Chemoprevention in Barrett’s esophagus and esophageal adenocarcinoma

Alkhayyat, Motasem; Kumar, Prabhat; Sanaka, Krishna; Thota, Prashanthi N.

doi:10.1177/17562848211033730

Cited by 7 publications

(4 citation statements)

References 87 publications

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“…The protective effect was increased with the combined use of both (HR = 0.22; 95% CI 0.06–0.85) [ 68 ]. Other case-control studies have also supported the association between statin use and a reduction in EAC risk [ 69 ].…”

Section: Epidemiology and Risk Factorsmentioning

confidence: 85%

Cancer Risk in Barrett’s Esophagus: A Clinical Review

Beydoun

Stabenau

Altman

et al. 2023

IJMS

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Esophageal adenocarcinoma (EAC) is rapidly increasing in incidence and is associated with a poor prognosis. Barrett’s esophagus (BE) is a known precursor of esophageal adenocarcinoma. This review aims to explore Barrett’s esophagus, esophageal adenocarcinoma, and the progression from the former to the latter. An overview of the definition, diagnosis, epidemiology, and risk factors for both entities are presented, with special attention being given to the areas of debate in the literature. The progression from Barrett’s esophagus to esophageal adenocarcinoma is reviewed and the relevant molecular pathways are discussed. The definition of Barrett’s esophagus remains debated and without international consensus. This, alongside other factors, has made establishing the true prevalence of Barrett’s esophagus challenging. The degree of dysplasia can be a histological challenge, but is necessary to guide clinical management. The progression of BE to EAC is likely driven by inflammatory pathways, pepsin exposure, upregulation of growth factor pathways, and mitochondrial changes. Surveillance is maintained through serial endoscopic evaluation, with shorter intervals recommended for high-risk features.

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Section: Epidemiology and Risk Factorsmentioning

confidence: 85%

Cancer Risk in Barrett’s Esophagus: A Clinical Review

Beydoun

Stabenau

Altman

et al. 2023

IJMS

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“…Taking into account the role of acid secretion in esophageal epithelial damage, proton pump inhibitors appear to be actually the only treatment that can interfere with the worsening of histological damage. Indeed, numerous studies have shown that acid-suppressing proton pump inhibitor therapy stabilizes the activity of cellular proliferative cells in the BE and consequently can prevent dysplasia and have a positive impact on reducing the risk of cancer in the esophagus [ 61 , 62 , 63 , 64 , 65 , 66 ] especially if the therapy is continuous and long-term [ 67 ]. The mechanism by which proton pump inhibitors exert a protective effect is nonetheless unclear.…”

Section: Discussionmentioning

confidence: 99%

“…In BE, metaplastic cells have a higher proliferative rate and are in line with what has been demonstrated both in vitro and in vivo, in esophageal adenocarcinoma cell lines under acid exposure through the production of agents by mitogens that transmit signals regulating cell growth and proliferation, and contextually decrease apoptosis [ 64 ]. Hillmann et al [ 67 ] and other Authors [ 63 , 64 , 65 ], demonstrated that these drugs stabilize the proliferation of epithelial cells already in the short term suggesting that the prolongation of the duration will limit the hyperplasia of the basal cell layer [ 68 , 69 ]. Our results are in agreement with this hypothesis; we monitored the patients after one year of follow-up by observing a decrease in Ki67 expression, a sign of a decrease in cell proliferation, and contextually a decrease in FAS-mediated supplementary metabolic activities, a sign of loss of cellular metabolic demand.…”

Section: Discussionmentioning

confidence: 99%

Variation in Fatty Acid Synthase, Ki67 and p53 Esophageal Mucosa Expressions in Barrett’s Esophagus Patients Treated for One Year with Two Esomeprazole Different Regimens

Crispino

Ciarambino

Giordano

2023

CIMB

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Barrett’s esophagus (BE) is an acquired pre-malignant condition that results from chronic gastroesophageal reflux. The malignant transformation occurred in 0.5% of patients/year and was independent of medical and endoscopic conservative treatments. Fatty acid synthase (FAS) is a multifunctional enzyme that catalyzes the synthesis of long-chain fatty acids from acetyl-coenzyme A, malonyl-coenzyme A, a reduced form of nicotinamide adenine dinucleotide phosphate (NADPH), and adenosine triphosphate. Activation of FAS is closely linked to malignant transformation. The aim of the present study was to evaluate the variation of FAS, p53, and Ki67 expressions in two groups of 21 BE patients each, after one year of continuous (group A) or discontinuous (group B) treatment with esomeprazole 40 mg/day in comparison to the initial expression. In both the two groups of BE patients, biopsies were taken from pathologic sites of the mucosa for histological and immuno-histochemical detection of FAS, Ki67, and p53 at entry and after one year of Esomeprazole 40 mg treatment. FAS expression was positive when a strong granular cytoplasmic staining was observed in esophageal cells. Ki67 and p53 were defined as positive when nuclear staining was clearly detected at ×10 magnification. FAS expression was reduced in 43% of patients treated with Esomeprazole continuously in comparison to the 10% of patients treated with Esomeprazole on demand (p = 0.002). Ki67 expression was reduced in 28% of continuously treated patients in comparison to 5% of patients treated on demand (p = 0.001). The p53 expression decreased in 19% of continuously treated patients in comparison to an increase in 2 patients (9%) treated on demand (p = 0.05). Continuously Esomeprazole treatment could help in the diminution of metabolic and proliferative activities in the esophageal columnar epithelium and in part it can help prevent the oxidative damage against cellular DNA, resulting in a diminution in p53 expression.

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“…Silicosis caused by asbestos fibers or silica dust is related to lung cancer 21 . Barrett's esophagitis is related to esophageal cancer 22,23 …”

Section: Inflammation and Tumorsmentioning

confidence: 99%

Research Progress on the Relationship Between Inflammation and Colorectal Cancer

Zhang

Qiao

2021

Annals of Gastroent Surgery

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Colorectal cancer (CRC), as one of the most prevalent types of cancer worldwide and the most common gastrointestinal malignant tumor, has become the third largest fatality rate of malignant tumor. [1][2][3] As people change their lifestyle in recent years, together with the environmental pollution influence factors, the incidence of CRC is on the rise in the world. CRC is easily misdiagnosed; those diagnosed in the early phase are less than 40% and for most of the patients at the time of definite diagnosis, the cancer has already metastasized. 4 Treatment with surgery is given priority, combined with radiotherapy and chemotherapy, but epidemiological data show that patients with CRC mortality are higher still. 5,6 In the middle of the nineteenth century, Virchow observed leukocyte infiltration in tumor tissues and first proposed the possible correlation between malignant tumors and inflammation. 7 With the deepening of such research, it has now been confirmed that chronic inflammation takes part in a tumor's start, proliferation, metastasis, aging, and apoptosis at various stages. Inflammation is also known as the seventh largest biological feature of malignant tumor. [7][8][9][10]

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Chemoprevention in Barrett’s esophagus and esophageal adenocarcinoma

Cited by 7 publications

References 87 publications

Cancer Risk in Barrett’s Esophagus: A Clinical Review

Cancer Risk in Barrett’s Esophagus: A Clinical Review

Variation in Fatty Acid Synthase, Ki67 and p53 Esophageal Mucosa Expressions in Barrett’s Esophagus Patients Treated for One Year with Two Esomeprazole Different Regimens

Research Progress on the Relationship Between Inflammation and Colorectal Cancer

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