
  11. Malfertheiner P, "Management of Helicobacter pylori infection-the Maastricht V", Florence Consensus Report, 2017, pp.66, 6~30
  12. Sugano K, "Effect of Helicobacter pylori eradication on the incidence of gastric cancer : a systematic review and metaanalysis", Gastric Cancer, 22, pp.435~445 (2019)
  13. Uemura N, "Helicobacter pylori infection and the development of gastric cancer", N Engl J Med, 345, pp.784~789 (2001)
  14. Malfertheiner P, "Helicobacter pylori treatment for gastric cancer prevention", N Engl J Med, 378, pp.1154~1156 (2018)
  15. Tan MC, "Gastric cancer risk stratification and surveillance after Helicobacter pylori eradication : 2020", Gastrointest Endosc, 90, pp.457~460 (2019)
  16. Rugge M, "Gastritis OLGA-staging and gastric cancer risk : a twelve-year clinico-pathological follow-up study", Aliment Pharmacol Ther, 31, pp.1104~1111 (2010)
  17. Rugge M, "Gastritis staging in clinical practice : the OLGA staging system", Gut, 56, pp.631~636 (2007)
  18. Dixon MF, "Classification and grading of gastritis: the updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994", Am J Surg Pathol, 20, pp.1161~1181 (1996)
  19. Rugge M, "Gastritis staging in the endoscopic follow-up for the secondary prevention of gastric cancer : a 5-year prospective study of 1755 patients", Gut, 68, pp.11~17 (2019)
  20. Kimura K, "An endoscopic recognition of the atrophic border and its significance in chronic gastritis", Endoscopy, 1, pp.87~97 (1969)
  21. Ito S, "Profile of Helicobacter pylori cytotoxin derived from two areas of Japan with different prevalence of atrophic gastritis", Gut, 39, pp.800~806 (1996)
  22. Hirata K, "CD44 variant 9 expression in primary early gastric cancer as a predictive marker for recurrence", Br J Cancer, 109, pp.379~386 (2013)
  23. Masuyama H, "Relationship between the degree of endoscopic atrophy of the gastric mucosa and carcinogenic risk", Digestion, 91, pp.30~36 (2015)
  24. Majima A, "Linked color imaging identifies important risk factors associated with gastric cancer after successful eradication of Helicobacter pylori", Gastrointest Endosc, 90, pp.763~769 (2019)
  25. Rugge M, "Gastric cancer prevention targeted on risk assessment : Gastritis OLGA staging", Helicobacter, 24, pp.e12571~ (2019)
  26. Minegishi Y, "Reduced Shh expression in TFF2-overexpressing lesions of the gastric fundus under hypochlorhydric conditions", J Pathol, 213, pp.161~169 (2007)
  27. Grötzinger C, "LI-cadherin : a marker of gastric metaplasia and neoplasia", Gut, 49, pp.73~81 (2001)
  28. Matsuzaki J, "Bile acids increase levels of microRNAs 221 and 222, leading to degradation of CDX2 during esophageal carcinogenesis", Gastroenterology, 145, pp.1300~1311 (2013)
  29. Dixon MF, "Bile reflux gastritis and intestinal metaplasia at the cardia", Gut, 51, pp.351~355 (2002)
  30. Huo X, "Deoxycholic acid causes DNA damage while inducing apoptotic resistance through NF-κB activation in benign Barrett’s epithelial cells", Am J Physiol Gastrointest Liver Physiol, 301, pp.G278~ (2011)
  31. Jenkins GJ, "Deoxycholic acid at neutral and acid pH, is genotoxic to oesophageal cells through the induction of ROS : the potential role of anti-oxidants in Barrett’s oesophagus", Carcinogenesis, 28, pp.136~142 (2007)
  32. McAdam E, "Reflux composition influences the level of NF-κB activation and upstream kinase preference in oesophageal adenocarcinoma cells", Int J Cancer, 136, pp.527~535 (2015)
  33. Cronin J, "Epidermal growth factor receptor(EGFR)is overexpressed in high-grade dysplasia and adenocarcinoma of the esophagus and may represent a biomarker of histological progression in Barrett’s esophagus(BE)", Am J Gastroenterol, 106, pp.46~56 (2011)
  34. Saito Y, "Development of a novel microRNA promoter microarray for ChIP-on-chip assay to identify epigenetically regulated microRNAs", Biochem Biophys Res Commun, 426, pp.33~37 (2012)
