The Efficacy of Linked Color Imaging in the Endoscopic Diagnosis of Barrett's Esophagus and Esophageal Adenocarcinoma
Ontology highlight
ABSTRACT:
SUBMITTER: Tokunaga M
PROVIDER: S-EPMC7542478 | biostudies-literature | 2020 Jan
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Esophageal adenocarcinoma is a major cause of cancer-related morbidity and mortality in Western countries. The incidences of esophageal adenocarcinoma and its precursor Barrett's esophagus have increased substantially in the last four decades. Current care guidelines recommend that endoscopy be used for the early detection and monitoring of patients with Barrett's esophagus; however, the efficacy of this approach is unclear. To prevent the increasing morbidity and mortality from esophageal adenocarcinoma, there is a tremendous need for early detection and surveillance biomarker assays that are accurate, low-cost, and clinically feasible to implement. The last decade has seen remarkable advances in the development of minimally invasive molecular biomarkers, an effort led in large part by the Early Detection Research Network (EDRN). Advances in multi-omics analysis, the development of swallowable cytology collection devices, and emerging technology have led to promising assays that are likely to be implemented into clinical care in the next decade. In this review, an updated overview of the molecular pathology of Barrett's esophagus and esophageal adenocarcinoma and emerging molecular biomarker assays, as well as the role of EDRN in biomarker discovery and validation, will be discussed.See all articles in this CEBP Focus section, "NCI Early Detection Research Network: Making Cancer Detection Possible."
| S-EPMC7710621 | biostudies-literature
Project description:Background and aimThe study aims to clarify the endoscopic features and clinicopathological differences in superficial Barret's esophageal adenocarcinoma (s-BEA) derived from short-segment Barrett's esophagus (SSBE) and long-segment Barrett's esophagus (LSBE).MethodsWe reviewed data of 130 patients (141 lesions) with pathologically confirmed s-BEA (SSBE: 95 patients and 95 lesions; LSBE: 35 patients and 46 lesions). We analyzed endoscopic and clinicopathological features of s-BEA in patients with SSBE and LSBE.ResultsThe distribution of lesions according to macroscopic findings were as follows (s-BEA in SSBE vs LSBE): flat type (0-IIb), 3.2% (3/95) vs 32.6% (15/46) (P < 0.001); accompanied type 0-IIb, 2.1% (2/95) vs 21.7% (10/46) (P < 0.001); and complex type (0-I + IIb, 0-IIa + IIc, etc.), 30.5% (29/95) vs 50.0% (23/46) (P = 0.025). Complex-type s-BEAs had high incidences of T1b invasions and poorly differentiated components (simple type: 22.5% [20/89] and 18.0% [16/89]; complex type: 59.6% [31/52] and 44.2% [23/52], P < 0.001 and P = 0.002, respectively). In SSBE, 72.6% (69/95) of lesions were located at the right anterior wall (P = 0.01). All flat-type or depressed-type lesions derived from SSBE were identified as reddish areas, whereas only 65.2% (15/23) from LSBE were identified as reddish areas (P < 0.001).ConclusionsIn LSBE, flat-type, accompanied-type 0-IIb, and complex-type lesions were significantly more prevalent. Furthermore, complex-type s-BEAs tended to have T1b invasions and poorly differentiated components. S-BEAs in LSBE should be more carefully evaluated on endoscopic appearance including flat-type and complex-type lesions than in SSBE.
