Unsuspected field changes in the esophageal mucosa of patients with esophageal cancer

1990 ◽  
Vol 3 (2) ◽  
pp. 93-106 ◽  
Author(s):  
O. J. Traynor ◽  
P. J. Byrne ◽  
R. C. Stuart ◽  
G. Keye ◽  
N. Nolan ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Esophageal Mucosa

Probability of Transition of Normal Esophageal Mucosa and Precancerous Lesion to the Esophageal Cancer

2021 ◽  
Author(s):  
Zhiyu Chen ◽  
Yong YU ◽  
Xue YANG ◽  
Jing-Xuan WANG ◽  
Wen-Qiang Wei ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Carcinoma In Situ ◽  
Markov Models ◽  
Transition Probabilities ◽  
Health State ◽  
Severe Dysplasia ◽  
Esophageal Mucosa ◽  
Mild Dysplasia ◽  
Pathological Stages

Abstract Background: To estimate the transition probabilities of esophageal cancer（EC） and its precancerous lesions by Markov model, which could provide important information for EC screening about choosing reasonable screening and follow-up intervals.Methods: The transition probabilities among pathological stages were estimated by establishing Markov models for the natural history of EC and repeatedly adjusting and calibrating Markov models by comparing the modeled incidence and distributions of pathological stages (alone or combined) with observed data in real-world condition. Results: In one year, the probabilities were 0.024, 0.05, 0.12 for people from health state progressing to mild dysplasia (mD), mild dysplasia (mD) to moderate dysplasia (MD), and moderate dysplasia (MD) to severe dysplasia/carcinoma in situ (SD/CIS), respectively. The age-specific transition probabilities were 0.08~0.18 for severe dysplasia/carcinoma in situ (SD/CIS) progressing to intramucosal carcinoma(IC), 0.4~0.87 for intramucosal carcinoma (IC) to submucosal carcinoma (T1N0M0) (SC), and 0.2~0.85 for submucosal carcinoma (T1N0M0) (SC) to invasive carcinoma (INC). The progression probabilities increased with age and the severity of the disease. Based on the estimated transition probabilities, we predicted the incidence of EC and distributions of its pathological stages. Comparisons between modeled results with observed data confirmed the validation of our transition probabilities.Conclusions: An esophageal cancer transition model in high-risk areas of China has been established with validity. It could be a point of reference for further economic evaluation and policy formulation of esophageal cancer screening.

The association between smoking and LINE-1 hypomethylation (global DNA hypomethylation) in normal esophageal epithelium of patients with esophageal squamous cell carcinoma.

2012 ◽  
Vol 30 (4_suppl) ◽  
pp. 41-41
Author(s):  
Shiro Iwagami ◽  
Yoshifumi Baba ◽  
Masayuki Watanabe ◽  
Hironobu Shigaki ◽  
Keisuke Miyake ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Cancer ◽  
Squamous Cell ◽  
Methylation Level ◽  
Continuous Variable ◽  
Smoking History ◽  
Esophageal Mucosa ◽  
Esophageal Epithelium ◽  
Dna Hypomethylation

41 Background: DNA methylation is a major epigenetic mechanism in X-chromosome inactivation, imprinting and repression of transposable elements and endogenous retroviral sequences. Global DNA hypomethylation appears to play an important role in genomic instability, leading to cancer development. DNA methylation in the long interspersed nucleotide element-1, L1 (LINE-1) repetitive element is a good indicator of global DNA methylation level. Smoking and alcohol is extremely important as the etiology of esophageal squamous cell carcinoma. Nonetheless, whether or not smoking and alcohol affect LINE-1 methylation level in normal esophageal epithelium of esophageal cancer patients remains uncertain. Methods: We quantified LINE-1 methylation of normal esophageal mucosa using pyrosequencing technology in 118 resected esophageal squamous cell carcinomas. The data on smoking (Brinkman index, absence or presence) and alcohol amount are available in all cases. We excluded preoperatively treated cases. Results: LINE-1 methylation in normal esophageal epithelium of esophageal cancer patients ranged from 57.1 to 92.8 of 0-100 scale (N=118; mean 81.2; median 80.0; standard deviation 7.2). LINE-1 methylation level (continuous variable) was significantly associated with Brickman index (continuous variable) (r=0.12, p=0.0002); heavy smoker had lower LINE-1 methylation level of normal esophageal mucosa. LINE-1 methylation level was lower in patients with smoking history (mean 79.7) than in patients without smoking history (mean 83.2) (p=0.034). Alcohol assumption was not associated with LINE-1 methylation level (r=0.003, p=0.58). Conclusions: Smoking was associated with LINE-1 hypomethylation in esophageal normal epithelium, suggesting the possibility of epigenetic field effects caused by cigarette in esophageal tumorigenesis. Considering that DNA methylation alterations are reversible and can thus be targets for chemoprevention, our findings may have clinical implication.

scholarly journals Prevalence and modern aspects of the treatment of patients with Barrett’s esophagus

