[1] D. Ricard, A. Idbaih, F. Ducray, M. Lahutte, K. Hoang-Xuan, and J. Y. Delattre, “Primary brain tumours in adults,” Lancet, vol. 379, no. 9830, pp. 1984–1996, 2012.
[2] R. L. Siegel, K. D. Miller, and A. Jemal, “Cancer Statistics , 2018,” CA. Cancer J. Clin., vol. 68, no. 1, pp. 7–30, 2018.
[3] C. A. Graham and T. F. Cloughesy, “Brain Tumor Treatment: Chemotherapy and Other New Development,” Semin. Oncol. Nurs., vol. 20, no. 4, pp. 260–272, 2004.
[4] I. B. Adams and B. R. Martin, “Cannabis : pharmacology and toxicology in animals and humans,” Addiction, vol. 91, no. 11, pp. 1585–1614, 1996.
[5] A. C. Howlett, C. S. Breivogel, S. R. Childers, S. A. Deadwyler, R. E. Hampson, and L. J. Porrino, “Cannabinoid physiology and pharmacology: 30 Years of progress,” Neuropharmacology, vol. 47, pp. 345–358, 2004.
[6] P. Śledziński, J. Zeyland, R. Słomski, and A. Nowak, “The current state and future perspectives of cannabinoids in cancer biology,” Cancer Med., vol. 7, no. 3, pp. 765–775, 2018.
[7] G. Velasco, C. Sánchez, and M. Guzmán, “Towards the use of cannabinoids as antitumour agents,” Nat. Rev. Cancer, vol. 12, no. 6, pp. 436–444, 2012.
[8] C. A. Dumitru, I. E. Sandalcioglu, and M. Karsak, “Cannabinoids in Glioblastoma Therapy: New Applications for Old Drugs,” Front. Mol. Neurosci., vol. 11, no. 156, pp. 1–7, 2018.
[9] S. D. McAllister et al., “Cannabinoids selectively inhibit proliferation and induce death of cultured human glioblastoma multiforme cells,” J. Neurooncol., vol. 74, no. 1, pp. 31–40, 2005.
[10] G. Velasco, I. Galve-Roperh, C. Sánchez, C. Blázquez, and M. Guzmán, “Hypothesis: Cannabinoid therapy for the treatment of gliomas?,” Neuropharmacology, vol. 47, no. 3, pp. 315–323, 2004.
[11] M. Begg et al., “Evidence for novel cannabinoid receptors,” Pharmacol. Ther., vol. 106, no. 2, pp. 133–145, 2005.
[12] L. A. Matsuda, S. J. Lolait, M. J. Brownstein, A. C. Young, and T. I. Bonner, “Structure of a cannabinoid receptor and functional expression of the cloned cDNA,” Nature, vol. 346, no. 6284, pp. 561–564, 1990.
[13] S. Munro, K. . Thomas, and M. Abu-Shaar, “Molecular Characterization of a Peripheral Receptor for Cannabinoids,” Nature, vol. 365, no. 6441, pp. 61–65, 1993.
[14] R. G. Pertwee and R. A. Ross, “Cannabinoid receptors and their ligands,” Prostaglandins Leukot. Essent. Fat. Acids, vol. 66, no. 2–3, pp. 101–121, 2002.
[15] K. Mackle, “Distribution of Cannabinoid Receptors in the Central and Peripheral Nervous System,” Handb. Exp. Pharmacol., vol. 168, pp. 299–325, 2005.
[16] E. S. Onaivi, H. Ishiguro, S. Gu, and Q. R. Liu, “CNS effects of CB2 cannabinoid receptors: Beyond neuro-immuno-cannabinoid activity,” J. Psychopharmacol., vol. 26, no. 1, pp. 92–103, 2011.
[17] M. L. De Jesús, C. Hostalot, J. M. Garibi, J. Sallés, J. J. Meana, and L. F. Callado, “Opposite Changes in Cannabinoid CB1 and CB2 Receptor Expression in Human Gliomas,” Neurochem. Int., vol. 56, no. 6–7, pp. 829–833, 2010.
[18] E. Ciaglia et al., “Cannabinoid receptor CB1 regulates STAT3 activity and its expression dictates the responsiveness to SR141716 treatment in human glioma patients’ cells,” Oncotarget, vol. 6, no. 17, pp. 15464–15481, 2015.
[19] X. Wu et al., “Alteration of Endocannabinoid System in Human Gliomas,” J. Neurochem., vol. 120, no. 5, pp. 842–849, 2012.