  35. Saito Y, "Chromatin remodeling at Alu repeats by epigenetic treatment activates silenced microRNA-512-5p with downregulation of Mcl-1 in human gastric cancer cells", Oncogene, 28, pp.2738~2744 (2009)
  36. Suzuki R, "Aberrant methylation of microRNA-34b", c is a predictive marker of metachronous gastric cancer risk, 2014, pp.49, 1135~1144
  37. Asada K, "Demonstration of the usefulness of epigenetic cancer risk prediction by a multicentre prospective cohort study", Gut, 64, pp.388~396 (2015)
  38. Garcia M, "In vitro culture and phenotypic and molecular characterization of gastric stem cells from human stomach", Helicobacter, 22, pp.12351~ (2017)
  39. Zavros Y, "Initiation and maintenance of gastric cancer : a focus on CD44 variant isoforms and cancer stem cells", Cell Mol Gastroenterol Hepatol, 4, pp.55~63 (2017)
  40. Lau WM, "CD44v8-10 is a cancerspecific marker for gastric cancer stem cells", Cancer Res, 74, pp.2630~2641 (2014)
  41. Ishimoto T, "CD44 variant regulates redox status in cancer cells by stabilizing the xCT subunit of system xc(-)and thereby promotes tumor growth", Cancer Cell, 19, pp.387~400 (2011)
  42. Miyoshi S, "Inhibiting xCT improves 5-fluorouracil resistance of gastric cancer induced by CD44 variant 9 expression", Anticancer Res, 38, pp.6163~6170 (2018)
  43. Ishimoto T, "Chronic inflammation with Helicobacter pylori infection is implicated in CD44overexpression through miR-328 suppression in the gastric mucosa", J Gastroenterol, 50, pp.751~757 (2015)
  44. Bertaux-Skeirik N, "CD44 variant isoform 9 emerges in response to injury and contributes to the regeneration of the gastric epithelium", J Pathol, 242, pp.463~475 (2017)
  45. Tsugawa H, "Cancer stem-cell marker CD44v9-positive cells arise from Helicobacter pylori-infected CAPZA1-overexpressing cells", Cell Mol Gastroenterol Hepatol, 8, pp.319~334 (2019)
  46. Higashi H, "SHP-2 tyrosine phosphatase as an intracellular target of Helicobacter pylori CagA protein", Science, 295, pp.683~686 (2002)
  47. Nguyen LT, "Helicobacter pylori virulence and the diversity of gastric cancer in Asia", J Med Microbiol (2008)
  48. Azuma T, "Distinct diversity of the cag pathogenicity island among Helicobacter pylori strains in Japan", J Clin Microbiol, 42, pp.2508~2517 (2004)
  49. Tsugawa H, "Reactive oxygen speciesinduced autophagic degradation of Helicobacter pylori CagA is specifically suppressed in cancer stem-like cells", Cell Host Microbe, 12, pp.764~777 (2012)
  50. Tsugawa H, "CAPZA1 determines the risk of gastric carcinogenesis by inhibiting Helicobacter pylori CagA-degraded autophagy", Autophagy, 15, pp.242~258 (2019)
  51. Wada T, "Functional role of CD44v-xCT system in the development of spasmolytic polypeptide-expressing metaplasia", Cancer Sci, 104, pp.1323~1329 (2013)
  52. Heider KH, "Differential expression of CD44 splice variants in intestinal-and diffusetype human gastric carcinomas and normal gastric mucosa", Cancer Res, 53, pp.4197~4203 (1993)
  53. Bertaux-Skeirik N, "CD44plays a functional role in Helicobacter pylori-induced epithelial cell proliferation", PLoS Pathog, 11, pp.e1004663~ (2015)
  54. Sougleri IS, "Helicobacter pylori CagA protein induces factors involved in the epithelial to mesenchymal transition(EMT)in infected gastric epithelial cells in an EPIYA-phosphorylation-dependent manner", FEBS J, 283, pp.206~220 (2016)
  55. Costa AM, "Helicobacter pylori activates matrix metalloproteinase 10 in gastric epithelial cells via EGFR and ERK-mediated pathways", J Infect Dis, 213, pp.1767~1776 (2016)
  56. Nam YH, "CagA phosphorylation-dependent MMP-9 expression in gastric epithelial cells", Helicobacter, 16, pp.276~283 (2011)
