- Email: [email protected]
Primary Seminal Vesicle Carcinoma Detected at Transurethral Resection of Prostate
Case Report Primary Seminal Vesicle Carcinoma Detected at Transurethral Resection of Prostate Lars Egevad, Roy Ehrnström, Ulf Håkansson, and Magnus Grabe We present a case of primary seminal vesicle carcinoma detected at transurethral resection. The clinical presentation, radiologic findings, and pathologic features of these tumors are reviewed. Grossly, seminal vesicle carcinoma is poorly circumscribed and solid or solid/cystic and may be misinterpreted as an abscess or hemorrhage on radiologic examination. Although a definitive diagnosis often cannot be given until after complete resection, we describe the findings indicative of seminal vesicle origin, including papillary histologic architecture, sometimes with mucinous differentiation, and a characteristic immunophenotype positive for CA-125 and cytokeratin 7, but negative for prostate-specific antigen and cytokeratin 20. UROLOGY 69: 778.e11–778.e13, 2007. © 2007 Elsevier Inc.
P
rimary seminal vesicle carcinoma (SVC) is a very rare tumor, and only 51 well-documented cases have been reported.1 The diagnosis is generally based on a combination of morphologic, immunohistochemical, and clinical findings, including radiologic examination. It is difficult to make a definitive diagnosis using biopsy, and surgical resection is usually required to determine whether the epicenter is in the seminal vesicles and whether it is primary to this site. We present a case of primary SVC suspected at transurethral resection of the prostate (TURP) and subsequently verified after procto-cysto-prostatectomy.
CASE REPORT A 73-year-old man with hematuria and hematospermia was first examined in March 2004. Digital rectal examination showed an enlarged multilobular right seminal vesicle that was confirmed by ultrasonography. The prostate volume was estimated at 85 cm3. The cystoscopy findings and serum prostate-specific antigen (PSA) level were normal (1.7 ng/ mL). Urinary cytology showed dissociated high-grade malignant cells with pleomorphic nuclei and no signs of adenocarcinoma differentiation. Computed tomography (CT) scan showed a multilobular, 12-cm-diameter, low-attenuated expansile process close to the prostate and on the site of the right seminal vesicle (Fig. 1). A diagnosis of abscess or hemorrhage was considered because of the partially cystic appearance. The patient underwent chest x-ray and CT of chest and abdomen without signs of malignancy elsewhere. He denied previous cancer, and his pathology record did not contain any malignant diagnoses. Because the patient had From the International Agency for Research on Cancer, Lyon, France; and Departments of Urology AND Pathology, Malmö University Hospital, Malmö, Sweden Address for correspondence: Lars Egevad, M.D., Ph.D., Pathology Group, International Agency for Research on Cancer (IARC), 150 Cours Albert Thomas, Lyon 69372 Cedex 08, France. E-mail: [email protected] Submitted: September 15, 2006; accepted (with revisions): December 7, 2007
© 2007 Elsevier Inc. All Rights Reserved
Figure 1. Front view of CT scan showing multilobular, lowattenuated, expansile process close to prostate and on site of right seminal vesicle (asterisk). Urinary bladder was dislocated.
hematospermia and lower urinary tract symptoms indicating bladder outlet obstruction, as well as a normal serum PSA value, we decided to perform diagnostic TURP with no preceding transrectal biopsy. This was done in February 2005, and adenocarcinoma was found on histologic examination. The tumor had columnar-stratified epithelium with elongated nuclei and a predominantly papillary architecture similar to ductal carcinoma of the prostate. However, immunostains for PSA and prostate-specific acid phosphatase (PSAP) were negative. Furthermore, cytokeratin (CK) 7 and CK20 were negative, and p53, carcinoembryonic antigen, and CA-125 were positive. High-molecular-weight CK was diffusely positive without a basal cell pattern. In view of the clinical and radiologic findings, a diagnosis of primary SVC was suggested. Another CT scan showed that the 0090-4295/07/$32.00 778.e11 doi:10.1016/j.urology.2007.02.011
Figure 2. Gross features of resection specimen. Tumor was poorly circumscribed and had solid areas (long arrow) and cystic cavities (asterisk). Rectal wall was infiltrated, but rectal mucosa (short arrow) was not penetrated.
Figure 3. In resection specimen, tumor had cystic and papillary architecture. Hematoxylin-eosin stain, original magnification ⫻50.