[20] J. Held-Feindt, L. Dörner, G. Sahan, H. M. Mehdorn, and R. Mentlein, “Cannabinoid receptors in human astroglial tumors,” J. Neurochem., vol. 98, no. 3, pp. 886–893, 2006.
[21] M. Schley et al., “Predominant CB2 receptor expression in endothelial cells of glioblastoma in humans,” Brain Res. Bull., vol. 79, no. 5, pp. 333–337, 2009.
[22] C. Calatozzolo et al., “Expression of cannabinoid receptors and neurotrophins in human gliomas,” Neurol. Sci., vol. 28, no. 6, pp. 304–310, 2007.
[23] S. Sarfaraz, F. Afaq, V. M. Adhami, and H. Mukhtar, “Cannabinoid Receptor as a Novel Target for the Treatment of Prostate Cancer,” Cancer Res., vol. 65, no. 5, pp. 1635–1641, 2005.
[24] A. Carracedo et al., “Cannabinoids Induce Apoptosis of Pancreatic Tumor Cells via Endoplasmic Reticulum Stress-Related Genes,” Cancer Res., vol. 66, no. 13, pp. 6748–6755, 2006.
[25] X. Xu et al., “Overexpression of Cannabinoid Receptors CB1 and CB2 Correlates with Improved Prognosis of Patients with Hepatocellular Carcinoma,” Cancer Genet. Cytogenet., vol. 171, no. 1, pp. 31–38, 2006.
[26] D. Zheng et al., “The Cannabinoid Receptors are Required for Ultraviolet-Induced Inflammation and Skin Cancer Development,” Cancer Res., vol. 68, no. 10, pp. 3992–3998, 2008.
[27] J. Guindon and A. G. Hohmann, “The endocannabinoid system and cancer: Therapeutic implication,” Br. J. Pharmacol., vol. 163, no. 7, pp. 1447–1463, 2011.
[28] A. Preet et al., “Cannabinoid Receptors, CB1 and CB2, as Novel Targets for Inhibition of Non-Small Cell Lung Cancer Growth and Metastasis,” Cancer Prev. Res., vol. 4, no. 1, pp. 65–75, 2011.
[29] A. M. Wasik and B. Sander, “Cannabinoid Receptors in Mantle Cell Lymphoma,” Cell Cycle, vol. 14, no. 3, pp. 291–292, 2015.
[30] M. Pyszniak, J. Tabarkiewicz, and J. J. Łuszczki, “Endocannabinoid System as a Regulator of Tumor Cell Malignancy - Biological Pathways and Clinical Significance.,” Onco. Targets. Ther., vol. 9, no. 2, pp. 4323–36, 2016.
[31] G. Larrinaga et al., “Cannabinoid CB1 Receptor is Downregulated in Clear Cell Renal Cell Carcinoma,” J. Histochem. Cytochem., vol. 58, no. 12, pp. 1129–1134, 2010.
[32] S. Furuse et al., “Reduction of Bone Cancer Pain by Activation of Spinal Cannabinoid Receptor 1 and its Expression in the Superficial Dorsal Horn of the Spinal Cord in a Murine Model of Bone Cancer Pain,” Anesthesiology, vol. 111, no. 1, pp. 173–186, 2009.
[33] S. B. Gustafsson et al., “High Tumour Cannabinoid CB1 Receptor Immunoreactivity Negatively Impacts Disease-Specific Survival in Stage II Microsatellite Stable Colorectal Cancer,” PLoS One, vol. 6, no. 8, pp. 1–11, 2011.
[34] S. C. Chung et al., “A high cannabinoid CB1 receptor immunoreactivity is associated with disease severity and outcome in prostate cancer,” Eur. J. Cancer, vol. 45, no. 1, pp. 174–182, 2009.
[35] G. S. Stoyanov, D. L. Dzhenkov, M. Kitanova, I. S. Donev, and P. Ghenev, “Correlation Between Ki-67 Index , World Health Organization Grade and Patient Survival in Glial Tumors With Astrocytic Differentiation,” Cureus, vol. 9, no. 6, pp. 1396–1405, 2017.
[36] D. Walsh, K. A. Nelson, and F. A. Mahmoud, “Establised and potential applications of cannabinoids in oncology,” Support Cancer Care, vol. 11, no. 3, pp. 137–143, 2003.
[37] M. B. Bridgeman and D. T. Abazia, “Medicinal Cannabis : History , Pharmacology , And Implications for the Acute Care Setting,” Pharm. Ther., vol. 42, no. 3, pp. 180–188, 2017.