| S-EPMC7027738 | biostudies-literature
Project description:Endoscopic surveillance of patients with Barrett's Esophagus (BE) is recommended to detect esophageal adenocarcinoma (EAC) and its dysplasia precursors, but survival benefits are unclear. Using Surveillance, Epidemiology, and End Results (SEER) and linked Medicare data, we sought to determine the impact of a prior BE diagnosis on survival in patients with EAC.Our analysis focused on patients over age 65 with primary EAC diagnosed in a SEER region from 2000-2011 and enrolled in Medicare. We identified patients with preexisting BE prior to EAC diagnosis and compared this group to EAC patients without a prior BE diagnosis. A Cox Proportional Hazards model compared survival and included variables such as age, sex, cancer stage, treatment, and medical comorbidities.Among 4,978 SEER-Medicare patients identified with EAC, 577 (12%) had preexisting BE; 4,401 (88%) did not. BE patients had overall lower stage (28.5% stage I vs. 12.8% stage IV) than those without preexisting BE (16.4% stage I vs. 30.6% stage IV). Overall survival was better among patients in the BE group (hazard ratio (HR), 0.56; 95% confidence interval (CI), 0.50-0.61); this benefit persisted in the adjusted model (HR, 0.72; 95%, 0.65-0.80). After adjusting for lead-time bias, the HRs attenuated to the null, with an unadjusted HR of 0.96 (95% CI: 0.86-1.05, P=0.39) and adjusted HR of 0.99 (CI: 0.89-1.10, P=0.92).Survival outcomes in patients with a BE diagnosis prior to EAC were statistically better in both the unadjusted and adjusted Cox proportional hazards model. However, this benefit appears to be predominantly lead-time and length-time bias.
| S-EPMC5856156 | biostudies-literature
Project description:BACKGROUND:Efforts to reduce mortality from esophageal adenocarcinoma (EA) have focused on screening and surveillance of Barrett's esophagus (BE). AIMS:We sought to determine the frequency of prior diagnosis of BE in patients with EA and to evaluate the impact of a prior BE diagnosis on mortality in EA patients. METHODS:This was a retrospective cohort study of patients diagnosed with EA in the VA during 2002-2016. We compared the distributions of EA stage and receipt of treatment between EA patients with and without a prior BE diagnosis and used Cox proportional hazards models to compare mortality risk (all-cause and cancer specific) unadjusted and adjusted for stage and treatment to assess their impact on any survival differences. RESULTS:Among 8564 EA patients, only 4.9% had a prior BE diagnosis. The proportion with prior BE diagnosis increased from 3.2% in EA patients diagnosed during 2005-2007 to 7.0% in those diagnosed during 2014-2016. EA patients with a prior BE diagnosis were more likely to have stage 1 disease and receive any treatment. A prior BE diagnosis was associated with lower all-cause mortality risk (hazard ratio [HR] unadjusted for stage, 0.69; 95% CI, 0.61-0.80), which was largely explained by the earlier stage of EA at the time of diagnosis (HR adjusted for stage, 0.87; 95% CI, 0.75-0.99). There was no evidence of lead time bias or length time bias. CONCLUSIONS:Prior diagnosis of BE was associated with better survival, largely due to earlier EA stage at diagnosis.
| S-EPMC6185782 | biostudies-literature
Project description:Background: Barrett's esophagus and esophageal adenocarcinoma cases are increasing as gastroesophageal reflux disease increases. Using artificial intelligence (AI) and linked color imaging (LCI), our aim was to establish a method of diagnosis for short-segment Barrett's esophagus (SSBE). Methods: We retrospectively selected 624 consecutive patients in total at our hospital, treated between May 2017 and March 2020, who experienced an esophagogastroduodenoscopy with white light imaging (WLI) and LCI. Images were randomly chosen as data for learning from WLI: 542 (SSBE+/- 348/194) of 696 (SSBE+/- 444/252); and LCI: 643 (SSBE+/- 446/197) of 805 (SSBE+/- 543/262). Using a Vision Transformer (Vit-B/16-384) to diagnose SSBE, we established two AI systems for WLI and LCI. Finally, 126 WLI (SSBE+/- 77/49) and 137 LCI (SSBE+/- 81/56) images were used for verification purposes. The accuracy of six endoscopists in making diagnoses was compared to that of AI. Results: Study participants were 68.2 ± 12.3 years, M/F 330/294, SSBE+/- 409/215. The accuracy/sensitivity/specificity (%) of AI were 84.1/89.6/75.5 for WLI and 90.5/90.1/91.1/for LCI, and those of experts and trainees were 88.6/88.7/88.4, 85.7/87.0/83.7 for WLI and 93.4/92.6/94.6, 84.7/88.1/79.8 for LCI, respectively. Conclusions: Using AI to diagnose SSBE was similar in accuracy to using a specialist. Our finding may aid the diagnosis of SSBE in the clinic.
