References:
[1]. Goschzik, T., et al., Genomic Alterations of Adamantinomatous and Papillary Craniopharyngioma. J Neuropathol Exp Neurol, 2017. 76(2): p. 126-134.
[2]. Preda, V., et al., The Wnt signalling cascade and the adherens junction complex in craniopharyngioma tumorigenesis. Endocr Pathol, 2015. 26(1): p. 1-8.
[3]. Hölsken, A., et al., Adamantinomatous and papillary craniopharyngiomas are characterized by distinct epigenomic as well as mutational and transcriptomic profiles. Acta Neuropathol Commun, 2016. 4: p. 20.
[4]. Brastianos, P.K., et al., Exome sequencing identifies BRAF mutations in papillary craniopharyngiomas. Nat Genet, 2014. 46(2): p. 161-5.
[5]. Brown, H.A., P.G. Thomas and C.W. Lindsley, Targeting phospholipase D in cancer, infection and neurodegenerative disorders. Nat Rev Drug Discov, 2017. 16(5): p. 351-367.
[6]. Martini, M., et al., PI3K/AKT signaling pathway and cancer: an updated review. Ann Med, 2014. 46(6): p. 372-83.
[7]. Alzahrani, A.S., PI3K/Akt/mTOR inhibitors in cancer: At the bench and bedside. Semin Cancer Biol, 2019. 59: p. 125-132.
[8]. Gehringer, F., et al., Physiological levels of the PTEN-PI3K-AKT axis activity are required for maintenance of Burkitt lymphoma. Leukemia, 2020. 34(3): p. 857-871.
[9]. Ho, C.J. and S.M. Gorski, Molecular Mechanisms Underlying Autophagy-Mediated Treatment Resistance in Cancer. Cancers (Basel), 2019. 11(11).
[10]. Wang, Y., et al., Clinical and prognostic role of annexin A2 in adamantinomatous craniopharyngioma. J Neurooncol, 2017. 131(1): p. 21-29.
[11]. Nelson, W.G., et al., Specific keratins as molecular markers for neoplasms with a stratified epithelial origin. Cancer Res, 1984. 44(4): p. 1600-3.
[12]. Quentmeier, H., et al., Immunocytochemical analysis of cell lines derived from solid tumors. J Histochem Cytochem, 2001. 49(11): p. 1369-78.
[13]. Zhang, N., [Vimentin and tumor diagnosis]. Zhonghua Bing Li Xue Za Zhi, 1990. 19(2): p. 122-4.
[14]. Martinez-Barbera, J.P. and R. Buslei, Adamantinomatous craniopharyngioma: pathology, molecular genetics and mouse models. J Pediatr Endocrinol Metab, 2015. 28(1-2): p. 7-17.
[15]. Amit, S., et al., Axin-mediated CKI phosphorylation of beta-catenin at Ser 45: a molecular switch for the Wnt pathway. Genes Dev, 2002. 16(9): p. 1066-76.
[16]. Davies, H., et al., Mutations of the BRAF gene in human cancer. Nature, 2002. 417(6892): p. 949-54.
[17]. Haston, S., et al., MAPK pathway control of stem cell proliferation and differentiation in the embryonic pituitary provides insights into the pathogenesis of papillary craniopharyngioma. Development, 2017. 144(12): p. 2141-2152.
[18]. Davis, W.J., P.Z. Lehmann and W. Li, Nuclear PI3K signaling in cell growth and tumorigenesis. Front Cell Dev Biol, 2015. 3: p. 24.
[19]. Shingu, T., et al., Synergistic augmentation of antimicrotubule agent-induced cytotoxicity by a phosphoinositide 3-kinase inhibitor in human malignant glioma cells. Cancer Res, 2003. 63(14): p. 4044-7.
[20]. Sourbier, C., et al., The phosphoinositide 3-kinase/Akt pathway: a new target in human renal cell carcinoma therapy. Cancer Res, 2006. 66(10): p. 5130-42.
[21]. Mallon, R., et al., Antitumor efficacy of PKI-587, a highly potent dual PI3K/mTOR kinase inhibitor. Clin Cancer Res, 2011. 17(10): p. 3193-203.
[22]. Zhao, H.F., et al., Recent advances in the use of PI3K inhibitors for glioblastoma multiforme: current preclinical and clinical development. Mol Cancer, 2017. 16(1): p. 100.
[23]. Mohlin, S., et al., Anti-tumor effects of PIM/PI3K/mTOR triple kinase inhibitor IBL-302 in neuroblastoma. EMBO Mol Med, 2019. 11(8): p. e10058.
[24]. Shayesteh, L., et al., PIK3CA is implicated as an oncogene in ovarian cancer. Nat Genet, 1999. 21(1): p. 99-102.
[25]. Downward, J., Ras signalling and apoptosis. Curr Opin Genet Dev, 1998. 8(1): p. 49-54.