Figure 4. Goblet cells and pools of mucin found in some areas. Desmoplasia seen around infiltrating acini. Hematoxylin-eosin stain, original magnification ⫻100.
(Fig. 4). The architecture was sometimes reminiscent of seminal vesicle tissue, and the tumor was surrounded by smooth muscle cells. No in situ component was found. Unequivocal infiltration in the desmoplastic stroma had occurred, and tumor had invaded the prostate and rectal wall. Immunohistochemically, the tumor was positive for high-molecular-weight CK, CK7, carcinoembryonic antigen, and CA-125, but negative for CK20 and PSA. Occasional cells were positive for PSAP. The clinical, radiologic, gross, histologic, and immunohistochemical findings were compatible with primary SVC. Six months later, metastases were found in the abdominal wall, and fine needle aspiration cytology showed malignant cells compatible with the previously diagnosed SVC. Antiandrogen medication was given. At the last follow-up visit, the patient was doing well without disease progression.
COMMENT tumor diameter had increased to 15 cm. After 50 Gy of neoadjuvant radiotherapy, the tumor was considered resectable, and the patient underwent cysto-prostatectomy, including rectal resection and iliac lymph node dissection in July 2005. Urine deviation was performed with an ileal conduit (Bricker), and the patient underwent terminal sigmoidoscopy. A 12 ⫻ 8 ⫻ 7-cm tumor was found between the urinary bladder and rectum. The tumor was attached to, and had infiltrated, the bladder wall from the outside, but no gross penetration to the bladder mucosa was seen. It had solid and cystic, white to yellow cut surfaces and was poorly circumscribed (Fig. 2). The tumor was centered on the seminal vesicle, filling out the central zone but had also invaded the transition and peripheral zones. The histologic architecture of the tumor was papillary and cystic (Fig. 3). The papillary fronds were lined with columnar epithelium with severe atypia. Occasional goblet cells and pools of mucin were seen 778.e12
The seminal vesicle is often invaded by locally advanced prostate cancer, but it rarely harbors primary tumors. Most malignant tumors arising in the seminal vesicle are adenocarcinomas.1 SVC typically presents with advanced, symptomatic disease. Among the most common presenting symptoms are hematuria and hematospermia, but urinary infection, dysuria, painful defecation, and general pelvic pain have also been reported.1–3 These symptoms are quite nonspecific, and, when they occur as the presenting symptoms of cancer, other malignancies are far more common than SVC. CT scans and ultrasonography may be helpful for localizing the tumor to the seminal vesicle before surgery.4 –7 The radiologic findings are usually described as consistent with a solid or cystic mass between the rectum and bladder or prostate. Sometimes, an expansion of the seminal vesicle is evident. The partially cystic nature of SVC can be suggestive of an old hemorrhage or abscess rather than cancer.7 UROLOGY 69 (4), 2007
In many previous case reports, the descriptions of macroscopic features of SVC have been very brief or omitted entirely. It seems that SVC has two main gross patterns. Some tumors have firm, gritty cut surfaces,8 with poor circumscription,9 and others are predominantly cystic1 and often filled with turbid red or brown fluid5,9 or pus and necrotic material.2 Grossly, papillary tumors in the cyst wall have been described.1,5 In the present case, a combination of solid, white, poorly circumscribed cut surfaces and several cystic spaces was found. Unlike some of the previously reported cases, the cyst fluid was clear, with no signs of hemorrhage. The histologic hallmark of SVC is adenocarcinoma with papillary growth1,3,5,9 –13; however, poorly differentiated carcinomas have also been described.4,6,12 An in situ component may be present and gives support to a seminal vesicle origin in poorly differentiated cases.6 In many cases, some mucinous differentiation is present,5,8,10,13 sometimes with goblet cells. Desmoplasia is seen around infiltrating glands.8 These features are not typical of prostatic acinar adenocarcinoma. Papillary growth is seen in ductal carcinoma of the prostate, but those tumors are positive for PSA and lack mucinous differentiation. The diagnostic difficulty occurs when a papillary component is missing or not sampled by biopsy. The morphology on TURP in our case was compatible with ductal carcinoma, but a PSA stain was negative. Extensive immunohistochemistry was performed on the TURP specimen, because the clinical and radiologic findings were suggestive of primary SVC. It might seem unlikely that a