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Testicular germ cell tumors (TGCTs) are the most commonly diagnosed malignancies in younger men. The monitoring of disease course and recurrence is supported by traditional tumor markers, including α-fetoprotein (AFP). AFP is physiologically synthesized in the liver and can be detected at increased levels in testicular cancer patients as well as under other benign liver diseases, which have been reported as a misleading cause of interpretation of TGCTs clinical course. A cluster of stem cell-associated microRNAs has been reported to outperform traditional tumor markers in newly diagnosed TGCTs, but the value of these microRNAs to differentiate between specific and unspecific AFP elevations, has never been reported. We report here a patient with chronic hepatitis B and normal liver related blood values presenting with a surgically removed primary TGCT and elevated AFP levels. Clinical staging revealed a suspect retroperitoneal metastatic lymph node together with other risk factors and first line treatment with PEB chemotherapy was administered. During curative treatment significantly rising AFP levels led to the assumption of chemo-resistant disease, mandating the initiation of salvage chemotherapy and surgical removal of the putative lymph node metastases. The AFP levels continuously decreased with the interruption of chemotherapeutic agents, indicating a chemotherapy-induced liver toxicity on the basis of pre-existing liver disease. MiR-371a-3p serum levels were not detectable in serum samples with elevated AFP levels. In conclusion, miR-371a-3p may be a reliable biomarker to differentiate between non-specific AFP elevations in TGCTs patients.

Dramatic success in cancer immunotherapy has been achieved over the last decade with the introduction of checkpoint inhibitors, leading to response rates higher than with chemotherapy in certain cancer types. These responses are often restricted to cancers that have a high mutational burden and show pre-existing T-cell infiltrates. Despite extensive efforts, therapeutic vaccines have been mostly unsuccessful in the clinic. With the introduction of next generation sequencing, the identification of individual mutations is possible, enabling the production of personalized cancer vaccines. Combining immune check point inhibitors to overcome the immunosuppressive microenvironment and personalized cancer vaccines for directing the host immune system against the chosen antigens might be a promising treatment strategy.