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Research ArticleResearch Article

Mucin-Producing Urothelial-Type Adenocarcinoma of the Prostate (a Case Report and Review of the Literature)

Haitao Niu, Guang Sun, Jiwu Chang and Yibing Zhang
Chinese Journal of Clinical Oncology October 2006, 3 (5) 370-372;
Haitao Niu
Department of Urology, Second Hospital of Tianjin Medical University, Institute of Urology, Tianjin 300211, China.
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Guang Sun
Department of Urology, Second Hospital of Tianjin Medical University, Institute of Urology, Tianjin 300211, China.
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Jiwu Chang
Department of Urology, Second Hospital of Tianjin Medical University, Institute of Urology, Tianjin 300211, China.
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Yibing Zhang
Department of Urology, Second Hospital of Tianjin Medical University, Institute of Urology, Tianjin 300211, China.
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Abstract

OBJECTIVE To report clinical and pathologic findings of one case of mucin-producing urothelial-type adenocarcinoma of the prostate, and to discuss the diagnosis and prognosis of this disease.

METHODS The patient was a 60-year-old man who had an 8-month history of urinary frequency and dysuria culminating in an aggravating condition for 10-days. Laboratory results were tPSA 3.0 and fPSA 0.4. An ultrasound and digital rectal exam showed no abnormal findings, so he was diagnosed as having benign prostatic hyperplasia, and underwent a transurethral prostate resection.

RESULTS The findings during the operation resembled benign prostatic hyperplasia (BPH), whereas the pathological exam showed that the prostatic construction was deranged in the tumor infiltrating region, with many mucin lakes and signet ring cell in the cancer tissue. Immunohistochemical staining revealed that the cancer tissue was negative for prostate-specific antigen (PSA) and postive for carcinoembryonic antigen (CEA). Final diagnosis: mucin-producing urothelial-type adenocarcinoma of the prostate. After 5D Gy radiotherapy, the patient was free of recurrent signs and metastasis up to 8 months after operation.

CONCLUSION Mucin-producing urothelial-type adenocarcinoma of the prostate is extremely rare. Its differential diagnosis mainly includes conventional prostatic adenocarcinoma with mucin production and secondary adenocarcinoma. The diagnosis and treatment of this disease should be further investigated.

KEYWORDS:

keywords

  • mucin -producing urothelial-type adenocarcinoma
  • prostate
  • diagnosis

Mucin-producing urothelial-type adenocarcinoma of the prostate is an extremely rare neoplasm with only 4 cases having been reported in the literature. We present the 5th case of this disease in a 60-year-old man. The clinical and histological features of this disease are summarized based on our case and literature review.

MATERIALS AND METHODS

A 60-year-old male patient presented with a voiding disorder and urination urgency in April, 2005. A digital rectal exam (DRE) revealed that the prostate was elastic, large and painless without nodules. Rectoprostatic sulci were found to be prominent with no hardness. His serum PSA was 3.0 ng/ml. An examination of urine flow showed a maximum flow rate (MFR) of 7 ml/s and an average flow rate (AFR) of 4 ml/s. Ultrasonography (US) revealed the prostate volume was 60 mL and residual urine was 110 ml. The prostatic internal echo was not even, some calculi were visible and the marginal capsule was not clear. The preoperative diagnosis of this patient was BPH, so a transurethral resection of the prostate (TURP) was performed. During the operation, urethrascopy showed small amounts of mucoid material covering the prostatic urethra, especially on the left apical-posterior aspect of the gland. The anterior urethra and urinary bladder were found to be normal. The prostate was deeply resected with a 24 F resectoscope with no mucoid secretion released from the prostate in the course of resection, but the left lobe of the gland was heavily adhesive with the prostate capsule.

