1. Epidemiology, Diagnosis, and Management of Esophageal Adenocarcinoma
Joel H. Rubenstein, Nicholas J. Shaheen 
Gastroenterology 
Volume 149, Issue 2, Pages e1 (August 2015)
DOI: /j.gastro
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2. Figure 1
Global differences in the incidence of histological subtypes of esophageal cancer. Age-standardized incidence rate (ASR) per 100,000 of (A) EAC and (B) SCC in men. AC, adenocarcinoma; SCC, squamous cell carcinoma.
Reproduced with permission from Arnold et al.7
Gastroenterology  , e1DOI: ( /j.gastro )
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3. Figure 2
Trend of incidence of EAC in the United States. The graph shows the incidence of EAC and incidence-based mortality from 1975 to 2009 according to data from the Surveillance, Epidemiology, and End Results (SEER) Cancer Registry.9 From 1975 to 1997, the incidence of EAC increased at an annual percentage change (APC) of 8.4 (95% CI, 7.7–9.1), whereas the APC was 1.6 (95% CI, 0.0–3.3) from 1997 to For incidence-based mortality, the APC was 8.0 from 1978 to 1998 (95% CI, 7.2–8.8) and 1.1 from 1998 to 2009 (95% CI, 0.7–2.9). All rates were age adjusted to the 2000 standard population using 19 age groups.
Reproduced with permission from Hur et al.9
Gastroenterology  , e1DOI: ( /j.gastro )
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4. Figure 3
Risk factors for EAC. The primary risk factors for EAC include male sex, advancing age, white race, GERD, obesity, and tobacco use. The effect of obesity is likely mediated both through a mechanical effect promoting GERD and a hormonal effect through alterations in circulating adipokines and other peptides and appears to be a major risk factor for both Barrett’s esophagus and EAC. A deranged gastroesophageal junction, noted with a large hiatal hernia, allows free reflux of gastric contents. H pylori infection protects against EAC, and Barrett’s esophagus is its only known precursor.
Gastroenterology  , e1DOI: ( /j.gastro )
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5. Figure 4
Tumor depth staging for EAC. There are 4 main layers of the esophageal wall: mucosa, submucosa, muscularis propria, and adventitia. The mucosa is further divided into the epithelium, lamina propria, and muscularis mucosae. Dysplasia is confined to the epithelium. Intramucosal tumors (T1a) invade the lamina propria or muscularis mucosae. Tumors that invade the submucosa are classified as T1b. T2 tumors invade the muscularis propria, T3 tumors invade the adventitia, and T4 tumors invade adjacent structures.
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6. Figure 5
Endoscopic management of early EAC. Depth of invasion, as assessed by EMR or ESD, is the key to appropriate subsequent therapy. BE, Barrett’s esophagus; LVI, lymphovascular invasion.
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7. Supplementary Figure 1
Survival after esophagectomy according to T classification in pN0 M0 disease. (A) Current (2002) classification. The numbers of patients in each classification and traced at 5 years, respectively, were as follows: Tis, 44 and 21; T1, 98 and 26; T2, 31 and 8; T3, 57 and 12; and T4, 4 and 0. (B) Proposed subclassification of T1 into T1a (intramucosal, n = 66, 18 traced at 5 years) and T1b (submucosal, n = 32, 8 traced at 5 years). Shown for reference are Tis (high-grade dysplasia) and T2. Vertical bars represent 68% confidence limits.
Reproduced with permission from Rice et al.86
Gastroenterology  , e1DOI: ( /j.gastro )
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8. Supplementary Figure 2
Durability of complete eradication for intramucosal adenocarcinoma compared with Barrett’s esophagus of varying degrees of dysplasia. (A) Overall recurrence rate of the cohort. (B) Recurrence rate broken out by baseline histology. IMC (T1a) has a higher recurrence rate than nondysplastic Barrett’s esophagus. LGD, low-grade dysplasia; HGD, high-grade dysplasia; IMC, intramucosal adenocarcinoma (T1a).
Reproduced with permission from Pasricha et al.118
Gastroenterology  , e1DOI: ( /j.gastro )
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