Seminal vesicle leiomyosarcoma: Case report and literature review.

INTRODUCTION AND BACKGROUND: Primary leiomyosarcoma of the seminal vesicle is an extremely rare and highly malignant disease with less than 15 cases reported. CASE DESCRIPTION: A 34-year-old man presented with acute urinary symptoms. Imagen studies showed an abdominal mass (80 mm × 65 mm × 50 mm) with contrast enhancement, compressing the right side of the bladder but with a clear cleavage level between surrounding organs. The patient underwent a transrectal US-guided biopsy which was informed as compatible with leiomyosarcoma by immunohistochemical characterization. We performed a cystoprostatectomy and pelvic lymphadenectomy plus radiotherapy. Pathology showed a 7.5 cm × 6 cm nodular para-vesical Leiomyosarcoma histological grade 2 with 0/22 lymph nodes involved. Twelve months after the surgery no recurrences have presented. CONCLUSION: A multi-disciplinary therapeutic approach, combined with close follow-up, is mandatory to obtain good outcomes in such rare and challenging cases.

The MICA-NKG2D axis in clear cell renal cell carcinoma bolsters MICA as target in immuno-oncology.

NKG2D is a major natural killer (NK) cell-activating receptor that recognizes eight ligands (NKG2DLs), including MICA, and whose engagement triggers NK cell effector functions. As NKG2DLs are upregulated on tumor cells but tumors can subvert the NKG2D-NKG2DL axis, NKG2DLs constitute attractive targets for antibody (Ab)-based immuno-oncology therapies. However, such approaches require a deep characterization of NKG2DLs and NKG2D cell surface expression on primary tumor and immune cells. Here, using a bioinformatic analysis, we observed that MICA is overexpressed in renal cell carcinoma (RCC), and we also detected an association between the NKG2D-MICA axis and a diminished overall survival of RCC patients. Also, by flow cytometry (FC), we observed that MICA was the only NKG2DL over-expressed on clear cell renal cell carcinoma (ccRCC) tumor cells, including cancer stem cells (CSC) that also coexpressed NKG2D. Moreover, tumor-infiltrating leukocytes (TIL), but not peripheral blood lymphoid cells (PBL) from ccRCC patients, over-expressed MICA, ULBP3 and ULBP4. In addition, NKG2D was downregulated on peripheral blood NK cells (PBNK) from ccRCC patients but upregulated on tumor-infiltrating NK cells (TINK). These TINK exhibited impaired degranulation that negatively correlated with NKG2D expression, diminished IFN-γ production, upregulation of TIM-3, and an impaired glucose intake upon stimulation with cytokines, indicating that they are dysfunctional, display features of exhaustion and an altered metabolic fitness. We conclude that ccRCC patients exhibit a distorted MICA-NKG2D axis, and MICA emerges as the forefront NKG2DL for the development of targeted therapies in ccRCC.