tumor centered on the seminal vesicle would be diagnosed by TURP, but a previously reported case was also found in a TURP specimen.1 This probably reflects that with the aid of radiology and immunohistochemistry, we now have a greater ability to accurately diagnose advanced cases of SVC with deep infiltration of the prostate. It should also be considered that normal seminal vesicle mucosa is sometimes sampled at TURP, which means that TURP has the potential to reach the base of the seminal vesicle. All published reports on the immunohistochemistry of SVC have shown that these tumors are negative for PSA and also usually for PSAP. CA-125 was positive in our case, similar to most other reports,1,5,14 although tumors negative for CA-125 have also been described.6,14 Carcinoembryonic antigen has been positive in most cases, including ours,1,4,6,7,9,10,12,13 but exceptional cases have been negative.1,5 The staining for CK7 has usually been strongly positive and CK20 negative.1,14 Similar to our case, Oxley et al.6 reported a positive high-molecular-weight CK stain. This keratin profile might be helpful in the differential diagnosis against adenocarcinomas primary to the prostate (usually CK7 and CK20 negative) or rectum (usually CK7 negative and CK20 positive). Urinary bladder adenocarcinomas are also usually CK7 positive and CK20 negative and must be distinguished from SVC on the basis of the topography, morphology, and lack of CA-125 expression.1 A negative PSA or PSAP stain might, by itself, have limited
UROLOGY 69 (4), 2007
diagnostic value because this can occur as an artifact. However, in conjunction with the other markers, the immunostaining pattern is suggestive of cancer of a nonprostatic origin. The diagnostic criteria for SVC shifted after CT,13 ultrasonography,4 and immunohistochemistry4,5,13,14 were introduced. Dalgaard and Giertsen11 proposed in 1956 that to qualify for SVC, a tumor must be a papillary or anaplastic carcinoma, localized exclusively or mainly to the seminal vesicle, and primary carcinoma should not be found in any site of the body. Benson et al.13 added that some degree of mucin production is required. These criteria are stricter than necessary today when both radiologic techniques and immunohistochemistry are available to support a seminal vesicle origin. In the present case, the cancer had infiltrated the prostate and the walls of the urinary bladder and rectum. However, with a characteristic histologic and immunohistochemical profile and a typical tumor distribution, we consider that a definitive diagnosis of primary SVC can be made even in some locally advanced cases. Acknowledgment. To Professor Jonathan Epstein, Johns Hopkins Hospital, Baltimore, Maryland for reviewing the slides and confirming the diagnosis. References 1. Thiel R, and Effert P: Primary adenocarcinoma of the seminal vesicles. J Urol 168: 1891–1896, 2002. 2. Williamson RC, Slade N, and Feneley RC: Seminal vesicle tumours. J R Soc Med 71: 286 –288, 1978. 3. Kawahara M, Matsuhashi M, Tajima M, et al: Primary carcinoma of seminal vesicle: diagnosis assisted by sonography. Urology 32: 269 –272, 1988. 4. Oguchi K, Takeuchi T, Kuriyama M, et al: Primary carcinoma of the seminal vesicle (cross-imaging diagnosis). Br J Urol 62: 383– 384, 1988. 5. Ohmori T, Okada K, Tabei R, et al: CA125-producing adenocarcinoma of the seminal vesicle. Pathol Int 44: 333–337, 1994. 6. Oxley JD, Brett MT, Gillatt DA, et al: Seminal vesicle carcinoma. Histopathology 34: 562–563, 1999. 7. Zenklusen HR, Weymuth G, Rist M, et al: Carcinosarcoma of the prostate in combination with adenocarcinoma of the prostate and adenocarcinoma of the seminal vesicles: a case report with immunocytochemical analysis and review of the literature. Cancer 66: 998 –1001, 1990. 8. Davis NS, Merguerian PA, DiMarco PL, et al: Primary adenocarcinoma of seminal vesicle presenting as bladder tumor. Urology 32: 466 – 468, 1988. 9. Gohji K, Kamidono S, and Okada S: Primary adenocarcinoma of the seminal vesicle. Br J Urol 72: 514 –515, 1993. 10. Chinoy RF, and Kulkarni JN: Primary papillary adenocarcinoma of the seminal vesicle. Indian J Cancer 30: 82– 84, 1993. 11. Dalgaard JB, and Giertsen JC: Primary carcinoma of the seminal vesicle; case and survey. Acta Pathol Microbiol Scand 39: 255– 267, 1956. 12. Tanaka T, Takeuchi T, Oguchi K, et al: Primary adenocarcinoma of the seminal vesicle. Hum Pathol 18: 200 –202, 1987. 13. Benson RC Jr, Clark WR, and Farrow GM: Carcinoma of the seminal vesicle. J Urol 132: 483– 485, 1984. 14. Ormsby AH, Haskell R, Jones D, et al: Primary seminal vesicle carcinoma: an immunohistochemical analysis of four cases. Mod Pathol 13: 46 –51, 2000.