2018 ◽  
pp. 24-27
Author(s):  
V. V. Tsukanov ◽  
A. V. Vasyutin ◽  
N. N. Butorin ◽  
Yu. L. Tonkikh ◽  
O. V. Peretyatko ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Barrett’S Esophagus ◽  
Barrett's Esophagus ◽  
Prolonged Treatment ◽  
Main Task ◽  
Esophageal Mucosa ◽  
Adenocarcinoma Of The Esophagus ◽  
Small Doses ◽  
Inflammatory Drugs ◽  
Endoscopic Methods

The article analyzes the prevalence and principles in treatment of Barrett’s esophagus. The prevalence of Barrett’s esophagus varies widely from region to region of the world and has ethnic differences. The use of endoscopic methods and the histological examination of the biopsies of esophageal mucosa are of utmost importance in the diagnosis of this pathology. The prevention of esophageal cancer is the main task in managing patients with Barrett’s esophagus. The length of the Barrett’s esophagus segment, the presence and extent of dysplasia is of the greatest importance to select tactics for managing patients. Endoscopic methods are widely used for the eradication of metaplasia sites, among which the radiofrequency ablation is the most effective one. Prolonged treatment with proton pump inhibitors is safe and reduces the risk of transformation of Barrett’s esophagus into adenocarcinoma of the esophagus. There is evidence that small doses of aspirin, nonsteroidal anti-inflammatory drugs, statins and ursodeoxycholic acid have the preventive effect on the development of esophageal cancer. However, the possibilities of using these drugs for this purpose are still limited. Anti-reflux surgery still holds relevance, but at the same time, it has no advantages over the drug therapy for the prevention of esophageal cancer.

scholarly journals A Dilemma in Staging of Esophageal Cancer: How Should We Stage ypT0 N2 M0 Esophageal Cancer after Neoadjuvant Therapy?

2015 ◽  
Vol 2015 ◽  
pp. 1-4
Author(s):  
Sebahattin Celik ◽  
Remzi Erten ◽  
Abdulsamed Batur ◽  
Burak Suvak
Keyword(s):  
Esophageal Cancer ◽  
Lymph Nodes ◽  
Neoadjuvant Therapy ◽  
Cell Cancer ◽  
Locally Advanced ◽  
Neoadjuvant Treatment ◽  
Complete Response ◽  
Resection Margins ◽  
Pathology Report ◽  
Esophageal Mucosa

Background. Since neoadjuvant treatment in esophageal cancer began to become popular, a complete pathological response at the primary tumour site has been commonly reported. An issue of conflict is whether complete response in the esophageal lumen means that the esophagus is completely tumour-free. Another important issue is whether lymph nodes that are retrieved from pathologically complete response cases are also tumour-free or not. There is a gap in the esophageal cancer staging system for ypT0 N2 M0 tumours that have received neoadjuvant therapy. Here, we will discuss the problem about staging of esophageal cancer associated with neoadjuvant therapy.Case. A female aged 40 years complaining of dysphagia was diagnosed as having locally advanced thoracic esophageal cancer. Neoadjuvant therapy decision was taken by oncology committee. Six weeks after neoadjuvant therapy, with a curative intention, minimal invasive surgery was performed. The pathology report was as follows. “There were no neoplastic cells in the suspected area of the esophageal mucosa upon examination with all staining. There was no cancer at resection margins. Four metastatic lymph nodes were infiltrated with squamous cell cancer.”Conclusion. Despite the growing use of neoadjuvant treatment in locally advanced esophageal cancer in world, we do not have a protocol for the evaluation of these patients’ pathology reports. We believe that new studies and new ideas are needed to resolve this dilemma associated with neoadjuvant therapy.

Prognostic significance of LINE-1 methylation level in esophageal squamous cell carcinoma.

2012 ◽  
Vol 30 (4_suppl) ◽  
pp. 26-26 ◽  
Author(s):  
Yoshifumi Baba ◽  
Shiro Iwagami ◽  
Masayuki Watanabe ◽  
Hironobu Shigaki ◽  
Satoshi Ida ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Cancer ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Methylation Level ◽  
Prognostic Significance ◽  
Esophageal Mucosa ◽  
Dna Hypomethylation

