Primary diseases of the seminal vesicles (SV) are very rare entities.Nonneoplastic lesions of the seminal vesicles include amyloidosis, inflammation, calcification and calculi, radiation-induced changes, and basal cell proliferation.Seminal vesicles are frequently involved by tumors originating elsewhere, in particular by prostatic adenocarcinoma, urothelial carcinoma, and rectal adenocarcinoma. On the contrary, primary tumors of the seminal vesicles are rare. Among these, the most common is seminal vesicle adenocarcinoma. To date, less than 100 cases have been reported in literature. Morphologically, primary SV adenocarcinoma is described as a papillary or sheetlike growth architecture, with trabecular and glandular patterns, composed by hobnail tumor cells, frequently with mucinous differentiation. On the contrary, mesenchymal tumors include benign lesions such as leiomyoma, schwannoma, fibroma, paraganglioma, solitary fibrous tumor, cystadenoma, and mixed epithelial and stromal tumors (MEST).Cystadenoma is a rare benign tumor, while MESTs are biphasic tumors with stromal and benign epithelial components. Histological features such as stromal atypia, mitotic activity, nuclear pleomorphism, and tumor necrosis distinct MEST in low-, intermediate-, and high-grade tumors.In recent years, multiple studies reported a link between tumorigenesis and tumor microenvironment. In this regard, the molecular mechanisms connecting prostate cancer (PCa) progression and the host microenvironment have been described and include extracellular matrix (ECM), myofibroblasts, cancer-associated fibroblasts (CAFs), neuroendocrine cells, adipose tissue, and the immune-modulatory cells. Of note, only one study evaluated the influence of seminal vesicle's tumor microenvironment (SVME) on prostate cancer cells so far. Besides, in vivo experiments in NOD/SCID mice clarified the influence of SVME on PCa progression. As such, the injection of PC3 cells into the prostate or the SV resulted in different tumor aggressiveness, and the incidence of retroperitoneal lymph node metastases was significantly higher in mice models receiving SV injection. These findings demonstrated that SVs (rather than the prostate) offer a stimulating tumor microenvironment for growth and invasion of prostate cancer cells.
Keywords: Adenocarcinoma; Benign tumors; Cancer-associated fibroblasts; Cystadenoma; Experimental models; Extracellular matrix; MEST; Malignant tumors; Mesenchymal tumors; Microenvironment; Mixed epithelial and stromal tumors; Myofibroblasts; Prostate cancer; Seminal vesicles; Tumorigenesis.