| S-EPMC11012507 | biostudies-literature
Project description:Preliminary studies suggested a possible correlation of microbiota with Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), where the need for tools to ameliorate its poor prognosis is mandatory. We explored the potential signature of esophageal microbiota and its predicted functional profile along the continuous spectrum from BE to EAC. We analyzed through 16S-based amplicon sequencing the mucosal microbiota and the microbiota-related functional predictions in 10 BE and 6 EAC patients compared with 10 controls, exploring also potential differences between the metaplastic mucosa (BEM) and the adjacent normal areas of BE patients (BEU). BEM and EAC showed a higher level of ? and ?-diversity. BEM evidenced a decrease of Streptococcus and an increase of Prevotella, Actinobacillus, Veillonella, and Leptotrichia. EAC displayed a striking reduction of Streptococcus, with an increase of Prevotella, Veillonella and Leptotrichia. LefSe analysis identified Leptotrichia as the main taxa distinguishing EAC. BEM showed a decreased ?-diversity compared with BEU and a reduction of Bacteroidetes, Prevotella and Fusobacterium. Functional predictions identified peculiar profiles for each group with a high potential for replication and repair in BEM; an upregulated energy, replication and signaling metabolisms, with the fatty-acids biosynthesis and nitrogen and D-alanine pathways down-regulated in EAC. Our pilot study identifies a unique microbial structure and function profile for BE and EAC, as well as for metaplastic and near-normal areas. It proposes a new concept for BE, which could be intended not only as the histological, but, also, as the microbial closest precursor of EAC. This requires further larger follow-up studies, but opens intriguing horizons towards innovative diagnostic and therapeutic options for EAC.
| S-EPMC7199943 | biostudies-literature
Project description:PurposeEsophageal adenocarcinoma is a highly aggressive malignancy that frequently develops from Barrett's esophagus, a premalignant pathologic change occurring in the lower end of the esophagus. Identifying Barrett's esophagus patients at high risk of malignant transformation is essential to the prevention of esophageal adenocarcinoma. Although microRNA (miRNA) expression signatures have been associated with the etiology and prognosis of several types of cancers, their roles in the development of esophageal adenocarcinoma have not been extensively evaluated.Experimental designIn this study, we analyzed the expression patterns of 470 human miRNAs using Agilent miRNA microarray in 32 disease/normal-paired tissues from 16 patients diagnosed with Barrett's esophagus of either low- or high-grade dysplasia, or esophageal adenocarcinoma.ResultsUsing unsupervised hierarchical clustering and class comparison analyses, we found that miRNA expression profiles in tissues of Barrett's esophagus with high-grade dysplasia were significantly different from their corresponding normal tissues. Similar findings were observed for esophageal adenocarcinoma, but not for Barrett's esophagus with low-grade dysplasia. The expression patterns of selected miRNAs were further validated using quantitative reverse transcription real-time PCR in an independent set of 75 pairs of disease/normal tissues. Finally, we identified several miRNAs that were involved in the progressions from low grade-dysplasia Barrett's esophagus to esophageal adenocarcinoma.ConclusionsWe showed that miRNAs were involved in the development and progression of esophageal adenocarcinoma. The identified significant miRNAs that may become potential targets for early detection, chemoprevention, and treatment of esophageal cancer.