778.e13
P
rimary seminal vesicle carcinoma (SVC) is a very rare tumor, and only 51 well-documented cases have been reported.1 The diagnosis is generally based on a combination of morphologic, immunohistochemical, and clinical findings, including radiologic examination. It is difficult to make a definitive diagnosis using biopsy, and surgical resection is usually required to determine whether the epicenter is in the seminal vesicles and whether it is primary to this site. We present a case of primary SVC suspected at transurethral resection of the prostate (TURP) and subsequently verified after procto-cysto-prostatectomy.
CASE REPORT A 73-year-old man with hematuria and hematospermia was first examined in March 2004. Digital rectal examination showed an enlarged multilobular right seminal vesicle that was confirmed by ultrasonography. The prostate volume was estimated at 85 cm3. The cystoscopy findings and serum prostate-specific antigen (PSA) level were normal (1.7 ng/ mL). Urinary cytology showed dissociated high-grade malignant cells with pleomorphic nuclei and no signs of adenocarcinoma differentiation. Computed tomography (CT) scan showed a multilobular, 12-cm-diameter, low-attenuated expansile process close to the prostate and on the site of the right seminal vesicle (Fig. 1). A diagnosis of abscess or hemorrhage was considered because of the partially cystic appearance. The patient underwent chest x-ray and CT of chest and abdomen without signs of malignancy elsewhere. He denied previous cancer, and his pathology record did not contain any malignant diagnoses. Because the patient had From the International Agency for Research on Cancer, Lyon, France; and Departments of Urology AND Pathology, Malmö University Hospital, Malmö, Sweden Address for correspondence: Lars Egevad, M.D., Ph.D., Pathology Group, International Agency for Research on Cancer (IARC), 150 Cours Albert Thomas, Lyon 69372 Cedex 08, France. E-mail: [email protected] Submitted: September 15, 2006; accepted (with revisions): December 7, 2007
© 2007 Elsevier Inc. All Rights Reserved
Figure 1. Front view of CT scan showing multilobular, lowattenuated, expansile process close to prostate and on site of right seminal vesicle (asterisk). Urinary bladder was dislocated.
hematospermia and lower urinary tract symptoms indicating bladder outlet obstruction, as well as a normal serum PSA value, we decided to perform diagnostic TURP with no preceding transrectal biopsy. This was done in February 2005, and adenocarcinoma was found on histologic examination. The tumor had columnar-stratified epithelium with elongated nuclei and a predominantly papillary architecture similar to ductal carcinoma of the prostate. However, immunostains for PSA and prostate-specific acid phosphatase (PSAP) were negative. Furthermore, cytokeratin (CK) 7 and CK20 were negative, and p53, carcinoembryonic antigen, and CA-125 were positive. High-molecular-weight CK was diffusely positive without a basal cell pattern. In view of the clinical and radiologic findings, a diagnosis of primary SVC was suggested. Another CT scan showed that the 0090-4295/07/$32.00 778.e11 doi:10.1016/j.urology.2007.02.011
Figure 2. Gross features of resection specimen. Tumor was poorly circumscribed and had solid areas (long arrow) and cystic cavities (asterisk). Rectal wall was infiltrated, but rectal mucosa (short arrow) was not penetrated.
Figure 3. In resection specimen, tumor had cystic and papillary architecture. Hematoxylin-eosin stain, original magnification ⫻50.
Figure 4. Goblet cells and pools of mucin found in some areas. Desmoplasia seen around infiltrating acini. Hematoxylin-eosin stain, original magnification ⫻100.
