The Kirsten rat sarcoma virus (KRAS) gene provides instructions on creating K-Ras proteins that are part of the RAS/MAPK signalizing pathway. KRAS genes are a type of oncogene that can cause normal cells in the body to become cancerous. The frequency and role of genomic alterations in testicular germ cell tumors (TGCTs) is largely unexplored. A recent study published in Frontiers in Oncology evaluated the mutation profile of a 15-driver gene panel and copy number variation of KRAS genes to determine the correlation between KRAS and TGCTs.
A test group of 97 patients with TGCT was recruited for the study from the Barretos Cancer Hospital in Brazil. Fifty-one patients underwent real-time polymerase chain reaction (PCR) to determine the KRAS gene’s copy number variation (CNV), while 65 patients underwent mutation analysis using the TruSight Tumor 15 panel. Sample categories were compared using univariate analysis in relation to mutational frequencies, and survival analysis was conducted through the Kaplan-Meier method and log-rank test.
The study results demonstrated that KRAS copy number gain was a frequent event, occurring in 80.4% of TGCT cases, and resulted in a worse prognosis compared with the group that experienced no KRAS copy gain. Several different variants were found in 11 of 15 genes in the panel among the 65 TGCT cases, with the TP53 gene as the most recurrently mutated driver gene.
Further studies are needed to learn more about the molecular landscape of TGCT. However, this study demonstrates the potential of utilizing TGCT as a biomarker for germ cell tumors and utilizing variants for choosing targeted therapies.
