Cancer Science & Therapy

Background: Pure testicular yolk sac tumours are extremely rare among adults, and there is no prior report of spinal cord compression syndrome due to yolk sac testis tumour metastasis in an adult.

Case presentation: Here we describe the case of a 26-year-old male with a testicular yolk sac tumour that was found when a vertebral metastasis caused spinal cord compression. Symptoms included lower back pain and a growing painless testicular mass. Treatment comprised emergency surgical spinal cord decompression and orchidectomy, followed by 3 cycles of bleomycin, etoposide, and platinum (BEP) chemotherapy, and then 3 cycles of etoposide and platinum and 40 Gy vertebral radiotherapy. One year later, cement leaked into the spinal duct, prompting a return of compression syndrome. Corporectomy was performed, followed by osteosynthesis. The patient’s treatment was consolidated with 34 months and zoledronic acid administration. Although spinal metastasis from a yolk sac tumour is extremely rare, it must be considered in young adults with a testicular mass who exhibit pain or limb numbness. Such cases warrant rapid surgical decompression and radical orchidectomy, followed by adjuvant chemotherapy.

Conclusion: Our case is atypical due to the patient’s age and the disease presentation. Spinal cord compression syndrome caused by yolk sac tumor metastasis is extremely rare in adulthood, and usually has a bad prognosis when diagnosed late.

Objectives: Burkitt lymphoma is a kind of non-Hodgkin B-cell-derived malignancy originating from germinal centre B cells. FAM54A has been proven to be involved in various physiological and pathological processes of cancers, but the biological function of FAM54A in Burkitt lymphoma remains unclear. Thus, the aim of our research was to elucidate the roles of FAM54A in the proliferation, apoptosis and cell cycle of Burkitt lymphoma.

Methods: A Burkitt lymphoma cell line (Namalwa) was chosen to perform the following experiments. FAM54AshRNA and negative control-shRNA lentiviruses that were synthesized by Qiagen were used to transfect targeted cells to knockdown FAM54A or as a negative control. Then, cell proliferation, cell cycle and cell apoptosis were detected by using MTS assay, propidium iodide staining and Annexin V-APC staining, respectively.

Results: Our results showed that high expression of FAM54A protein was found in the Namalwa cell line. Furthermore, MTS analysis revealed that knockdown of FAM54A obviously inhibited cell proliferation in Namalwa cells. Moreover, cell cycle analysis showed that knockdown of FAM54A induced Namalwa cell apoptosis and arrested the cell cycle in G2/M phase.

Conclusion: These findings suggest that FAM54A is essential for Namalwa cell proliferation and may be a potential therapeutic target for the treatment of Burkitt lymphoma.