(Fig. 4). The architecture was sometimes reminiscent of seminal vesicle tissue, and the tumor was surrounded by smooth muscle cells. No in situ component was found. Unequivocal infiltration in the desmoplastic stroma had occurred, and tumor had invaded the prostate and rectal wall. Immunohistochemically, the tumor was positive for high-molecular-weight CK, CK7, carcinoembryonic antigen, and CA-125, but negative for CK20 and PSA. Occasional cells were positive for PSAP. The clinical, radiologic, gross, histologic, and immunohistochemical findings were compatible with primary SVC. Six months later, metastases were found in the abdominal wall, and fine needle aspiration cytology showed malignant cells compatible with the previously diagnosed SVC. Antiandrogen medication was given. At the last follow-up visit, the patient was doing well without disease progression.
COMMENT tumor diameter had increased to 15 cm. After 50 Gy of neoadjuvant radiotherapy, the tumor was considered resectable, and the patient underwent cysto-prostatectomy, including rectal resection and iliac lymph node dissection in July 2005. Urine deviation was performed with an ileal conduit (Bricker), and the patient underwent terminal sigmoidoscopy. A 12 ⫻ 8 ⫻ 7-cm tumor was found between the urinary bladder and rectum. The tumor was attached to, and had infiltrated, the bladder wall from the outside, but no gross penetration to the bladder mucosa was seen. It had solid and cystic, white to yellow cut surfaces and was poorly circumscribed (Fig. 2). The tumor was centered on the seminal vesicle, filling out the central zone but had also invaded the transition and peripheral zones. The histologic architecture of the tumor was papillary and cystic (Fig. 3). The papillary fronds were lined with columnar epithelium with severe atypia. Occasional goblet cells and pools of mucin were seen 778.e12
The seminal vesicle is often invaded by locally advanced prostate cancer, but it rarely harbors primary tumors. Most malignant tumors arising in the seminal vesicle are adenocarcinomas.1 SVC typically presents with advanced, symptomatic disease. Among the most common presenting symptoms are hematuria and hematospermia, but urinary infection, dysuria, painful defecation, and general pelvic pain have also been reported.1–3 These symptoms are quite nonspecific, and, when they occur as the presenting symptoms of cancer, other malignancies are far more common than SVC. CT scans and ultrasonography may be helpful for localizing the tumor to the seminal vesicle before surgery.4 –7 The radiologic findings are usually described as consistent with a solid or cystic mass between the rectum and bladder or prostate. Sometimes, an expansion of the seminal vesicle is evident. The partially cystic nature of SVC can be suggestive of an old hemorrhage or abscess rather than cancer.7 UROLOGY 69 (4), 2007
In many previous case reports, the descriptions of macroscopic features of SVC have been very brief or omitted entirely. It seems that SVC has two main gross patterns. Some tumors have firm, gritty cut surfaces,8 with poor circumscription,9 and others are predominantly cystic1 and often filled with turbid red or brown fluid5,9 or pus and necrotic material.2 Grossly, papillary tumors in the cyst wall have been described.1,5 In the present case, a combination of solid, white, poorly circumscribed cut surfaces and several cystic spaces was found. Unlike some of the previously reported cases, the cyst fluid was clear, with no signs of hemorrhage. The histologic hallmark of SVC is adenocarcinoma with papillary growth1,3,5,9 –13; however, poorly differentiated carcinomas have also been described.4,6,12 An in situ component may be present and gives support to a seminal vesicle origin in poorly differentiated cases.6 In many cases, some mucinous differentiation is present,5,8,10,13 sometimes with goblet cells. Desmoplasia is seen around infiltrating glands.8 These features are not typical of prostatic acinar adenocarcinoma. Papillary growth is seen in ductal carcinoma of the prostate, but those tumors are positive for PSA and lack mucinous differentiation. The diagnostic difficulty occurs when a papillary component is missing or not sampled by biopsy. The morphology on TURP in our case was compatible with ductal carcinoma, but a PSA stain was negative. Extensive immunohistochemistry was performed on the TURP specimen, because the clinical and radiologic findings were suggestive of primary SVC. It might seem unlikely that a tumor centered on the seminal vesicle would be diagnosed by TURP, but a previously