Small Glands in the Prostate

Deloar Hossain, M.D.

Specimen Type:

Prostate

History:

A 57-year-old male with an elevated serum PSA (6.3 ng/ml) underwent prostate needle biopsies.

Pathologic Features:

At low magnification, there are a good number of small glands infiltrating between normal prostatic glands (Fig 1, 2). Some glands have abortive lumen (Fig 3). The glands display marked architectural distortion, including variation in size, shape, and spacing. The glands are lined by cells with enlarged hyperchromatic nuclei and scant cytoplasm (Fig 4). Nucleoli can also be appreciated (Fig 5). These small acini demonstrate cytoplasmic reaction with 34BE12 and nuclear staining for p63.

Differential Diagnosis:

  • Prostatic adenocarcinoma
  • Atypical basal cell hyperplasia
  • Basal cell carcinoma

Prostatic adenocarcinoma: Prostatic adenocarcinoma is the most common malignancy in the prostate. The diagnosis is based on 1) architecture: infiltrative small glands or cribriform glands too large or irregular to represent high-grade PIN; 2) Single cell layer (absence of basal cells); 3) Nuclear atypia: nuclear and nucleolar enlargement.

Atypical basal cell hyperplasia: Basal cell hyperplasia consists of a proliferation of basal cells two or more cells in thickness at the peripheral of prostatic acini. The proliferation may protrude into the acinar lumen, retaining the overlying secretory luminal epithelium. It sometimes appears as small nests of cells surrounded by compressed stroma. The nests may be solid or cystically dilated and occasionally punctuated by irregular round luminal spaces, creating a cribriform pattern. Atypical basal cell hyperplasia is identical to basal cell hyperplasia except for the presence of large prominent nucleoli. This lesion is significant because of the potential for misdiagnosis as adenocarcinoma.

Basaloid and adenoid cystic carcinoma: It is extraordinarily rare in the prostate with only about 30 reported cases. Clinically, patients present with obstructive symptoms and serum PSA was slightly increased (to 4.5 and 4.6 ng/ml) in few of reported cases. Microscopically, the basaloid proliferation should be infiltrative with a prominent cribriform architecture. Cordlike, glandular and nested basaloid patterns can be also be present. Cytologically, small ovoid basaloid cells with scant amount of cytoplasam and finely stippled chromatin are present. Tumor is positive for 34BE12. Variable reactive with PSA and PAP has been reported although many cases are negative. Although the clinical behavior of basaloid carcinoma of the prostate remains unknown due to its rarity, no evidence of metastatic disease was reportedly present in these cases.

 

Diagnosis:

Atypical small acinar proliferation highly suspicious for but not diagnostic of malignancy.

The case presented here has all the morphologic features of prostatic adenocarcinoma in terms of architecture and cytology except for the positive staining for p63 and high-molecular weight cytokeratin (34BE12). Prostatic adenocarcinma is considered to be derived from the secretory compartment of double-layered prostatic epithelium rather than basal cell compartment. Therefore, absence of basal cells is the major criterion for diagnosis of prostatic adenocarcinoma in addition to cytologic atypia and architecture distortion. Cancer cells should be negative for basal cell markers. However, in a study of prostatectomy-proven prostatic adenocarcinma (reference 3), p63, a sensitive basal cell marker, was found to be positive in 4 of 70 cases (6%) and the staining intensity was weak and occurred in less than 1% of the cells. It was also noted that tumors that stained positive for p63 were more likely to be high grade than those that did not. Thus, the case presented here is more likely representing such rare case of high-grade prostatic adenocarcinoma with aberrant p63 experience. Although the cells stain positively for basal cell markers, typical small acinar pattern and lack of cribriform and/or nested basaloid patterns argue against basal cell hyperplasia and basaloid/adenoid cystic carcinoma.

References:

  1. Montironi R, Mazzucchelli R, Stramazzotti D, Scarpelli M, Lopez Beltran A, Bostwick DG.Basal cell hyperplasia and basal cell carcinoma of the prostate: a comprehensive review and discussion of a case with c-erbB-2 expression. J Clin Pathol. 2005 Mar;58(3):290-6.
  2. Iczkowski KA, Ferguson KL, Grier DD, Hossain D, Banerjee SS, McNeal JE, Bostwick DG. Adenoid cystic/basal cell carcinoma of the prostate: clinicopathologic findings in 19 cases. Am J Surg Pathol. 2003 Dec;27(12):1523-9.
  3. Parsons JK, Gage WR, et al. p63 protein expression is rare in prostate adenocarcinoma: implications for cancer diagnosis and carcinogenesis. Urology. 2001 Oct;58(4):619-24.