  57. Yin Y, "Helicobacter pylori potentiates epithelial : mesenchymal transition in gastric cancer : links to soluble HB-EGF, gastrin and matrix metalloproteinase-7", Gut, 59, pp.1037~1045 (2010)
  58. Lv YP, "Helicobacter pylori-induced matrix metallopeptidase-10 promotes gastric bacterial colonization and gastritis", Sci Adv, 5, pp.eaau6547~ (2019)
  59. Hung KH, "Host single nucleotide polymorphisms of MMP-9-1562", TIMP1 372 have gender differences in the risk of gastric intestinal metaplasia after Helicobacter pylori infection, 2009, pp.14, 580~587
  60. Krakowiak MS, "Matrix metalloproteinase 7 restrains Helicobacter pylori-induced gastric inflammation and premalignant lesions in the stomach by altering macrophage polarization", Oncogene, 34, pp.1865~1871 (2015)
  61. Ogden SR, "Matrix metalloproteinase-7 and premalignant host responses in Helicobacter pylori-infected mice", Cancer Res, 70, pp.30~35 (2010)
  62. Maldonado-Contreras A, "Structure of the human gastric bacterial community in relation to Helicobacter pylori status", ISME J, 5, pp.574~579 (2011)
  63. Jo HJ, "Analysis of gastric microbiota by pyrosequencing : minor role of bacteria other than Helicobacter pylori in the gastric carcinogenesis", Helicobacter, 21, pp.364~374 (2016)
  64. Schulz C, "The active bacterial assemblages of the upper GI tract in individuals with and without Helicobacter infection", Gut, 67, pp.216~225 (2018)
  65. Lofgren JL, "Lack of commensal flora in Helicobacter pylori-infected INS-GAS mice reduces gastritis and delays intraepithelial neoplasia", Gastroenterology, 140, pp.210~220 (2011)
  66. Lertpiriyapong K, "Gastric colonisation with a restricted commensal microbiota replicates the promotion of neoplastic lesions by diverse intestinal microbiota in the Helicobacter pylori INS-GAS mouse model of gastric carcinogenesis", Gut, 63, pp.54~63 (2014)
  67. Ferreira RM, "Gastric microbial community profiling reveals a dysbiotic cancer-associated microbiota", Gut, 67, pp.226~236 (2018)
  68. Yang I, "Different gastric microbiota compositions in two human populations with high and low gastric cancer risk in Colombia", Sci Rep, 6, pp.18594~ (2016)
  69. Mukaisho K, "Two distinct etiologies of gastric cardia adenocarcinoma : interactions among pH, Helicobacter pylori, and bile acids", Front Microbiol, 6, pp.412~ (2015)
  70. Suo M, "Thioproline prevents carcinogenesis in the remnant stomach induced by duodenal reflux", Cancer Lett, 237, pp.256~262 (2006)
  71. Samloff IM, "Relationships among serum pepsinogen I, serum pepsinogen II, and gastric mucosal histology: a study in relatives of patients with pernicious anemia", Gastroenterology, 83(1 Pt 2), pp.204~209 (1982)
  72. Song M, "Serum pepsinogen 1 and anti-Helicobacter pylori IgG antibodies as predictors of gastric cancer risk in Finnish males", Aliment Pharmacol Ther, 47, pp.494~503 (2018)
  73. Oishi Y, "The serum pepsinogen test as a predictor of gastric cancer : the Hisayama study", Am J Epidemiol, 163, pp.629~637 (2006)
  74. Ren JS, "Serum pepsinogens and risk of gastric and oesophageal cancers in the General Population Nutrition Intervention Trial cohort", Gut, 58, pp.636~642 (2009)
  75. Ikeda F, "Combination of Helicobacter pylori antibody and serum pepsinogen as a good predictive tool of gastric cancer incidence : 20-year prospective data from the Hisayama study", J Epidemiol, 26, pp.629~636 (2016)
  76. Leja M, "Pepsinogen testing for evaluation of the success of Helicobacter pylori eradication at 4 weeks after completion of therapy", Medicina(Kaunas), 50, pp.8~13 (2014)
  77. Hirata K, "Improvement of reflux symptom related quality of life after Helicobacter pylori eradication therapy", J Clin Biochem Nutr, 52, pp.172~178 (2013)
  78. Isomoto H, "Circulating ghrelin levels in patients with various upper gastrointestinal diseases", Dig Dis Sci, 50, pp.833~838 (2005)
