Cystic retroperitoneal metastasis from testicular seminoma, radiologically mimicking as lymphangioma

Background Retroperitoneal nodal metastasis in a primary testicular tumor is not uncommon and usually presents as solid or solid-cystic nodal masses. A completely cystic appearance with fluid attenuation or fluid signal intensity on computed tomography (CT) and magnetic resonance imaging (MRI), respectively, is an uncommon presentation. There are many case reports of different types of cystic retroperitoneal masses; however, to our knowledge, metastatic retroperitoneal cystic masses showing fluid attenuation/fluid signal intensity on CT/ MRI secondary to primary testicular seminoma masquerading as cystic lymphangioma has been rarely reported in the medical literature. Our case report reports a case of a metastatic retroperitoneal cystic mass in a known case of testicular seminoma patient, which was misdiagnosed as cystic lymphangioma initially based on imaging. Case presentation A 55-year-old—patient presented to our hospital with abdominal pain, which was on and off in character. The patient underwent routine ultrasound abdomen, CT and MRI, which revealed multiple cystic lesions in the retroperitoneum. Initially, a provisional diagnosis of cystic lymphangioma was made based on the utterly cystic nature of the lesion and the presence of calcification. However, fine-needle aspiration cytology (FNAC) confirmed the metastatic origin of the lesion and was strengthened by the previous clinical history of orchidectomy. Conclusion The treatment strategy for cystic retroperitoneal masses varies depending on the cause and its nature, so differentiation between the cystic masses is essential. Metastasis should also be kept in the differentials in all cystic retroperitoneal masses. Moreover, clinical history and FNAC can assist in making the correct diagnosis.

CNV Hotspots in Testicular Seminoma Tissue and Seminal Plasma

Seminoma (SE) is the most frequent type of testicular tumour, affecting predominantly young men. Early detection and diagnosis of SE could significantly improve life quality and reproductive health after diagnosis and treatment. Copy number variation (CNV) has already been associated with various cancers as well as SE. In this study, we selected four genes (MAGEC2, NANOG, RASSF1A, and KITLG) for CNV analysis in genomic DNA (gDNA), which are located on chromosomes susceptible to gains, and whose aberrant expression was already detected in SE. Furthermore, CNV was analysed in cell-free DNA (cfDNA) from seminal plasma. Analysis was performed by droplet digital polymerase chain reaction (ddPCR) on gDNA from SE and nonmalignant testicular tissue. Seminal plasma cfDNA from SE patients before and after surgery was analysed, as well as from healthy volunteers. The CNV hotspot in gDNA from SE tissue was detected for the first time in all analysed genes, and for two genes, NANOG and KITLG it was reflected in cfDNA from seminal plasma. Although clinical value is yet to be determined, presented data emphasize a potential use of CNV as a potential SE biomarker from a liquid biopsy.

The m6A Methyltransferase METTL3 Promotes Cisplatin Resistance and Invasion in Testicular Seminoma via BCL2

Background: Methyltransferase-like 3 (METTL3) involves in promoting tumor progression through tumor-related genes N6-methyladenosine (m6A) modification. Our previous study found that METTL3 plays an important role in seminoma chemosensitivity. BCL-2 is a key cause of cisplatin resistance in many tumors. Therefore, we want to explore whether METTL3 affects cisplatin resistance of seminoma by regulating BCL-2.Methods: In this study, we downregulated and overexpressed METTL3 in TCam-2 cisplatin resistant cells (TCam-2/CDDP). Then, m6A RNA methylation quantification of BCL-2 and cell viability assay, cell apoptosis analysis and cell invasion assay were investigated under the condition of with or without cis‐dichlorodiammine platinum (CDDP) treatment. Results: Consistent with our previous results, METTL3 significantly affects the chemosensitivity of TCam-2/CDDP. After METTL3 downregulated, the proliferation and anti-apoptosis ability of TCam-2/CDDP cells significantly weakened. Correspondingly, overexpression of METTL3 could promote the chemoresistance. However, the phenotype could be partly reversed by decreasing the expression of BCL-2. Moreover, we found that the m6A modification of BCL-2 is more abundant in cisplatin-resistant strains. Knockdown and overexpression of METTL3 significantly affected the m6A modification and the protein level of BCL-2 in TCam-2/CDDP. Finally, we found that METTL3 also promoted the invasion ability of TCam-2/CDDP cells via BCL2.Conclusion: This study revealed that METTL3 promotes anti-apoptosis and invasion of TCam-2/CDDP through BCL-2. And it indicated that METTL3 and BCL-2 may be an effective treatment target for CDDP-resistance seminoma.