RESULTS

The transurethral resection of the prostate produced 25 g of tissue fragments. Histologic sections showed detached fragments of mucin-producing adenocarcinoma with glandular and cribriform architecture infiltrating the prostatic parenchyma. The tumor cells were tall and columnar with marked atypical nuclei. Mucin pools and irregular small glandular alveoli were visible. In addition, there were numerous irregular satellite foci. Large hyperchromatic signet ring cells with a vacuolized cytoplasm and peripherally positioned nucleus were detected (Fig.l). Immunohistochemically, the tumor showed totally negative staining for PSA and was diffusely positive for CEA (Figs.2, 3). The gastrointestinal tract was investigated in order to exclude a secondary prostate tumor. There were no pathological findings of tumor markers (PSA, CEA), abdominal CT or colonoscopic indications. Thorax CT, lumber MRI, and a bone scan were also normal. These investigations showed that the prostate tissue was the source of the primary pathology. Taken together, the morphology and immunophénotype and the other exams all supported mucin-producing urothelial-type adenocarcinoma involving the prostate.

Fig. 1.
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Fig. 1.

Microscopic features of mucin-producing urothelia-type adenocarcinoma of the prostate (H&E), reduced from × 100.

Fig. 2.
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Fig. 2.

Negative staining for PSA, reduced from × 100.

Fig. 3.
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Fig. 3.

Focally positive staining for CEA, reduced from × 100.

Radical prostatectomy or radiotherapy were recommended for the patient as treatment alternatives. Because the patient rejected radical prostatectomy, a total of 50 Gy radiotherapy (25 x2 Gy) was applied after TURP. At 12 months after treatment, thoracoabdominal CT, bone scintigraphy and tumor markers (PSA, CEA) were found to be normal.

DISCUSSION

Adenocarcinoma arising in the male urethra can originate from urethritis glandularis of the urothelium and/or squamous mucosa, especially when the metaplasia is of an intestinal type. Other sources include periurethral structures such as Cowper's (bulbourethral) or Littre's glands. It may be quite difficult to determine the source of these tumors as they may be diagnosed late in the course of the disease and after telltale precursor lesions have been obliterated by the growing mass.[1] Tran et al.[2] reported that these tumors most likely arise from malignant transformation of the urethritis glandularis involving the urothelium lining the prostatic urethra or proximal prostatic ducts, followed by the development of adenocarcinoma in situ and invasive adenocarcinoma.

Establishing the correct diagnosis of urothelial-type adenocarcinoma involving the prostate is extremely important for several reasons. Correct diagnosis can prevent patients being subjected to extensive and invasive investigations to exclude the presence of a primary tumor in their gastrointestinal tract. It may be possible to avoid these investigations, the discomfort and risks associated with them, and the potential delay in the initiation of treatment if the correct diagnosis had been established at the time of prostate biopsy or transurethral resection. In addition, establishing the correct diagnosis will prevent the potential initiation of inappropriate hormone therapy that might occur if the tumor were to be misconstrued as a variant of acinar-type prostatic adenocarcinoma. The histopatholical changes in mucin-producing urothelial-type adenocarcinoma of the prostate are similar to conventional prostatic adenocarcinoma with mucin producing and secondary adenocarcinoma involving the prostate. It is very difficult to make a correct diagnosis only from a histopathological examination. An immunohistochemical panel mainly including PSA and CEA can be very helpful in establishing the correct diagnosis.

Conventional prostatic adenocarcinoma that is mucin-producing mainly includes mucinous carcinoma (MC), signet-ring cell carcinoma (SRCC) and mucinous carcinoma with signet-ring cells (MCSRC). P1 Saito et al. [4]reported that the positive rates for serum PSA in these tumors were 77.8%, 33.3% and 0% respectively, and others have indicated that the positive rates for immunohistochemical staining of PSA is 90.3%, 81.8% and 60.3% respectively.131 However the urothelial-type adenocarcinoma of the prostate, is quite different. Immunohistochemically, our case and the four published cases all showed negative findings for PSA, but were positive for CEA. In radical prostatectomy specimens, the diagnosis of mucin-producing urothelial-type adenocarcinoma of the prostate may be more apparent, given the greater likelihood of finding precursor lesions such as glandular metaplasia of the urothelium, or urethritis glandularis, and adenocarcinoma in situ.

