Bravo LE, Quijano-Lievano ML

Language: Spanish
References: 16
Page: 162-166
PDF size: 252.66 Kb.

ABSTRACT

The objective of this work is to analyze the conceptual development of the sequential model of gastric carcinogenesis proposed by Professor Pelayo Correa, highlighting its transdisciplinary integration and its relevance for understanding population variations in the progression of the precancerous cascade and opportunities for prevention in Latin America. Correa’s model originated from epidemiological observations in Colombia and evolved into an integrative framework that combines natural history, pathology, molecular biology, host genetics, and bacterial virulence. The precancerous cascade –chronic gastritis, atrophy, intestinal metaplasia, dysplasia, and carcinoma– was validated as a dynamic and potentially reversible process modulated by the persistence of Helicobacter pylori. The chemoprevention trial conducted in Nariño demonstrated that H. pylori eradication accelerates regression of precursor lesions and substantially alters the trajectory of the cascade. A major conceptual contribution of the model is the incorporation of host-pathogen coevolution: incompatibility between human lineages and H. pylori strains of different ancestry helps explain the striking differences in disease risk among neighboring populations. This multilevel articulation –from natural history to molecular and evolutionary determinants– provides a robust foundation for primary prevention strategies and risk-based surveillance of precursor lesions. Correa’s work illustrates that chronic, long-lasting diseases require analytical approaches that inte- grate multiple biological and population-level dimensions. His model underscores H. pylori eradication as a key intervention point in gastric cancer prevention. In Latin America, where high-risk populations coexist with limited resources, this transdisciplinary framework offers guidance for cost-effective prevention and surveillance strategies adapted to diverse epidemiological and socio-environmental contexts.

REFERENCES

1. Correa P, Llanos G. Morbidity and mortality from cancer in Cali,Colombia. J Natl Cancer Inst. 1966;36(4):717-45. https://doi.org/10.1093/jnci/36.4.717

2. Correa P, Cuello C, Duque E. Carcinoma and intestinal metaplasia of thestomach in Colombian migrants. J Natl Cancer Inst. 1970;44(2):297-306.https://doi.org/10.1093/jnci/44.2.297

3. Correa P, Haenszel W, Cuello C, Tannenbaum S, Archer M. A model forgastric cancer epidemiology. Lancet. 1975;306(7924):58-60. https://doi.org/10.1016/S0140-6736(75)90498-5

4. Haenszel W, Correa P, Cuello C, Guzman N, Burbano LC, Lores H,Muñoz J. Gastric cancer in Colombia. II. Case-control epidemiologic studyof precursor lesions. J Natl Cancer Inst. 1976;57(5):1021-6. https://doi.org/10.1093/jnci/57.5.1021

5. Correa P, Haenszel W, Cuello C, Zavala D, Fontham E, Zarama G, et al.Gastric precancerous process in a high-risk population: cohort follow-up.Cancer Res. 1990;50(15):4737-40. Disponible en: https://pubmed.ncbi.nlm.nih.gov/2369748/

6. Cuello C, Correa P, Haenszel W, Gordillo G, Brown C, Archer M,Tannenbaum S. Gastric cancer in Colombia. I. Cancer risk and suspectenvironmental agents. J Natl Cancer Inst. 1976;57(5):1015-20. https://doi.org/10.1093/jnci/57.5.1015

7. IARC Working Group. IARC Monographs, vol. 61. Schistosomes, liverflukes and Helicobacter pylori. Lyon: International Agency for Research onCancer, IARC Publications,1994.

8. Uemura N, Okamoto S, Yamamoto S, Matsumura N, Yamaguchi S,Yamakido, et al. Helicobacter pylori infection and the development of gastriccancer. N Engl J Med. 2001;345(41):784-9. https://doi.org/10.1056/NEJMoa001999

9. Camargo MC, Yépez MC, Cerón C, Guerrero N, Bravo L, Correa P,Fontham E. Age at acquisition of Helicobacter pylori infection: comparisonof two areas with contrasting risk of gastric cancer. Helicobacter.2004;9(3):262-70. https://doi.org/10.1111/j.1083-4389.2004.00221.x

10. Pignatelli B, Bancel B, Esteve J, Malaveille C, Calmels S, Correa P, et al.Inducible nitric oxide synthase, antioxidant enzymes and H. pylori infectionin gastritis and gastric precancerous lesions in humans. Eur J Cancer Prev.1998;7(6):439-447. https://doi.org/10.1097/00008469-199812000-00003

11. Li CQ, Pignatelli B, Ohshima H. Increased oxidative and nitrativestress in human stomach associated with cagA-positive Helicobacterpylori infection and inflammation. Dig Dis Sci. 2001;46:836-44. https://doi.org/10.1023/A:1010764720524

12. Whary MT, Sundina N, Bravo LE, Correa P, Quinones F, Caro F, Fox J.Intestinal helminthiasis in Colombian children promotes a Th2 responseto Helicobacter pylori: possible implications for gastric carcinogenesis.Cancer Epidemiol Biomarkers Prev. 2005;14(6):1464-69. https://doi.org/10.1158/1055-9965.EPI-05-0095

13. Sung JJ, Lin SR, Ching JY, Zhou LY, To K, Wang RT, et al. Atrophy andintestinal metaplasia one year after cure of H. pylori infection: a prospective,randomized study. Gastroenterology. 2000;119(1):7-14. https://doi.org/10.1053/gast.2000.8550

14. Wong BCY, Lam S, Wong W-M, et al. Eradication of Helicobacter pylorisignificantly slows down the progression of precancerous lesions: a 5-yearprospective randomized study. Gastroenterology. 2002;122:A588.

15. Correa P, Fontham ET, Bravo JC, Bravo LE, Ruiz B, Zarama G, et al.Chemoprevention of gastric dysplasia: randomized trial of antioxidantsupplements and anti-Helicobacter pylori therapy. J Natl Cancer Inst.2000;92(23):1881-8. https://doi.org/10.1093/jnci/92.23.1881

16. Kodaman N, Pazos A, Schneider BG, Piazuelo B, Mera R, SobotaRS, et al. Human and Helicobacter pylori coevolution shapes the risk ofgastric disease. Proc Natl Acad Sci USA. 2014;111(4):1455-60. https://doi.org/10.1073/pnas.1318093111