Paratesticular rhabdomyosarcoma of a young adult

Sarcomas represent large and diverse group of malignant tumours, originating from mesenchymal cells. Nearly 15% of all childhood tumours and about 1% of all tumours in adults are sarcomas [1]. The incidence of adult soft tissue sarcomas in Europe is 5/100,000 [2]. Rhabdomyosarcoma accounts for 4.6% of all soft tissue sarcomas and it is the most common paediatric sarcoma, while it is extremely rare in adults [3]. The majority of scrotal neoplasms originate from the testicle itself. However, some may arise from mesenchymal elements of paratesticular tissue: spermatic cord, epididymis, and testicular envelopes. Only about 30% of all paratesticular neoplasms are malignant. Their real origin in comparison to anatomical structures is somewhat hard to determine; however, it is said that spermatic cord is the most common site (90%) [4]. The most common paratesticular neoplasm is soft tissue sarcoma: leiomyosarcoma, rhabdomyosarcoma, and liposarcoma being at the top of the list [5]. We report a rare case of a 25-year-old male who was admitted at our institution after surgical treatment in a small regional centre. Our diagnosis based on delivered paraffin-embedded tumour tissue samples was: Paratesticular pleomorphic rhabdomyosarcoma, high grade. Pathohistological report was: Tumour tissue consists of fusiform, oval, polygonal, spindle and numerous bizarre large rhabdomyoblasts, including multinucleated ones. Nuclei are hyperchromatic. In bizarre rhabdomyoblasts cytoplasm is abundant, eosinophilic, granular, rich in thick and thin filaments (Fig. 1). Tumour cells are forming nests and sheets. Stroma is variably myxoid with minor sclerotic areas. Microcystic formations are focally present. Minor elements of embryonal (spindle cell) and alveolar rhabdomyosarcoma as well as sclerosing rhabdomyosarcoma are also present (Fig. 2). Tumour is well vascularised. Mitotic activity is high (over 10 mitosis per 10 high power fields). Immunophenotype: vimentin + (monoclonal antibody, clone V9, DAKO, visualisation kit FLEX), desmin + (monoclonal antibody, clone D33, Lab Vision IHC System Solution, visualisation kit FLEX) (Figs. 3 and 4) and actin + (monoclonal antibody, clone HHF35, DAKO, visualisation kit FLEX), MyoD1 – (monoclonal antibody, clone 5.8A, DAKO, visualisation kit LP detection system), and S-100 protein – (polyclonal antibody, DAKO, visualisation kit FLEX, CD34–, CD99–, CD117–). The patient was initially treated in a small regional centre and was referred to a medical oncologist only after the first relapses, three months after the surgery. He was in a good physical shape, with no complications. He did not have any significant personal or family medical history. Serum alphaphetoprotein, lactate dehydrogenases, and