Quantitative analysis of p16 methylation in Barrett's carcinogenesis

Chueca, Eduardo; Valero, Alberto; Hördnler, Carlos; Puertas, Agustín Carlos Nebra; Carrera, Paola; García-González, María Asunción; Strunk, Mark; Lanas, Ángel; Piazuelo, Elena

doi:10.1016/j.anndiagpath.2020.151554

Cited by 2 publications

(2 citation statements)

References 24 publications

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“…In a recent study, lesion-containing sections of patients with LGD, HGD, and EAC were separated from histological sections by laser-capture microdissection, and p16 (encoded by CDKN2A) methylation analysis was performed with pyrosequencing. The authors reported that p16 methylation increased in parallel with the level of the carcinogenesis process [40].…”

Section: Rbp1mentioning

confidence: 99%

“…regulates the cell cycle tumor suppressor p16INK4A promotor: BE (3-77%, mean: 29%) [12] BD (11-75%, mean: 40%) [9] EAC (16-85%, mean: 51%) [14] NSE (0-43%, mean: 9%) [9] p14ARF promotor: BE (8%) [1] EAC (0-20%, mean: 7%) [3] NSE (0%) [1] p16INK4A [21,22,24,25,27,[30][31][32][33][34][40][41][42] p14ARF [24,25,27] DAPK positive mediator of gamma-interferon-induced programmed cell death tumor suppressor BE (50%) [1], BD (53%) [1], EAC (20-70%, mean: 50%) […”

Section: Cdkn2amentioning

confidence: 99%

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Epigenetic Alterations from Barrett’s Esophagus to Esophageal Adenocarcinoma

Ergün

Kıpçak

Bor

2023

IJMS

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Barrett’s esophagus (BE) is a disease entity that is a sequela of chronic gastroesophageal reflux disease that may result in esophageal adenocarcinoma (EAC) due to columnar epithelial dysplasia. The histological degree of dysplasia is the sole biomarker frequently utilized by clinicians. However, the cost of endoscopy and the fact that the degree of dysplasia does not progress in many patients with BE diminish the effectiveness of histological grading as a perfect biomarker. Multiple or more quantitative biomarkers are required by clinicians since early diagnosis is crucial in esophageal adenocancers, which have a high mortality rate. The presence of epigenetic factors in the early stages of this neoplastic transformation holds promise as a predictive biomarker. In this review, current studies on DNA methylations, histone modifications, and noncoding RNAs (miRNAs) that have been discovered during the progression from BE dysplasia to EAC were collated.

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Section: Rbp1mentioning

confidence: 99%

Section: Cdkn2amentioning

confidence: 99%

Epigenetic Alterations from Barrett’s Esophagus to Esophageal Adenocarcinoma

Ergün

Kıpçak

Bor

2023

IJMS

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The Aberrant Expression of Biomarkers and Risk Prediction for Neoplastic Changes in Barrett’s Esophagus–Dysplasia

Choi,

Bedford,

Pollack

2024

Cancers

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Background: Barrett’s esophagus (BE) is a pre-neoplastic condition associated with an increased risk of esophageal adenocarcinoma (EAC). The accurate diagnosis of BE and grading of dysplasia can help to optimize the management of patients with BE. However, BE may be missed and the accurate grading of dysplasia based on a routine histology has a considerable intra- and interobserver variability. Thus, well-defined biomarker testing remains indispensable. The aim of our study was to identify routinely applicable and relatively specific biomarkers for an accurate diagnosis of BE, as well as determining biomarkers to predict the risk of progression in BE–dysplasia. Methods: Retrospectively, we performed immunohistochemistry to test mucin 2(MUC2), trefoil factor 3 (TFF3), p53, p16, cyclin D1, Ki-67, beta-catenin, and minichromosome maintenance (MCM2) in biopsies. Prospectively, to identify chromosomal alterations, we conducted fluorescent in situ hybridization testing on fresh brush samples collected at the time of endoscopy surveillance. Results: We discovered that MUC2 and TFF3 are specific markers for the diagnosis of BE. Aberrant expression, including the loss and strong overexpression of p53, Ki-67, p16, beta-catenin, cyclin D1, and MCM2, was significantly associated with low-grade dysplasia (LGD), high-grade dysplasia (HGD), and EAC histology, with a relatively high risk of neoplastic changes. Furthermore, the aberrant expressions of p53 and p16 in BE-indefinite dysplasia (IND) progressor cohorts predicted the risk of progression. Conclusions: Assessing the biomarkers would be a suitable adjunct to accurate BE histology diagnoses and improve the accuracy of BE–dysplasia grading, thus reducing interobserver variability, particularly of LGD and risk prediction.

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Quantitative analysis of p16 methylation in Barrett's carcinogenesis

Cited by 2 publications

References 24 publications

Epigenetic Alterations from Barrett’s Esophagus to Esophageal Adenocarcinoma

Epigenetic Alterations from Barrett’s Esophagus to Esophageal Adenocarcinoma

The Aberrant Expression of Biomarkers and Risk Prediction for Neoplastic Changes in Barrett’s Esophagus–Dysplasia

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