Revision as of 05:03, 2 June 2018 by imported>Boghog(→Implications in cancer: no reviews yet, but added independent primary source that comes to similar conclusions)
GPC2 is highly expressed in about half of neuroblastoma cases and that high GPC2 expression correlates with poor overall survival, suggesting GPC2 as a therapeutic target in neuroblastoma.[5][6] GPC2 silencing inactivates Wnt/β-catenin signaling and reduces the expression of N-Myc, an oncogenic driver of neuroblastoma tumorigenesis. Immunotoxins and chimeric antigen receptor (CAR) T cells targeting GPC2 inhibit neuroblastoma growth in mouse models.[5]
↑Ivins JK, Litwack ED, Kumbasar A, Stipp CS, Lander AD (April 1997). "Cerebroglycan, a developmentally regulated cell-surface heparan sulfate proteoglycan, is expressed on developing axons and growth cones". Developmental Biology. 184 (2): 320–32. doi:10.1006/dbio.1997.8532. PMID9133438.
↑Herndon ME, Stipp CS, Lander AD (February 1999). "Interactions of neural glycosaminoglycans and proteoglycans with protein ligands: assessment of selectivity, heterogeneity and the participation of core proteins in binding". Glycobiology. 9 (2): 143–55. doi:10.1093/glycob/9.2.143. PMID9949192.
↑Bosse KR, Raman P, Zhu Z, Lane M, Martinez D, Heitzeneder S, et al. (September 2017). "Identification of GPC2 as an Oncoprotein and Candidate Immunotherapeutic Target in High-Risk Neuroblastoma". Cancer Cell. 32 (3): 295–309.e12. doi:10.1016/j.ccell.2017.08.003. PMID28898695.