[38] G. Velasco et al., “Cannabinoids and gliomas,” Mol. Neurobiol., vol. 36, no. 1, pp. 60–67, 2007.
[39] R. I. Wilson and R. A. Nicoll, “Endocannabinoid Signaling in the Brain,” Science (80-. )., vol. 296, no. 5568, pp. 678–682, 2002.
[40] A. Belous et al., “Mitochondrial P2Y-Like Receptors Link Cytosolic Adenosine Nucleotides to Mitochondrial Calcium Uptake,” J. Cell. Biochem., vol. 92, no. 5, pp. 1062–1073, 2004.
[41] M. Navarrete and A. Araque, “Endocannabinoids Mediate Neuron-Astrocyte Communication,” Neuron, vol. 57, no. 6, pp. 883–893, 2008.
[42] J. Liu et al., “Functional CB1 Cannabinoid Receptors in Human Vascular Endothelial Cells.,” Biochem. J., vol. 346, no. 3, pp. 835–840, 2000.
[43] A. C. Howlett, M. Bidaut-Russell, W. A. Devane, L. S. Melvin, M. R. Johnson, and M. Herkenham, “The cannabinoid receptor: biochemical, anatomical and behavioral characterization,” Trends Neurosci., vol. 13, no. 10, pp. 420–423, 1990.
[44] A. C. Hanyaloglu and M. von Zastrow, “Regulation of GPCRs by Endocytic Membrane Trafficking and Its Potential Implications,” Annu. Rev. Pharmacol. Toxicol., vol. 48, no. 1, pp. 537–568, 2008.
[45] L. Lanzetti and P. P. Di Fiore, “Endocytosis and cancer: An ‘Insider’ network with dangerous liaisons,” Traffic, vol. 9, no. 12, pp. 2011–2021, 2008.
[46] I. Mellman and Y. Yarden, “Endocytosis and cancer,” Curr. Opin. Cell Biol., vol. 5, no. 12, pp. 156–161, 2013.
[47] A. M. Kidger and S. M. Keyse, “The regulation of oncogenic Ras/ERK signalling by dual-specificity mitogen activated protein kinase phosphatases (MKPs),” Semin. Cell Dev. Biol., vol. 50, pp. 125–132, 2016.
[48] V. Serra et al., “PI3K inhibition results in enhanced HER signaling and acquired ERK dependency in HER2-overexpressing breast cancer,” Oncogene, vol. 30, no. 22, pp. 2547–2557, 2011.
[49] Y. Fujimori, M. Inokuchi, Y. Takagi, K. Kato, K. Kojima, and K. Sugihara, “Prognostic value of RKIP and p-ERK in gastric cancer,” J. Exp. Clin. Cancer Res., vol. 31, no. 1, pp. 30–38, 2012.
[50] Q. Z. Dong et al., “Derlin-1 is overexpressed in non-small cell lung cancer and promotes cancer cell invasion via EGFR-ERK-mediated up-regulation of MMP-2 and MMP-9,” Am. J. Pathol., vol. 182, no. 3, pp. 954–964, 2013.
[51] K. Buchegger et al., “The ERK/MAPK pathway is overexpressed and activated in gallbladder cancer,” Pathol. Res. Pract., vol. 213, no. 5, pp. 476–482, 2017.
[52] P. Ramaswamy, K. Goswami, N. D. Nanjaiah, D. Srinivas, and C. Prasad, “TNF-α mediated MEK-ERK signaling in invasion with putative network involving NF-κB and STAT-6: a new perspective in glioma,” Cell Biol. Int., vol. 11, no. 184, pp. 1–17, 2019.
[53] X. Xian, L. Tang, C. Wu, and L. Huang, “MiR-23b-3p and miR-130a-5p affect cell growth, migration and invasion by targeting CB1R via the Wnt/β-catenin signaling pathway in gastric carcinoma,” Onco. Targets. Ther., vol. 11, pp. 7503–7512, 2018.
[54] I. Kasacka, Z. Piotrowska, A. Filipek, and W. Lebkowski, “Comparative evaluation of cannabinoid receptors, apelin and S100A6 protein in the heart of women of different age groups,” BMC Cardiovasc. Disord., vol. 18, no. 1, pp. 2–9, 2018.
[55] S. L. Dunn, J. M. Wilkinson, A. Crawford, R. A. D. Bunning, and C. L. Le Maitre, “Expression of Cannabinoid Receptors in Human Osteoarthritic Cartilage: Implications for Future Therapies,” Cannabis Cannabinoid Res., vol. 1, no. 1, pp. 3–15, 2016.