Our findings also suggest the in vivo anti tumour effect of SP600125 treatment most likely be caused by the specific action of SP600125 to deplete base like tumour cells and maybe not to its non specific growth inhibitory effect on bulk tumour cells. In support of this concept, the outcome of the serial transplantation assays demonstrated that temporary administration of the reversible Aurora A inhibitor inhibitor of JNK is sufficient to provide a resilient, preventive effect against secondary tumor formation. Moreover, the results indicated that the in vivo SP600125 treatment depletes self-renewing, base like cells but has without any impact on the bulk tumour cells. But, it needs to be accepted that these findings do not exclude the possibility that the tumour initiating cells within established xenografts may not necessarily be stem like cells and that SP600125 also targets such non stem glioblastoma cells with tumour initiating potential. Intriguingly, SP600125 is currently increasingly delivered Meristem to the brain parenchyma via the intraventricular route in animal models of neurological conditions to boost neurological and biochemical features, including cognitive function. The reported neuro-protective activity of SP600125 causes it to be an even more appealing therapeutic option, and the reported findings also suggest that, in medical settings, the drug may be applied not only systemically but also intrathecally, for example via an Ommaya reservoir installed during surgery. It’s been well-documented that the JNK pathway is activated in astrocytic tumours in direct relationship with the WHO grade of malignancy however not in normal brain tissues, suggesting a role for JNK in the biology of astrocytic tumours including their most dangerous type, buy Gemcitabine glioblastoma. While a previous study utilising the serum cultured U87 cell line showed that JNK is indeed mixed up in growth of mass cultured glioblastoma cells as well as xenografts produced from them, the results also showed that such JNK involvement is modest. As this finding, which was also confirmed in this study, shows that JNK inhibition would have only a modest effect on the growth of volume glioblastoma cells, it alone might not support using JNK as a therapeutic target against glioblastoma. As a goal of glioblastoma therapy the identification of JNK as a key player in base like glioblastoma cells in this study, however, clearly supports use of JNK. Of note, the JNK pathway could be activated by upstream activities such as EGFR activation and PTEN reduction, both of which occur frequently in glioblastoma. But, JNK2a2, a JNK isoform constitutively activated through an autophosphorylation device independently of upstream triggering signs, is reportedly stated in nearly all human glioblastomas. Hence, targeting of the JNK pathway at or downstream of JNK may be warranted to regulate the pathway in glioblastoma cells.