26 Background: Genome-wide DNA hypomethylation plays a role in genomic instability and carcinogenesis. DNA methylation in the long interspersed nucleotide element-1, L1 (LINE-1) repetitive element is a good indicator of global DNA methylation level. LINE-1 methylation is a useful marker for predicting cancer prognosis and monitoring efficacy of adjuvant therapy. Esophageal squamous cell carcinoma, the major histological type of esophageal cancer in East Asian countries, is one of the most aggressive malignant tumors. Nonetheless, prognostic significance of LINE-1 hypomethylaiton in esophageal cancer remains uncertain. Methods: Using 217 curatively resected esophageal squamous cell carcinomas, we quantified LINE-1 methylation using bisulfite-PCR-pyrosequencing assay. Cox proportional hazards model was used to calculate mortality hazard ratio (HR), adjusted for clinical, epidemiologic, and pathological variables. Results: Esophageal cancers showed significantly lower LINE-1 methylation level compared to matched normal esophageal mucosa (p<0.0001; N=50). Tumoral LINE-1 methylation ranged from 24.8 to 91.8 of 0-100 scale (N=217; mean 64.5; median 65.0; standard deviation 12.8). LINE-1 hypomethylation was significantly associated with disease-free survival [log-rank p=0.0008; univariate HR= 2.31, 95% confidence interval (CI) 1.38-3.84, p=0.0017; multivariate HR=1.81, 95% CI 1.06-3.05, p=0.031] and overall survival (log-rank p=0.0013; univariate HR=2.21, 95% CI 1.33-3.60, p=0.0026; multivariate HR=1.87, 95% CI 1.12-3.08, p=0.018]. Conclusions: LINE-1 hypomethylation in esophageal cancer is associated with shorter survival, suggesting its role as a prognostic biomarker. Given that epigenetic changes, including DNA methylation alterations, are reversible and can thus be targets for therapy or chemoprevention, our findings may have considerable clinical implications.

scholarly journals Increased risk of esophageal squamous cell carcinoma associated with frequent and long-term consumption of salted meat and salted fat

2019 ◽  
Vol 47 (8) ◽  
pp. 3841-3849
Author(s):  
Lin Zhao ◽  
Yu-Chen Li ◽  
Jiang-Ping Wu ◽  
Yan-Jie Zhao ◽  
Rui-Bin Wang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Cancer ◽  
Case Control Study ◽  
Case Control ◽  
Esophageal Mucosa ◽  
Food Frequency ◽  
Increased Risk ◽  
Salted Meat ◽  
Control Study

Objective This study aimed to investigate the association between the consumption of salted meat and salted fat and esophageal cancer risk among individuals with normal esophageal mucosa or esophagitis. Methods This case-control study enrolled 216 individuals from Yanting County. Information on the consumption of salted meat and salted fat was collected using a food-frequency questionnaire validated among Yanting people. Results Higher intake frequencies (≥once a week) of salted meat and salted fat were associated with 2.40-fold and 7.37-fold increased risks of esophageal cancer among individuals with normal esophageal mucosa, while long-term intakes (≥6 months) increased the risks by 6.87-fold and 85.45-fold, respectively. Similarly, the odds ratios (ORs) of patients with esophagitis developing esophageal cancer from frequent intakes of salted meat and salted fat were 6.48 and 5.05, respectively, and the ORs associated with long-term intakes were 44.38 and 74.90, respectively. Conclusions Frequent and long-term consumption of salted meat and salted fat could increase the risk of esophageal cancer in individuals from Yanting with normal esophageal mucosa or esophagitis. Efforts should thus be made to reduce the consumption of these foods among people in this region.

scholarly journals Tissue Type Differences in ABCB1 Expression and Paclitaxel Tissue Pharmacokinetics in Patients With Esophageal Cancer

2021 ◽  
Vol 12 ◽  
Author(s):  
Ruben A. G. van Eerden ◽  
Leni van Doorn ◽  
Femke M. de Man ◽  
Niels Heersche ◽  
Michail Doukas ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Tumor Tissue ◽  
Treatment Resistance ◽  
Tissue Type ◽  
Esophageal Mucosa ◽  
Tissue Pharmacokinetics ◽  
Esophageal Tissue ◽  
Tumor Types ◽  
Transporter Expression ◽  
Concomitant Radiotherapy

Background: Data from previous work suggests that there is no correlation between systemic (plasma) paclitaxel exposure and efficacy in patients treated for esophageal cancer. In this trial, we investigated ATP-binding cassette efflux transporter expression and intratumoral pharmacokinetics of paclitaxel to identify changes which could be a first sign of chemoresistance.Methods: Patients with esophageal cancer treated with paclitaxel and carboplatin (± concomitant radiotherapy) were included. During the first and last cycle of weekly paclitaxel, blood samples and biopsies of esophageal mucosa and tumor tissue were taken. Changes in paclitaxel exposure and expression of ABCB1 (P-glycoprotein) over time were studied in both tumor tissue and normal appearing esophageal mucosa.Results: ABCB1 was significantly higher expressed in tumor tissue compared to esophageal tissue, during both the first and last cycle of paclitaxel (cycle 1: p &lt; 0.01; cycle 5/6: p = 0.01). Interestingly, ABCB1 expression was significantly higher in adenocarcinoma than in squamous cell carcinoma (p &lt; 0.01). During the first cycle, a trend towards a higher intratumoral paclitaxel concentration was observed compared to the esophageal mucosa concentration (RD:43%; 95%CI: −3% to 111% p = 0.07). Intratumoral and plasma paclitaxel concentrations were significantly correlated during the first cycle (AUC0–48 h: r = 0.72; p &lt; 0.01).Conclusion: Higher ABCB1 expression in tumor tissue, and differences between histological tumor types might partly explain why tumors respond differently to systemic treatment. Resistance by altered intratumoral paclitaxel concentrations could not be demonstrated because the majority of the biopsies taken at the last cycle of paclitaxel did contain a low amount of tumor cells or no tumor.

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