| S-EPMC2745487 | biostudies-literature
Project description:A proportion of patients with Barrett's esophagus (BE) are diagnosed with esophageal adenocarcinoma (EAC) within 1 year of an endoscopic examination that produced negative findings. These cases of missed cancers have not been well studied, despite current surveillance strategies for BE. We performed a systematic review and meta-analysis to determine the magnitude of missed EAC in cohorts of patients with BE.We searched MEDLINE, EMBASE, and Web of Science from their inception to May 31, 2015 to identify cohort studies of adults with BE (baseline nondysplastic BE ± BE with low-grade dysplasia) and at least a 3-year follow-up period, providing data on missed and incident EACs (diagnosed within 1 year and diagnosed more than 1 year after the initial endoscopy in which BE was diagnosed, respectively). The main outcome measure was pooled proportion of missed and incident EACs (of all EACs detected after initial endoscopy) among BE cohorts, using a random effects model.In a meta-analysis of 24 studies reporting on 820 missed and incident EACs, 25.3% were classified as missed (95% confidence interval: 16.4%-36.8%) and 74.7% as incident EACs (95% CI: 63.2%-83.6%), although there was substantial heterogeneity among studies (I2 = 74%). When the analysis was restricted to nondysplastic BE cohorts (15 studies), 23.9% of EACs were classified as missed (95% confidence interval: 15.3%-35.4%; I2 = 0%). In a meta-analysis of 10 studies with follow-up periods of ?5 years (a total of 239 EACs), 22.0% were classified as missed (95% confidence interval: 8.7%-45.5%), with substantial heterogeneity (I2 = 68%).Among adults with nondysplastic BE (or BE with low-grade dysplasia) at their index endoscopy and at least a 3-year follow-up period, 25% of EACs are diagnosed within 1 year after the index endoscopy. Additional resources should be allocated to detect missed EAC.
| S-EPMC4919075 | biostudies-literature
Project description:Esophageal adenocarcinoma is an increasingly common disease with a dismal 5-year survival rate of 10% to 15%. In the first systematic evaluation of the PD-1 pathway in esophageal adenocarcinoma, we identify expression of PD-L2 in cancer cells in 51.7% of esophageal adenocarcinomas. Epithelial PD-L1 was expressed on only 2% of cases, although PD-L1(+) immune cells were observed in 18% of esophageal adenocarcinomas. We also evaluated expression in the precursor lesion of esophageal adenocarcinoma, Barrett's esophagus, which emerges following gastric reflux-induced esophageal inflammation, and found PD-L2 expression in Barrett's esophagus but not in non-Barrett's esophagus esophagitis. Because the progression from squamous esophagitis to Barrett's esophagus is accompanied by a transition from a TH1 to TH2 immune response, we hypothesized that the TH2 cytokines IL4/IL13 could contribute to PD-L2 induction. We confirmed that these cytokines can augment PD-L2 expression in esophageal adenocarcinoma cell lines. These results suggest that the inflammatory environment in Barrett's esophagus and esophageal adenocarcinoma may contribute to the expression of PD-L2. Furthermore, the potential for PD-1 receptor blockade to be effective in esophageal adenocarcinomas with epithelial PD-L2 or immune cell PD-L1 expression should be evaluated in clinical trials.
| S-EPMC4596773 | biostudies-literature
Project description:Almost 50% of esophageal adenocarcinoma (EAC) patients progressed from Barrett's esophagus (BE). EAC is often diagnosed at late stages and is related to dismal prognosis. However, there are still no effective methods for stratification and therapy in BE and EAC. Two public datasets (GSE26886 and GSE37200) were analyzed to identify differentially expressed genes (DEGs) between BE and EAC. Then, a series of bioinformatics analyses were performed to explore potential biomarkers associated with BE-EAC. 27 up- and 104 down-regulated genes were observed between GSE26886 and GSE37200. The GO and KEGG enrichment analysis indicated that the DEGs were highly involved in tumorigenesis. Subsequently, Weighted Gene Co-Expression Network Analysis (WGCNA) were performed to explore the potential genes related to BE-EAC, which were validated in The Cancer Genome Atlas (TCGA) database, and 5 up-regulated genes (MYO1A, ACE2, COL1A1, LGALS4, and ADRA2A) and 3 down-regulated genes (AADAC, RAB27A, and P2RY14) were found in EAC. Meanwhile, ADRA2A and AADAC could contribute to EAC pathogenesis and progression. MYO1A, ACE2, COL1A1, LGALS4, ADRA2A, AADAC, RAB27A, and P2RY14 could be potential novel diagnostic and prognostic biomarkers in BE-EAC.
| S-EPMC9910260 | biostudies-literature