Key result
Surgical resection of giant paratesticular liposarcoma achieves ~30 months relapse-free survival in one patient.
Why the study?
Paratesticular liposarcomas are extremely rare malignant tumors with challenging diagnosis and limited data on molecular characterization and management.
Case Report (n=1)
Molecular analysis showing MDM2 and CDK4 co-amplification can support the histological diagnosis of rare paratesticular liposarcomas.
May support histological diagnosis of rare paratesticular liposarcomas; leaves open routine NGS use beyond case reports.
Paratesticular liposarcomas are extremely rare malignant tumors originating from fat tissues, with an often-challenging diagnosis. We present here the case of a 76-year-old man with a giant paratesticular liposarcoma, initially misdiagnosed as a scrotal hernia. After two years, the progressively enlarging mass underwent surgical resection, and a diagnosis of well-differentiated liposarcoma (lipoma-like subtype) was made. Post-operative treatments were not indicated, and the patient remains relapse free. Next generation sequencing performed on the neoplastic tissue showed co-amplification of MDM2 and CDK4. These alterations are molecular hallmarks of well-differentiated liposarcomas and corroborate the histological diagnosis. Clinical and molecular features of the presented case are in line with the majority of previously published experiences. In conclusion, the presence of a liposarcoma should be taken into account during the diagnostic workup of scrotal masses, in order to minimize the rate of misdiagnosis and improper management. Molecular analysis may support histological characterization of these rare entities and potentially disclose novel therapeutic targets.
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Pavone et al. (2022) conducted a case report in Giant paratesticular liposarcoma (n=1). Surgical resection was evaluated on Disease recurrence. Surgical resection of a giant paratesticular liposarcoma resulted in the patient remaining relapse-free at 30 months of follow-up, with molecular analysis confirming MDM2 and CDK4 co-amplification.
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