biologist, bichemist, researcher
Guillermo Velasco was born in Madrid, studied Biology and obtained his PhD degree (1997) at the School of Biology of the Complutense University, Madrid, Spain. After defending his PhD, he got an EMBO long-term fellowship to work in Philip Cohen’s laboratory at the MRC Protein Phosphorylation Unit (Dundee, Scotland) on a project aimed at studying the regulation and of the Rho-activated protein kinase (ROCK).
On the year 1999 he got a position as Assistant Teacher at the School of Chemistry of the Complutense University and since the year 2003 he is Associated professor of the Department of Biochemistry and Molecular Biology I.
On the year 2001 he started a line of research aimed at investigating the mechanisms underlying cannabinoid antitumoral action as well as at optimizing the potential clinical utilization of these agents in cancer therapies.
Different lines of research in his group are currently investigating the role of endoplasmic reticulum stress, autophagy, apoptosis, intracellular trafficking of ceramide and regulation of mTORC1 and mTORC2 in cannabinoid antitumoral action as well as the participation of growth factor receptor-activated pathways in the resistance to the antineoplasic actions of cannabinoids.
|2017||Towards the utilization of cannabinoids as anticancer agents||Abstract|
A large body of evidence shows that cannabinoids, in addition to their well-known palliative effects on some cancer-associated symptoms, can reduce tumour growth in animal models of cancer and specifically of gliomas. The mechanism of cannabinoid anticancer action relies, at least largely, on the ability of these agents to stimulate autophagy-mediated cancer cell death. Moreover,the combined administration of cannabinoids and temozolomide produces a strong anticancer effect, which correlates with an intense activation of the signalling route that triggers the activation of cytotoxic autophagy. Research conducted in our group has also led to the identification of mechanisms of resistance to cannabinoid anticancer action. For example, up-regulation of the growth factor Midlkine (MK) promotes resistance to cannabinoid anticancer action in gliomas via stimulation of the Anaplastic Lymphoma Kinase tyrosine kinase receptor (ALK); and could be a factor of bad prognosis in GBM patients. All these preclinical findings have facilitated the promotion of a clinical study to investigate the safety and efficacy of the combined administration of the cannabis-based medicine Sativex and temozolomide in recurrent GBM. In this presentation I will discuss these issues and also other possible future studies that may help to clarify whether cannabinoids may be useful as anticancer agents in patients with gliomas or other cancers.
|2017||Towards the utilization of cannabinoids as anticancer agents||Workshop|