Cysts and epithelial proliferations of the testicular collecting system (including rete testis).

Neoplastic and non-neoplastic proliferations of the testicular collecting system may be a source of diagnostic difficulty as they are rarely encountered and may have an appearance that leads to confusion with lesions arising in adjacent structures. The rete testis and epididymis are the 2 sites that are most likely to give rise to this unusual group of lesions. This article principally, although not exclusively, deals with those lesions that produce an intrascrotal mass. These include benign acquired or developmental cysts such as cystic dysgenesis of the rete testis or acquired cystic transformation of the rete testis, non-neoplastic epithelial proliferations such as adenomatous hyperplasia of the rete testis or cribriform hyperplasia of the epididymis, and benign or malignant neoplasms. Rete testis cystadenoma, including the sertoliform variant, and papillary cystadenoma of the epididymis are examples of benign tumors of the testicular collecting system that must be considered, the latter is the more likely of the 2 to be encountered. Primary carcinoma of either the rete testis or the epididymis is a rare occurrence; these entities are considered in some detail to allow for their recognition and distinction from other tumors that may occur in this region. Our own experience with 18 unpublished cases of lesions of the rete is also present.

The utility of tissue transglutaminase as a marker of apoptosis during treatment and progression of prostate cancer.

PURPOSE: To determine the extent of cell proliferation and apoptosis during treatment and progression of prostate cancer and to determine whether staining for tissue transglutaminase is a better histological marker than TUNEL for neoadjuvant androgen ablation treatment of localized prostate cancer. MATERIALS AND METHODS: Immunocytochemistry techniques were used on archival prostate tissue from four groups of men: 14 men with BPH, 18 men with untreated, localized prostate cancer, 21 men with localized prostate cancer who received neoadjuvant hormone therapy prior to prostatectomy and 18 men with metastatic androgen-independent prostate cancer. Cell proliferation was evaluated by staining for the Ki67 nuclear antigen, and apoptosis was evaluated by staining for DNA fragmentation (TUNEL technique) and tissue transglutaminase (tTG). Image analysis was used to quantitate the results. RESULTS: TUNEL staining increased by 37% in localized prostate cancer compared with BPH, with a further increase of 43% seen after neoadjuvant therapy, although variation was such that neither was statistically significant. In androgen-independent cancer, TUNEL staining was decreased compared with neoadjuvant hormone treated cancer (p = 0.02). Staining for tTG was not increased in untreated prostate cancer compared with BPH; however, staining more than doubled after neoadjuvant therapy, compared with untreated prostate cancer (p = 0.04). Staining for tTG was markedly decreased in androgen-independent cancer (p = 0.07 compared with BPH and p = 0.0004 compared with neoadjuvant hormone treated cancer). Ki67 immunoreactivity did not significantly change in localized prostate cancer, either before or after neoadjuvant therapy, compared with BPH, but it more than doubled in androgen-independent prostate cancer (p = 0.07 compared with BPH and p = 0.05 compared with untreated prostate cancer). CONCLUSIONS: This study shows that cell proliferation increases and apoptosis decreases as prostate cancer progresses to androgen independence, and, that of the markers used in this study, tissue transglutaminase most accurately reflects the anticipated effect of neoadjuvant hormone therapy on localized prostate cancer. An assessment of these parameters provides a valuable tool for appraising new prostate cancer therapies.