Cystitis glandularis with intestinal metaplasia overlies the invasive adenocarcinoma. This feature is often found in the adjacent benign urothelium, which is helpful to support a primary adenocarcinoma versus a metastatic tumor.
Adenocarcinoma in situ lesions consists of normal urothelial mucosa being replaced by glandular epithelium with prominent cytologic atypia. In this image, areas of in situ lesions as well as probable invasive areas are seen.
The neoplastic glands resemble colonic glands, sometimes with abundant extracellular mucin. Goblet cells are a feature in this case.
These glands resemble colonic adenocarcinoma, thus, could be categorized in the enteric histologic subtype. In the absence of an in situ component, one must strongly consider the possibility of direct invasion from bladder, rectum, prostate, appendix and endometrium, or metastasis from other primary sites. Thus, clinical history, imaging studies and IHC panels will be required to support this rare diagnosis of primary vesical adenocarcinoma. For example, primary vesical adenocarcinoma may stain similarly to colonic adenocarcinoma with focal CK7 positivity and CK20 positivity, however, nuclear staining for beta-catenin is detected in primary colonic adenocarcinoma, but not primary vesical adenocarcinoma.3
Primary adenocarcinomas of the bladder are uncommon, accounting for approximately 5 to 2.5% of all malignant bladder tumors. Metastatic adenocarcinomas are far more common. As with squamous carcinoma of the bladder, adenocarcinomas arise from metaplasia of the urothelium as a result of longstanding irritation. For example, adenocarcinomas constitute up to 90% of carcinomas in bladder extrophy (protrusion of the bladder wall through the abdominal wall due to a defect in development), account for ~15% of tumors in non-functioning bladders (such as in spinal cord injuries) and are also more common in Schistosomiasis infections.1,2
Certain authors divide primary adenocarcinomas of the bladder into urachal (those associated with the persistence of an urachal remnant) and nonurachal (not associated with a urachal remnant). We shall do the same here and discuss only the nonurachal adenocarcinomas. You can read about urachal adenocarcinomas of the bladder in our separate case (see link below) -- urachal adenocarcinomas account for approximately 1/3 of all bladder adenocarcinomas.2
Grossly, adenocarcinomas tend to be single discrete lesions whereas urothelial (transitional cell) carcinomas tend to be multifocal. Similar to urothelial carcinoma, the tumors may be papillary, nodular, ulcerated or flat.
Histologic subtypes include: (1) enteric - resembles colonic adenocarcinoma; (2) mucinous or colloid - tumor cells are surrounded by abundant mucin; (3) signet ring - single signet ring cells percolate through the mucosa and bladder wall, similar to gastric signet ring adenocarcinoma; (4) mixed - a mixture of histologic types; (5) adenocarcinoma not otherwise specified - a significant portion of bladder adenocarcinomas bear a resemblance to colonic glands (thus, enteric type), however, 'nonspecific' neoplastic glands that do not necessarily resemble colonic adenocarcinoma belong in this category.
Similar to urothelial carcinoma, these tumors tend to arise in males over age 50 (M:F ratio of ~3:1), with a peak incidence in the 6th decade. Hematuria, dysuria and mucosuria can be presenting symptoms.3
Most adenocarcinomas have infiltrated deeply at the time of diagnosis, which probably accounts for their poorer prognosis. 5 year survival rates range from 18 to 47%. Signet ring adenocarcinomas have a grim prognosis as they generally present at a high stage.2,3
1 Mills SE, ed. Sternberg's Diagnostic Surgical Pathology.4th Ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004: 2060-2062.
2 Fletcher CDM, ed. Diagnostic Histopathology of Tumors. 3rd Ed. Philadelphia, PA: Elsevier; 2007: 539-543.
3 Zhou M, Magi-Galluzzi, C. Genitourinary Pathology: Foundations in Diagnostic Pathology. Philadelphia, PA: Elvesier; 2006: 190-2.