Background Fibrosarcoma is a very rare tumor that arises from fibrous tissue. Less than 5% of fibrosarcoma originate from the urogenital tract. Penile fibrosarcoma, even more rare, is characterized by pain, enlargement, penile erection and urinary tract obstruction. To our knowledge, this is the second reported case named “fibrosarcoma of the corpus cavernosum”. Case presentation A 51-year-old male presented with a 1-month history of penis pain during erection. CT scan showed a soft tissue mass arising from the proximal part of the penis. We diagnosed it as penile sarcoma, performing local excision. The postoperative pathological result was moderately differentiated fibrosarcoma. 3 months later, CT scan showed the recurrence of the tumor, and multiple metastases. Although he received chemotherapy, he died 10 months after surgery. Conclusions Fibrosarcoma of the corpus cavernosum is rare and have poor prognosis. Total penile amputation may be the best treatment. The effects of chemotherapy are limited. No more effective treatment has been found for a disseminated disease to date.

Purpose Endometriosis is one of the most common, difficult, and complicated gynecological disorders. Vascular cell adhesion molecule 1 (VCAM-1) has been reported to be aberrantly expressed in patients with endometriosis. However, the exact role and mechanism of VCAM-1 in endometriosis remains unclear. Methods The expression of transforming growth factor beta 1 (TGF-β1) and VCAM-1 was determined by quantitative real-time polymerase chain reaction and western blotting. Human endometriotic cells were cultured and their responsiveness to TGF-β1 was evaluated by Cell Counting Kit-8, 5-ethynyl-2′-deoxyuridine, and transwell migration and invasion assays. Results The levels of TGF-β1 and VCAM-1 mRNA were upregulated in the endometriotic tissues. Knockdown of TGF-β1 in endometriotic cyst stromal cells caused a marked inhibition of cell proliferation, migration, and invasion. Treatment of endometriotic cyst stromal cells with TGF-β1 resulted in an obvious promotion of cell proliferation, migration, and invasion, and strikingly increased the protein expression of VCAM-1. Silencing of Smad3 abated TGF-β1-stimulated VCAM-1 expression. Furthermore, the promoting effects of TGF-β1 on the proliferation, migration, and invasion of endometriotic cyst stromal cells were blocked by silencing of VCAM-1. Conclusion Knockdown of VCAM-1 impedes TGF-β1-mediated proliferation, migration, and invasion of endometrial cells, thereby indicating that VCAM-1 may serve as a therapeutic target for endometriosis.

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