Basal Cell Carcinoma of the Prostate: A Case Report and Review of the Literature

ABSTRACT

We report a case of an adenoid cystic variant of basal cell carcinoma (BCC) of the prostate in a patient diagnosed following transurethral resection (TURP). A single focus of adenoid cystic carcinoma (ACC) was found. One year later the patient had an episode of hematuria, for which a second TURP was performed; the specimen showed diffuse ACC. The patient then underwent a total prostatectomy (TP). There was no remaining tumor. The patient has been followed for 6 years with no recurrence.

KEYWORDS: Adenoid cystic carcinoma; Basal cell carcinoma; Immunohistopathology; Prostate

CORRESPONDENCE: Mark S. Soloway, MD, Professor and Chairman, Department of Urology, University of Miami, Miller School of Medicine, P.O. Box 016960, Miami, FL 33101, USA. ()

INTRODUCTION

Prostate cancer is the most common cancer among men in the USA. The annual incidence is estimated to be 186 320 [1]. Basal cell hyperplasia (BCH) is a common benign lesion arising from the basal cell layer of the prostate. However, basal cell carcinoma (BCC) is a very rare tumor arising from the basal cells of the prostate, comprising <0.01% of="" malignant="" prostate="" tumors="" [2,3,4,5]. BCC was first described in 1974 by Frankel and Craig [6] as an extensive infiltration of nests of basaloid cells between normal prostate glands. BCC can be classified into two variants: (1) adenoid cystic carcinoma (ACC), and (2) basaloid carcinoma (BC) [5,7]. Both can occur in pure or mixed form with one pattern predominating [2,7].

BCC arises from the periurethral transition zone (TZ) of the prostate and usually presents with bladder outlet obstruction symptoms [8]. Diagnosis is commonly an incidental finding following transurethral resection (TURP) [9,10]. Needle biopsy and open prostatectomy are other methods of diagnosis [9, 10]. There are still no guidelines for the management of BCC [2]; however BCC has been considered to have an indolent biological potential which requires less aggressive treatment than adenocarcinoma [2,7,8].

CASE REPORT

A 61-year-old African American male with bladder-emptying symptoms was evaluated for benign prostatic hyperplasia (BPH). Because of an elevated PSA of 7.0 ng/mL, he underwent several prostate biopsies that were negative for cancer.

In April 2002, the patient underwent a TURP at another institution. The specimen showed a focus of nests of cells and cribriform acini with blue mucin and he was diagnosed with low grade ACC. Some acini showed marked cytologic atypia and perineural invasion. Immunostaining showed strong basal cell staining for high molecular weight cytokeratin (HMW-CK) 34ßE12 and p63. He was managed conservatively following the diagnosis.

The patient had an episode of hematuria in March 2003 and required another TURP at another institution. The surgeon resected 138 grams of prostate tissue. The pathology report showed diffuse ACC (Figure 1). The patient was referred to the authorsâ€™ institution and elected to have a total prostatectomy (TP) 2 months later. The pathology report revealed BCH and no evidence of ACC. There was no extra prostatic extension. The seminal vesicles and lymph nodes were free of tumor (Figure 2). The patient has been followed for 6 years with no evidence of local or biochemical recurrence.

DISCUSSION

Adenocarcinoma is the most common variant of prostate cancer. It arises from the secretory epithelium and usually occupies the peripheral zone (PZ). It is less likely than basaloid carcinoma to cause significant lower urinary tract symptoms (LUTS). Adenocarcinoma usually results in an elevated serum PSA and is diagnosed with a needle biopsy. Immunoreactivity for PSA and PSAP is characteristic of adenocarcinoma [8,11,12]. Lack of immunoreactivity for PSA suggests that the tumor is either poorly differentiated adenocarcinoma or originates from different cells [5].

In contrast to the above, the majority of patients with BCC are initially evaluated for BPH. Because their symptoms persist despite medical treatment and negative needle biopsies for cancer, they undergo a TURP and the diagnosis of BCC is established.

HMW-CK 34ßE12 is a specific marker for basal cells. Immunoreactivity for HMW-CK 34ßE12 is essential for identifying BCC and excluding poorly differentiated adenocarcinoma [7,8,10]. P63 is another marker that stains basal cells and rarely secretory cells [8], while cytokeratins 7 and 20 are specifically reactive for urothelial carcinoma that can invade the prostate [5,7]. Staining for C-erbB-2 oncoprotein, p53, and high level of Ki67 indicates a higher malignant potential [5,9].

