Adenocarcinoma

Esophagus
Carcinoma
Adenocarcinoma

Topic Completed: 1 June 2013

Revised: 26 February 2019

Copyright: 2003-2019, PathologyOutlines.com, Inc.

PubMed Search: Adenocarcinoma[TI] esophagus[TI] pathology free full text[sb]

See also: Arising in ectopic gastric mucosa, Gastroesophageal junction, Intramucosal carcinoma

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Table of Contents

Cite this page: Weisenberg E. Adenocarcinoma. PathologyOutlines.com website. http://www.pathologyoutlines.com/topic/esophagusadenocarcinoma.html. Accessed August 19th, 2019.

Definition / general

Malignant gland forming tumor of esophagus

Epidemiology

In developed world, incidence has increased, while incidence of squamous cell carcinoma has remained constant (Ann Oncol 2012;23:3155, J Natl Compr Canc Netw 2011;9:830)
50 - 70% of esophageal carcinomas are adenocarcinoma
In 2013, American Cancer Society estimates 17,990 new cases of esophageal carcinoma in US with 15,210 deaths
Mean age is ~60 years old; cases before age 50 are uncommon
~80% men
While the most substantial increase has been among white men, incidence is increasing in women and men of other ethnicities
Obesity and high BMI are strong risk factors, likely related to increased GERD and Barrett esophagus
Barrett esophagus is most important risk factor
Tobacco is moderate risk factor
Infection with cagA+ Helicobacter pylori appears to be protective against reflux esophagitis, the initial step in development of adenocarcinoma (pathway is reflux to Barrett esophagus to dysplasia to adenocarcinoma); increase in adenocarcinoma may be due, in part, to decline in prevalence of Helicobacter pylori (Cancer Res 1998;58:588, Cancer Prev Res (Phila) 2008;1:329)
H. pylori infection may cause atrophic gastritis, decreasing acid production and thus decreasing reflux disease

Sites

Generally in distal esophagus
Rarely may arise in submucosal glands or ectopic gastric mucosa

Pathophysiology

Dysplasia - carcinoma sequence in Barrett mucosa with stepwise accumulation of genetic mutations, especially p53 gene; additional changes involve HER2 / c-ERBB2, cyclin D1, cyclin E genes, RB, p16 genes

Clinical features

Insidious onset, dysphagia to solids, followed by dysphagia to all food
Extreme weight loss due to loss of nutrition and the tumor itself
Metastasis generally occurs early even in superficial tumors, due to extensive lymphatic network in esophagus that allows horizontal and longitudinal spread
Adenocarcinoma occurs in lower esophagus and lymph node metastases involve gastric and celiac lymph nodes
Visceral metastases to liver, lungs, pleura
Recurrences are common

Diagnosis

Overwhelming majority diagnosed by endoscopic biopsy

Radiology description

Imaging reveals mass in distal esophagus

Prognostic factors

Lymph node metastases, extracapsular lymph node involvement (Am J Surg Pathol 2006;30:171), depth of invasion (but see J Clin Oncol 2007;25:507), status of resection margins; possibly endoglin / CD105 (Hum Pathol 2005;36:955)
Postchemoradiation therapy prognostic factors in resection specimens:
1. Extent of residual carcinoma predicts survival based on 3 groups:
  - P0 (0% residual carcinoma)
  - P1 (1 - 50% residual carcinoma)
  - P2 (> 50% residual carcinoma, Am J Surg Pathol 2007;31:58)
2. Prominent mucin pools in patients with Barrett associated adenocarcinoma are associated with mucinous tumors but acellular mucin pools are NOT associated with poor survival, even if at radial margin (Am J Surg Pathol 2006;30:28)

Case reports

51 year old man with collision tumor with papillary adenocarcinoma and neuroendocrine carcinoma (Arch Pathol Lab Med 2000;124:411)

Treatment

5 year survival for nonresectable tumors is rare
Resection if primary treatment modality (if possible); may be preceded by neoadjuvant therapy - report Barrett metaplasia on proximal margin, if present
Adjuvant chemoradiation often given

Gross description

Usually distal esophageal tumor with invasion of gastric cardia; appears as flat patches to nodular masses; may have adjacent Barrett mucosa

Gross images

AFIP images

Adenocarcinoma in Barrett esophagus

Contributed by
Mark R. Wick, M.D.

In Barrett metaplasia

Contributed by
Dr. Elliot Weisenberg

Adenocarcinoma

Images hosted on other servers:

Polypoid tumor

Microscopic (histologic) description

Usually moderate or well differentiated, usually mucin producing (intestinal type mucosa), may have foci of squamous or endocrine differentiation
Usually has adjacent Barrett mucosa with high grade dysplasia (may be displaced by adenocarcinoma)
Rarely signet ring cells, papillary structures, Paneth cells, endocrine cells, pagetoid spread of tumor cells

Microscopic (histologic) images

AFIP images

Arising from Barrett epithelium

Contributed by
Mark R. Wick, M.D.

Metaplasia

Contributed by
Dr. Elliot Weisenberg

In lymphatics

Images hosted on other servers:

Arising from
Barrett epithelium:
moderately
differentiated

Adenocarcinoma / neuroendocrine carcinoma collision tumor

Positive stains

Rarely needed for diagnosis
PAS, Alcian blue and mucicarmine (for mucin), usually CK7 and CK19 (Am J Surg Pathol 2002;26:1213), AMACR (Hum Pathol 2006;37:1601); focal positivity is common for somatostatin and serotonin (Histopathology 1987;11:53)

Negative stains

CK20

Electron microscopy images

Images hosted on other servers:

Adenocarcinoma (site unspecified)

Differential diagnosis

High grade dysplasia (no single cell invasion, no infiltration of submucosa or muscularis mucosae), metastatic or adjacent gastric carcinoma (signet ring cells may be present; often CK20+ in background of intestinal metaplasia)
Note per AJCC criteria, cancers of the gastroesophageal junction are staged as esophageal carcinomas

Additional references

Am J Surg Pathol 1984;8:563, Am J Surg Pathol 2002;26:784 (achalasia due to adenocarcinoma)