The mainstay of treatment is surgical excision.
25% of NCs are atypical with an elevated Ki-67 labeling index >2%, and exhibit a more aggressive course with high propensity for local recurrence and/or craniospinal dissemination. Although no standard treatment regimen exists for these atypical cases, adjuvant stereotactic or conventional radiotherapy and/or chemotherapy are typically offered but yield inconsistent results.
Zhang et al., described a patient with a vasopressin-secreting atypical neurocytoma of the sellar and cavernous sinus region. Following subtotal resection via endoscopic transsphenoidal surgery, the residual tumor showed increased FDG uptake and high somatostatin receptor expression on a 68Ga-DOTA-TATE PET/CT scan. Somatostatin receptor ligand (SRL) therapy with lanreotide (120 mg Q28d) was initiated, and 4 years later the residual tumor remains stable with decreased FDG tumor uptake. Immunocytochemical somatostatin receptor 2 (SSTR2) and SSTR5 expression was further confirmed in > 80% in a series of neurocytoma tissues.
They described the first use of SRL therapy in atypical NC and the results support consideration of adjuvant SRL therapy in NC refractory to surgical removal. The findings further raise the possibility of SSTR-directed peptide receptor radionuclide therapy (PRRT) as NC therapy 1).
A study examined the antitumor function of oridonin in Central neurocytoma (CN) cells, and investigated the underlying molecular mechanism. An MTT assay suggested that treatment with oridonin was able to significantly inhibit the proliferation of CN cells. The annexin V-fluorescein isothiocyanate/propidium iodide assay and western blot analysis demonstrated that oridonin was able to induce apoptosis and alter the expression of apoptosis-associated proteins by downregulating anti-apoptotic protein, B-cell lymphoma-2 (Bcl-2), and upregulating pro-apoptosis proteins, Bcl-2-like protein 4, cleaved caspase-3 and cleaved poly(ADP-ribose) polymerase 1. Subsequently, the Wnt/β-catenin signaling pathway was examined. Western blot analysis indicated that oridonin markedly decreased the expression of β-catenin, cyclin D1 and v-myc avian myelocytomatosis viral oncogene homolog. Furthermore, β-catenin was silenced by small interference RNA or overexpressed in CN cells, and the effect on cell proliferation was examined. The results indicated that silencing of β-catenin enhanced the inhibitory effect of oridonin on cell growth, whereas the overexpression of β-catenin attenuated this effect. These data indicated that oridonin inhibited proliferation and induced apoptosis to exert its antitumor activity in CN cells by repressing Wnt/β-catenin signaling. Therefore, the present study suggested that oridonin might be an effective adjuvant agent, and that the Wnt/β-catenin signaling pathway may be a potent target for the therapy in CN 2).