BCC was considered to have an indolent biologic potential and a benign behavior that suggested less aggressive treatment than for conventional adenocarcinoma. Due to the assumed benign nature of the disease, the diagnostic TURP was thought to be an adequate therapeutic approach for the majority of BCC patients [10]. However, subcapsular prostatectomy, total prostatectomy, pelvic exenteration, radiotherapy, hormonal treatment, and chemotherapy are other treatment options that have been used for previously reported cases of BCC [2,8,11]. The lack of long-term outcome data for the majority of the BCC patients was a limitation for standard therapeutic guidelines [8].

Although the majority of reported cases of BCC had an indolent behavior, BCC can be a highly malignant tumor with a potential to invade adjacent structures and metastasize with a risk of local recurrence after a TURP [2,8]. The authors reviewed 10 recently reported cases of BCC with no associated conventional adenocarcinoma. Table 1 contains data on the outcome following primary treatment. The mean age was 65 years (range, 43-86 years). All 10 patients presented with obstructive symptoms and 7 were diagnosed initially with BPH. The diagnosis was established following TURP for 5 patients. Five out of 6 patients who had a TURP developed local recurrence. Six patients had metastasis and 2 rapidly deteriorated and died 8 and 9 months after presentation.

The patient in the present report was incidentally diagnosed with BCC following a TURP. He did not receive further treatment until he had local recurrence 11 months later. Following the TP, he is recurrence free at 6 years.

CONCLUSION

BCC can recur locally, metastasize, and cause mortality. Therefore, it should be treated with early definitive therapy and life-long follow-up

ACKNOWLEDGEMENTS

The authors acknowledge financial support from â€œCUREDâ€ and Mr. Vincent A. Rodriguez.

REFERENCES

Jemal A, Siegel R, Ward E, et al. Cancer statistics, 2008. CA Cancer J Clin. 2008;58(2):71-96.
Ayyathurai R, Civantos F, Soloway MS, Manoharan M. Basal cell carcinoma of the prostate: current concepts. BJU Int. 2007;99(6):1345-1349.
Minei S, Hachiya T, Ishida H, Okada K. Adenoid cystic carcinoma of the prostate: a case report with immunohistochemical and in situ hybridization staining for prostate-specific antigen. Int J Urol. 2001;8(8):S41-44
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;58(3):290-296.
Segawa N, Tsuji M, Nishida T, Takahara K, Azuma H, Katsuoka Y. Basal cell carcinoma of the prostate: report of a case and review of the published reports. Int J Urol. 2008;15(6):557-559.
Frankel K, Craig JR. Adenoid cystic carcinoma of the prostate. Report of a case. Am J Clin Pathol. 1974;62(5):639-645.
Begnami MD, Quezado M, Pinto P, Linehan WM, Merino M. Adenoid cystic/basal cell carcinoma of the prostate: review and update. Arch Pathol Lab Med. 2007;131(4):637-640.
Iczkowski KA, Ferguson KL, Grier DD, et al. Adenoid cystic/basal cell carcinoma of the prostate: clinicopathologic findings in 19 cases. Am J Surg Pathol. 2003;27(12):1523-1529.
Halat SK, MacLennan GT. Adenoid cystic/basal cell carcinoma of the prostate. J Urol. 2008;179(4):1576.
Ali TZ, Epstein JI. Basal cell carcinoma of the prostate: a clinicopathologic study of 29 cases. Am J Surg Pathol. 2007;31(5):697-705.
McKenney JK, Amin MB, Srigley JR, et al. Basal cell proliferations of the prostate other than usual basal cell hyperplasia: a clinicopathologic study of 23 cases, including four carcinomas, with a proposed classification. Am J Surg Pathol. 2004;28(10):1289-1298.
Mastropasqua MG, Pruneri G, Renne G, De Cobelli O, Viale G. Basaloid cell carcinoma of the prostate. Virchows Arch. 2003;443(6):787-791.
Terris MK. The appearance of adenoid cystic carcinoma of the prostate on transrectal ultrasonography. BJU Int. 1999;83(7):875-876.
Hudson E, Rashid M, Carter AC, Lester JF. Basaloid carcinoma of the prostate: a case report and review of the literature. Eur J Cancer Care (Engl). 2008;17(5):509-511.

To Cite this Article: Eldefrawy A, Katkoori D, De Los Santos R, Manoharan M, Soloway MS. Basal cell carcinoma of the prostate: a case report and review of the literature. UIJ 2009 Jun;2(3). doi:10.3834/uij.1944-5784.2009.06.11

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