At the current time, there is no standard treatment protocol for patients with MiT family translocation RCC. Future studies will utilize emerging genomic technologies to identify prognostic factors and therapeutic targets in these neoplasms.
One study found that high chromosome copy number alterations in Xp11 translocation RCC are associated with aggressive behavior. Another found that chromosome 17q gain correlated with older age and worse outcome which corroborates the effect of age reported by Ellis et al. Expression profiling studies have demonstrated that the MET receptor tyrosine kinase is induced by TFE3 gene fusions, and this represents a targetable protein. Whole genome DNA and RNA sequencing studies have recently been performed on a small number of cases, and it is hoped that these studies and others will identify therapeutic targets. MiT family translocation RCC do express high levels of phosphorylated S6, a marker of activation of the mammalian target of rapamycin (mTOR) pathway. This finding suggests that the potential utility of mTOR inhibitors in MiT family translocation RCC, and several case reports have documented their efficacy though others have not. Two other genetically Xp11 confirmed Xp11 translocation RCC reported in the literature have responded to sunitinib, suggesting possible efficacy of tyrosine kinase inhibitors in treating these neoplasms.