CRITICAL REVIEW: BARRETS OESOPHAGUS – METAPLASIA – DYSPLASIA – MALIGNANT TRANSFORMAYION PHENOTYPICAL CHARACTERISTICS AND PROGRESSION MARKERS
DOI:
https://doi.org/10.52340/jecm.2022.718Keywords:
Barret’s oesophagus, metaplasia, dysplasia, malignant transformationAbstract
Oesophageal adenocarcinoma represents the 6th common cause of cancer related deaths. Frequently oesophageal adenocarcinomas are developed from Barret’s oesophagus, which represents the metaplastic lesion of the lower third of the oesophagus, when squamous epithelium is replaced by glandular epithelium. It has been shown, that Barret’s metaplasia bears the risk of progression into dysplasia and later into malignant disease. However, this risk is different in different patients. Nowadays, there are many ongoing studies investigating the molecular markers of the progression of Barret’s oesophagus, which on the other hand represents an important information for the proper clinical management of this lesion. We discuss the potential markers of Barret’s oesophagus progression and related problematic issues in presented critical review.
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R. L. Siegel and K. D. Miller, “Cancer Statistics , 2020,” vol. 70, no. 1, pp. 7–30, 2020.
R. L. Siegel, K. D. Miller, and A. Jemal, “Cancer statistics, 2019.,” CA. Cancer J. Clin., vol. 69, no. 1, pp. 7–34, Jan. 2019.
H. Sung et al., “Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries.,” CA. Cancer J. Clin., Feb. 2021.
Y. Peters et al., “Barrett oesophagus.,” Nat. Rev. Dis. Prim., vol. 5, no. 1, p. 35, May 2019.
Y. M. Fouad, I. Mostafa, R. Yehia, and H. El-Khayat, “Biomarkers of Barrett’s esophagus,” World J. Gastrointest. Pathophysiol., vol. 5, no. 4, pp. 450–456, Nov. 2014.
I. Ç. Türkmen, N. Başsüllü, S. Uraz, M. A. Yerdel, R. Memışoğlu, and G. Bülbül Doğusoy, “CDX2, COX2 and MUC2 expressions in Barrett’s esophagus: can they be useful in determination of the dysplasia?,” Turk Patoloji Derg., vol. 28, no. 3, pp. 251–258, 2012.
L. Zhang et al., “Barrett’s Esophagus and Intestinal Metaplasia,”Frontiers in Oncology, vol. 11. p. 2325, 2021.
M. Krothapalli et al., “Evaluation of p53 protein expression in Barrett esophagus,” Indian J. Pathol. Microbiol., vol. 61, no. 2, pp. 170–175, Apr. 2018.
V. J. A. Konda and R. F. Souza, “Biomarkers of Barrett’s Esophagus: From the Laboratory to Clinical Practice,” Dig. Dis. Sci., vol. 63, no. 8, pp. 2070–2080, Aug. 2018.
J. Que, K. S. Garman, R. F. Souza, and S. J. Spechler, “Pathogenesis and Cells of Origin of Barrett’s Esophagus,” Gastroenterology, vol. 157, no. 2, pp. 349-364.e1, 2019.
M. E. Vega et al., “Inhibition of Notch signaling enhances transdifferentiation of the esophageal squamous epithelium towards a Barrett’s-like metaplasia via KLF4.,” Cell Cycle, vol. 13, no. 24, pp. 3857–3866, 2014.
D. H. Wang and R. F. Souza, “Transcommitment: Paving the Way to Barrett’s Metaplasia.,” Adv. Exp. Med. Biol., vol. 908, pp. 183–212, 2016.
W. Kranc et al., “The origin, in vitro differentiation, and stemness specificity of progenitor cells.,” J. Biol. Regul. Homeost. Agents, vol. 31, no. 2, pp. 365–369, 2017.
W. Zhang and D. H. Wang, “Origins of Metaplasia in Barrett’s Esophagus: Is this an Esophageal Stem or Progenitor Cell Disease?,” Dig. Dis. Sci., vol. 63, no. 8, pp. 2005–2012, Aug. 2018.
J. J. Farrell et al., “TFF2/SP-deficient mice show decreased gastric proliferation, increased acid secretion, and increased susceptibility to NSAID injury,” J. Clin. Invest., vol. 109, no. 2, pp. 193–204, Jan. 2002.
K. Li et al., “mTOR signaling regulates gastric epithelial progenitor homeostasis and gastric tumorigenesis via MEK1-ERKs and BMP-Smad1 pathways ll ll mTOR signaling regulates gastric epithelial progenitor homeostasis and gastric tumorigenesis via MEK1-ERKs and BMP-Smad,” 2021.
S. G. Willet et al., “Regenerative proliferation of differentiated cells by mTORC1-dependent paligenosis,” EMBO J., vol. 37, no. 7, p. e98311, Apr. 2018.
Y. Yamamoto et al., “Mutational spectrum of Barrett’s stem cells suggests paths to initiation of a precancerous lesion,” Nat. Commun., vol. 7, p. 10380, Jan. 2016.
