Cited by 2kOpen Access
Jiangsu Cancer Hospital
ORCID: 0000-0002-3488-1059Publishes on Glioma Diagnosis and Treatment, Immune cells in cancer, Cancer, Hypoxia, and Metabolism. 296 papers and 11k citations.
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the effects they observed could be influenced by inhibition of other types of Trk receptors or signaling molecules downstream of Trk. We have recently started a series of experiments aiming to verify whether specific TrkB inhibition reduces glioma cell proliferation using ANA-12, a small-molecule selective TrkB antagonist. Our first results showed that ANA-12 effectively and dose-dependently reduces the viability of a human glioblastoma cell line with almost complete disappearance of cultured cells 72 hours after treatment (Fig. Therefore, selective TrkB inhibition might prove to be an effective experimental therapeutic strategy, possibly with fewer off-target toxicities compared with multitarget drugs in patients with astrocytomas harboring oncogenic TrkB.
cells, microglia and MDSCs constituted a higher percentage of GAMs than did macrophages. GAM profiling using flow cytometry studies revealed a continuum between the M1- and M2-like phenotype. Contrary to current dogma, GAMs exhibited distinct immunological functions, with the former aligned close to nonpolarized M0 macrophages.