To establish the correct diagnosis for mucin-producing urothelial-type adenocarcinoma of the prostate one must exclude the presence of a primary tumor in the gastrointestinal tract. Curtis et al[5]. Reported that an immunohistochemical panel which included CK7, CK20, 34bE12, PSA and CEA was very helpful in establishing the correct diagnosis, especially distinguishing between a urothelial-type adenocarcinoma and secondary adenocarcinoma of colonic origin involving the prostate. In their report, positive results for CEA, CK7, 34bE12 and negative findings for PSA indicated a primary mucin-producing urothelial-type adenocarcinoma of the prostate. In our case, we performed an abdominal CT, colonoscopy, thorax CT and lumber MRI to completely exclude secondary adenocarcinoma.

The rarity of urothelial-type adenocarcinoma involving the prostate prevents making any conclusions with respect to clinical characteristics, behavior and treatment, other than to indicate that hormonal therapy would be inappropriate. The first patient reported in the literature was a 73-year-old man treated by radical prostatectomy who remained well without evidence of métastasés through one year of follow-up. The second patient was a 68-year-old man treated by a simple retropubic prostatectomy with recurrence of the tumor 4 years later that was treated with radiation therapy resulting in a modest response. The third patient treated by TURP, died 9 months later with liver métastasés. The fourth patient was treated by radical prostatectomy and remained disease-free for over 16 months of follow-up.[5]

In summary, we have described one additional case of urothelial-type adenocarcinoma involving the prostate that had arisen in the prostatic urethra and/or proximal prostatic ducts. The documentation of more cases of urothelial-type adenocarcinoma involving the prostate is required to strengthen the contention that they arise in the prostatic urethra or proximal prostatic ducts, as well to determine the diagnostic standards, clinical behavior and establish optimal treatment.

  • Received August 11, 2006.
  • Accepted October 16, 2006.
  • Copyright © 2006 by Tianjin Medical University Cancer Institute & Hospital and Springer

References

  1. ↵
    1. Melicow MM,
    2. Roberts TW
    . Pathology and natural history of urethral tumors in males. Review of 142 cases. Urology. 1978;11:83–89.
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  2. ↵
    1. Tran KP,
    2. Epstein JI
    . Mucinous adenocarcinoma of urinary bladder type arising from the prostatic urethra. Distinction from mucinous adenocarcinoma of the prostate. Am J Surg Pathol. 1996;20:1346–1350.
    OpenUrl
    1. Rhee AC,
    2. Olgac S,
    3. Ohori M et al
    . Mucinous adenocarcinoma of the prostate: a case report of long-term disease-free survival and a review of the literature. Urology. 2004;63:779–780.
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  3. ↵
    1. Saito S,
    2. Iwaki H
    . Mucin -producing carcinoma of the prostate: review of 88 cases. Urology. 1999;54:141–144.
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  4. ↵
    1. Curtis MW,
    2. Evans AJ,
    3. Srigley JR
    . Mucin -producing urothelial-type adenocarcinoma of prostate: report of two cases of a rare and diagnostically challenging entity. Mod Pathol. 2005;18:585–590.
    OpenUrlCrossRefPubMed
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Cancer Biology and Medicine: 3 (5)
Chinese Journal of Clinical Oncology
Vol. 3, Issue 5
1 Oct 2006
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Mucin-Producing Urothelial-Type Adenocarcinoma of the Prostate (a Case Report and Review of the Literature)
Haitao Niu, Guang Sun, Jiwu Chang, Yibing Zhang
Chinese Journal of Clinical Oncology Oct 2006, 3 (5) 370-372;

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Mucin-Producing Urothelial-Type Adenocarcinoma of the Prostate (a Case Report and Review of the Literature)
Haitao Niu, Guang Sun, Jiwu Chang, Yibing Zhang
Chinese Journal of Clinical Oncology Oct 2006, 3 (5) 370-372;
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