N. Schoofs, R. Bisschops, and H. Prenen, “Progression of Barrett’s esophagus toward esophageal adenocarcinoma: an overview,” Ann. Gastroenterol., vol. 30, no. 1, pp. 1–6, 2017.
A. P. Thrift, “Global burden and epidemiology of Barrett oesophagus and oesophageal cancer,” Nat. Rev. Gastroenterol. Hepatol., vol. 18, no. 6, pp. 432–443, 2021.
F. Yousef, C. Cardwell, M. M. Cantwell, K. Galway, B. T. Johnston, and L. Murray, “The incidence of esophageal cancer and high-grade dysplasia in Barrett’s esophagus: a systematic review and meta-analysis.,” Am. J. Epidemiol., vol. 168, no. 3, pp. 237–249, Aug. 2008.
M. Sikkema, P. J. F. de Jonge, E. W. Steyerberg, and E. J. Kuipers, “Risk of esophageal adenocarcinoma and mortality in patients with Barrett’s esophagus: a systematic review and meta-analysis.,” Clin. Gastroenterol. Hepatol. Off. Clin. Pract. J. Am. Gastroenterol. Assoc., vol. 8, no. 3, pp. 235–44; quiz e32, Mar. 2010.
J. Alcedo et al., “Trends in Barrett’s esophagus diagnosis in Southern Europe: implications for surveillance,” Dis. Esophagus, vol. 22, no. 3, pp. 239–248, May 2009.
D. Pereira and P. Chaves, “Low risk of adenocarcinoma and high-grade dysplasia in patients with non-dysplastic Barrett’s esophagus : Results from a cohort from a country with low esophageal adenocarcinoma incidence,” 2016.
R. L. Juliano, “Addressing cancer signal transduction pathways with antisense and siRNA oligonucleotides,” NAR Cancer, vol. 2, no. 3, Sep. 2020.
J. A. Perez-fidalgo, “Cell proliferation inhibitors and apoptosis promoters,”EJC Suppl.,vol.15,pp.73–76, 2020.
G. Zhu et al., “Mutant p53 in Cancer Progression and Targeted Therapies,” Frontiers in Oncology, vol. 10. p. 2418, 2020.
V. T. Janmaat, S. H. van Olphen, K. E. Biermann, L. H. J. Looijenga, M. B. Bruno, and M. C. W. Spaander, “Use of immunohistochemical biomarkers as independent predictor of neoplastic progression in Barrett’s oesophagus surveillance: A systematic review and meta-analysis.,”PLoS One,vol.12, no.10, p.e0186305,2017.
A. Frenzel, F. Grespi, W. Chmelewskij, and A. Villunger, “Bcl2 family proteins in carcinogenesis and the treatment of cancer,” Apoptosis, vol. 14, no. 4, pp. 584–596, Apr. 2009.
A. A. Raouf, D. A. Evoy, E. Carton, E. Mulligan, M. M. Griffin, and J. V Reynolds, “Loss of Bcl-2 expression in Barrett’s dysplasia and adenocarcinoma is associated with tumor progression and worse survival but not with response to neoadjuvant chemoradiation.,” Dis. esophagus Off. J. Int. Soc. Dis. Esophagus, vol. 16, no. 1, pp. 17–23, 2003.
L. T. Li, G. Jiang, Q. Chen, and J. N. Zheng, “Ki67 is a promising molecular target in the diagnosis of cancer (review).,” Mol. Med. Rep., vol. 11, no. 3, pp. 1566–1572, Mar. 2015.
B. S. Volkweis, R. R. Gurski, L. Meurer, G. G. Pretto, G. da S. Mazzini, and M. I. Edelweiss, “Ki-67 Antigen Overexpression Is Associated with the Metaplasia-Adenocarcinoma Sequence in Barrett's Esophagus,” Gastroenterol. Res. Pract., vol. 2012, p. 639748, 2012.
J.-Y. Kim et al., “The value of phosphohistone H3 as a proliferation marker for evaluating invasive breast cancers: A comparative study with Ki67,” Oncotarget, vol. 8, no. 39, pp. 65064–65076, May 2017.
S. Nakashima, A. Shiozaki, D. Ichikawa, and S. Komatsu, “Anti-phosphohistone H3 as an Independent Prognostic Factor in Human Esophageal Squamous Cell Carcinoma,” vol. 468, pp. 461–467, 2013.
R. W. Phillips, H. F. J. Frierson, and C. A. Moskaluk, “Cdx2 as a marker of epithelial intestinal differentiation in the esophagus.,” Am. J. Surg. Pathol., vol. 27, no. 11, pp. 1442–1447, Nov. 2003.
D. M. Karamchandani et al., “Increasing diagnostic accuracy to grade dysplasia in Barrett ’ s esophagus using an immunohistochemical panel for CDX2 ,” Diagn. Pathol., pp. 1–13, 2016.
A. Creemers et al., “The dynamics of HER2 status in esophageal adenocarcinoma,” Oncotarget, vol. 9, no. 42, pp. 26787–26799, Jun. 2018.
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