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A 79-year-old man underwent a transrectal prostate needle biopsy with a prostate-specific antigen (PSA) level of 12.0 ng/ml. He was diagnosed with adenocarcinoma (Gleason score 4＋3, cT3aN0M0) and underwent radiation therapy. Eight months later, he was administered hormone therapy because of a rise in PSA level to 8.4 ng/ml. One year and 5 months later, he experienced back pain, and computed tomography revealed multiple lymphadenopathies and irregular prostate enlargement. The PSA level was 0.097 ng/ml. Re-biopsy of the prostate and biopsy of the lymph node were performed. Pathological examination revealed neuroendocrine differentiation of the prostate. The disease progressed rapidly, and the patient died 4 months after the biopsy. Neuroendocrine differentiation of prostate cancer is rare, and its development may not be consistent with PSA levels. Therefore, periodic imaging examinations should be conducted, even when PSA levels are low.

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Asymptomatic prostatitis is classified as category IV in NIH classification of prostatitis syndrome (1999). No report concerning this category has been present. We investigated this category histopathologically and clinically, in order to clarify the histopathological distribution and its correlation to the clinical features, in this study. Among 785 patients who were suspected prostate cancer because of their high prostatic specific antigen (PSA) values and to have a sextant prostate needle biopsy was performed between January, 1996 and December, 2000, 88 patients (11.2%) were diagnosed as NIH category IV prostatitis (asymptomatic prostatitis). We observed all pathological specimens stained with Hematoxylin-Eosine, and classified them into subtypes according to the classification criteria for prostatitis defined by True et al. (1999). We also investigated the relationship between histopathological distribution and clinical features such as PSA values, PSA density, the incidence of pyuria or bacteriuria. In the histopathological study, grade distributions were 12.5% (11/88) in mild, 71.6% (63/88) in moderate, and 15.9% (14/88) in severe. Location distributions were 2.3% (2/88) in glandular, 68.2% (60/88) in periglandular, and 29.5% (26/88) in stromal. No relationship between these subtypes and clinical features was recognized statistically. However, 7 patients (7.95%) were diagnosed as prostate cancers, later. Pyuria was found in 29.1% (23/79). Bacteriuria was present in 14.3% (11/77). Isolated bacteria were 4 strains of Enterococcus faccalis, 2 strains of each of Pseudomonas aeruginosa and Staphylococcus aureus, and one strain of each of Escherichia coli, Klebsiella oxytoca, Enterobacter cloacae, Enterobacter aerogenes, Staphylococcus haemolyticus, and Staphylococcus epidermidis. Gram positive rod, and Candida sp. No relationship between these subtypes and bacterial species was recognized. These results indicated that the incidence of NIII category IV prostatits was not low without correlation to any clinical features. However, we should pay attention to the presence of prostate cancer, because a small number of the patients were diagnosed as prostate cancer, later.

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BACKGROUND: A pathway consisting of bombesin, G-protein coupling receptors (GPCRs), metalloproteases, pro-heparin-binding epidermal growth factor (proHB-EGF), and epidermal growth factor receptor (EGFR) has been reported in prostate cancer cells. The occurrence of HB-EGF shedding from proHB-EGF in this pathway, however, has not been proven directly. In addition, it is still unclear how much this pathway contributes to the migration of prostate cancer cells. In this study, we tried to directly elucidate HB-EGF shedding in this pathway and to determine its contribution to the migration of prostate cancer cells. METHODS: RT-PCR and indirect immunofluorescence staining for HB-EGF and its receptors, such as EGFR and HER4/erbB4, were performed on PC-3 cells. The influences of bombesin, anti-EGFR neutralizing monoclonal antibody, HB-EGF, and HB-EGF shedding inhibitor on the migration of PC-3 cells were studied by means of in vitro wound assays. The amount of HB-EGF shed from PC-3 cells with alkaline phosphatase-tagged HB-EGF in the presence of bombesin was determined by measuring AP activity. Immunoprecipitations and phosphotyrosine Western blotting were performed to detect EGFR transactivated by bombesin. RESULTS: PC-3 expressed HB-EGF and EGFR, but not HER4/erbB4. PC-3 migrated in the presence of bombesin, but its migration was partly inhibited by the neutralizing antibody against EGFR. PC-3 also migrated in the presence of HB-EGF, but HB-EGF shedding inhibitor partly inhibited this phenomenon. HB-EGF was shed from PC-3 cells in the presence of bombesin, and this shedding was inhibited by HB-EGF shedding inhibitor. In addition, the EGFR on PC-3 was activated in the presence of bombesin and inactivated in the presence of HB-EGF shedding inhibitor. CONCLUSIONS: These results indicated that HB-EGF shedding and the following transactivation of EGFR occurs in this pathway and that this pathway partly contributes to the migration of prostate cancer cells.

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Papillary adenocarcinoma of the prostate, previously referred to as endometrioid carcinoma, is a variant of prostatic adenocarcinoma. Clinical and pathological evidence of involvement of the periurethral prostatic duct or verumontanum is usually required for definitive diagnosis of papillary adenocarcinoma. However, significant histologic and clinical features of papillary adenocarcinoma overlap with typical acinar carcinoma. Four cases of papillary adenocarcinoma were studied for the clinical features, histologic characteristics and immunohistochemical nature of prostatic specific antigen. In two cases, there were papillary regions, near the verumontanum, but in the other two cases, there were no papillary regions in the urethra. In two cases, acinar adenocarcinoma coexisted with papillary adenocarcinoma. All cases displayed positive immunohistochemical staining for prostatic specific antigen. In accordance with the observations of others, we suggest that papillary adenocarcinoma is one aspect of growth pattern of acinar adenocarcinoma, not a concept of a unique clinical and pathological entity.

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