  79. Suzuki H, "Plasma ghrelin concentration correlates with the levels of serum pepsinogen I and pepsinogen I", II ratio : a possible novel and noninvasive marker for gastric atrophy, 2004, pp.51, 1249~1254
  80. Kawashima J, "Circulating acylated ghrelin level decreases in accordance with the extent of atrophic gastritis", J Gastroenterol, 44, pp.1046~1054 (2009)
  81. Kuo HY, "Serum level of trefoil factor 2 can predict the extent of gastric spasmolytic polypeptide-expressing metaplasia in the H. pylori-infected gastric cancer relatives", Helicobacter, 22, pp.12320~ (2017)
  82. Kaise M, "The combination of serum trefoil factor 3 and pepsinogen testing is a valid nonendoscopic biomarker for predicting the presence of gastric cancer : a new marker for gastric cancer risk", J Gastroenterol, 46, pp.736~745 (2011)
  83. Lee HS, "Screening biomarker as an alternative to endoscopy for the detection of early gastric cancer : the combination of serum trefoil factor family 3 and pepsinogen", Gastroenterol Res Pract, 2018, pp.1024074~ (2018)
  84. Huang Z, "Serum trefoil factor 3 is a promising non-invasive biomarker for gastric cancer screening : a monocentric cohort study in China", BMC Gastroenterol, 14, pp.74~ (2014)
  85. Matsuzaki J, "Circulating microRNAs and extracellular vesicles as potential cancer biomarkers : a systematic review", Int J Clin Oncol, 22, pp.413~420 (2017)
  86. Gao Y, "Diagnostic and prognostic value of circulating tumor DNA in gastric cancer : a meta-analysis", Oncotarget, 8, pp.6330~6340 (2017)
  87. Rosenfeld N, "MicroRNAs accurately identify cancer tissue origin", Nat Biotechnol, 26, pp.462~469 (2008)
  88. Kosaka N, "Secretory mechanisms and intercellular transfer of microRNAs in living cells", J Biol Chem, 285, pp.17442~17452 (2010)
  89. Valadi H, "Exosome-mediated transfer of mRNAs and microRNAs is a novel mechanism of genetic exchange between cells", Nat Cell Biol, 9, pp.654~659 (2007)
  90. Shin VY, "A threemiRNA signature as promising non-invasive diagnostic marker for gastric cancer", Mol Cancer, 14, pp.202~ (2015)
  91. Liu R, "A five-microRNA signature identified from genome-wide serum microRNA expression profiling serves as a fingerprint for gastric cancer diagnosis", Eur J Cancer, 47, pp.784~791 (2011)
  92. Zhou X, "Diagnostic value of a plasma microRNA signature in gastric cancer : a microRNA expression analysis", Sci Rep, 5, pp.11251~ (2015)
  93. Hou CG, "Diagnostic and prognostic value of serum microRNA-206 in patients with gastric cancer", Cell Physiol Biochem, 39, pp.1512~1520 (2016)
  94. Zhu C, "A five-microRNA panel in plasma was identified as potential biomarker for early detection of gastric cancer", Br J Cancer, 110, pp.2291~2299 (2014)
  95. Link A, "MicroRNAs as non-invasive diagnostic biomarkers for gastric cancer : current insights and future perspectives", World J Gastroenterol, 24, pp.3313~3329 (2018)
  96. Kloten V, "Multicenter evaluation of circulating plasma microRNA extraction technologies for the development of clinically feasible reverse transcription quantitative PCR and next-generation sequencing analytical work flows", Clin Chem, 65, pp.1132~1140 (2019)
  97. Li D, "The diagnostic performance of serum LIM homeobox transcription factor 1 alpha in patients with gastric cancer", Medicine(Baltimore), 98, pp.e15783~ (2019)
  98. Zhou X, "Identification of the long non-coding RNA H19 in plasma as a novel biomarker for diagnosis of gastric cancer", Sci Rep, 5, pp.11516~ (2015)
  99. Tan H, "Diagnostic value of circular RNAs as effective biomarkers for cancer : a systematic review and meta-analysis", Onco Targets Ther, 12, pp.2623~2633 (2019)
  100. Best MG, "Tumor-educated platelets as a noninvasive biomarker source for cancer detection and progression monitoring", Cancer Res, 78, pp.3407~3412 (2018)

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