reported case was also found in a TURP specimen.1 This probably reflects that with the aid of radiology and immunohistochemistry, we now have a greater ability to accurately diagnose advanced cases of SVC with deep infiltration of the prostate. It should also be considered that normal seminal vesicle mucosa is sometimes sampled at TURP, which means that TURP has the potential to reach the base of the seminal vesicle. All published reports on the immunohistochemistry of SVC have shown that these tumors are negative for PSA and also usually for PSAP. CA-125 was positive in our case, similar to most other reports,1,5,14 although tumors negative for CA-125 have also been described.6,14 Carcinoembryonic antigen has been positive in most cases, including ours,1,4,6,7,9,10,12,13 but exceptional cases have been negative.1,5 The staining for CK7 has usually been strongly positive and CK20 negative.1,14 Similar to our case, Oxley et al.6 reported a positive high-molecular-weight CK stain. This keratin profile might be helpful in the differential diagnosis against adenocarcinomas primary to the prostate (usually CK7 and CK20 negative) or rectum (usually CK7 negative and CK20 positive). Urinary bladder adenocarcinomas are also usually CK7 positive and CK20 negative and must be distinguished from SVC on the basis of the topography, morphology, and lack of CA-125 expression.1 A negative PSA or PSAP stain might, by itself, have limited
UROLOGY 69 (4), 2007
diagnostic value because this can occur as an artifact. However, in conjunction with the other markers, the immunostaining pattern is suggestive of cancer of a nonprostatic origin. The diagnostic criteria for SVC shifted after CT,13 ultrasonography,4 and immunohistochemistry4,5,13,14 were introduced. Dalgaard and Giertsen11 proposed in 1956 that to qualify for SVC, a tumor must be a papillary or anaplastic carcinoma, localized exclusively or mainly to the seminal vesicle, and primary carcinoma should not be found in any site of the body. Benson et al.13 added that some degree of mucin production is required. These criteria are stricter than necessary today when both radiologic techniques and immunohistochemistry are available to support a seminal vesicle origin. In the present case, the cancer had infiltrated the prostate and the walls of the urinary bladder and rectum. However, with a characteristic histologic and immunohistochemical profile and a typical tumor distribution, we consider that a definitive diagnosis of primary SVC can be made even in some locally advanced cases. Acknowledgment. To Professor Jonathan Epstein, Johns Hopkins Hospital, Baltimore, Maryland for reviewing the slides and confirming the diagnosis. References 1. Thiel R, and Effert P: Primary adenocarcinoma of the seminal vesicles. J Urol 168: 1891–1896, 2002. 2. Williamson RC, Slade N, and Feneley RC: Seminal vesicle tumours. J R Soc Med 71: 286 –288, 1978. 3. Kawahara M, Matsuhashi M, Tajima M, et al: Primary carcinoma of seminal vesicle: diagnosis assisted by sonography. Urology 32: 269 –272, 1988. 4. Oguchi K, Takeuchi T, Kuriyama M, et al: Primary carcinoma of the seminal vesicle (cross-imaging diagnosis). Br J Urol 62: 383– 384, 1988. 5. Ohmori T, Okada K, Tabei R, et al: CA125-producing adenocarcinoma of the seminal vesicle. Pathol Int 44: 333–337, 1994. 6. Oxley JD, Brett MT, Gillatt DA, et al: Seminal vesicle carcinoma. Histopathology 34: 562–563, 1999. 7. Zenklusen HR, Weymuth G, Rist M, et al: Carcinosarcoma of the prostate in combination with adenocarcinoma of the prostate and adenocarcinoma of the seminal vesicles: a case report with immunocytochemical analysis and review of the literature. Cancer 66: 998 –1001, 1990. 8. Davis NS, Merguerian PA, DiMarco PL, et al: Primary adenocarcinoma of seminal vesicle presenting as bladder tumor. Urology 32: 466 – 468, 1988. 9. Gohji K, Kamidono S, and Okada S: Primary adenocarcinoma of the seminal vesicle. Br J Urol 72: 514 –515, 1993. 10. Chinoy RF, and Kulkarni JN: Primary papillary adenocarcinoma of the seminal vesicle. Indian J Cancer 30: 82– 84, 1993. 11. Dalgaard JB, and Giertsen JC: Primary carcinoma of the seminal vesicle; case and survey. Acta Pathol Microbiol Scand 39: 255– 267, 1956. 12. Tanaka T, Takeuchi T, Oguchi K, et al: Primary adenocarcinoma of the seminal vesicle. Hum Pathol 18: 200 –202, 1987. 13. Benson RC Jr, Clark WR, and Farrow GM: Carcinoma of the seminal vesicle. J Urol 132: 483– 485, 1984. 14. Ormsby AH, Haskell R, Jones D, et al: Primary seminal vesicle carcinoma: an immunohistochemical analysis of four cases. Mod Pathol 13: 46 –51, 2000.
778.e13