Review and preprint alert!!

This has been a great week for our lab with respect to publications!! Continue reading if you want to know more about the metabolic features of medulloblastoma (MB) or the role of ALK promoting agressiveness in pancreatic cancer (PDAC)…

First, we are happy to finally see our mini-review Metabolic determinants of stemness in medulloblastoma by Martín-Rubio et al. published in World Journal of Stem Cells. In this article, we summarize the current literature about the metabolic features of medulloblastoma and medulloblastoma cancer stem cells. In fact, recent evidence suggests that metabolic features among MB groups and even among the different cell subpopulations within a tumour are highly heterogeneous and importantly, the metabolic features of MB-CSCs remain absolutely unknown nowadays. Additionally, we discuss the current pre-clinical data and clinical trials testing metabolic targeting approaches for medulloblastoma treatment.

Metabolic features of medulloblastoma and medulloblastoma cancer stem cells. Medulloblastoma (MB) tumours show activation of metabolic pathways such as glycolysis and fatty acid synthesis. MB cancer stem cells (MB-CSCs) display several markers, including cluster of differentiation 133 (CD133), CD15, and nestin (NES). Increased autophagy and glycolysis have been detected in MB-CSCs compared to more differentiated cells. In addition, hypoxic conditions induce the expansion of MB-CSCs. On the other hand, MB-CSCs show decreased mitochondrial activity and reactive oxygen species. ROS: Reactive oxygen species

Next, we are very excited about our new pre-print deposited on bioRxiv ALK signaling drives tumorigenicity and chemoresistance of pancreatic ductal adenocarcinoma cells by Beatriz Parejo-Alonso et al, in which we describe the role of the tyrosine kinase receptor ALK promoting tumorigenicity and chemoresistance in PDAC. This receptor is preferentially overexpressed and phosphorylated in CSCs, regulating processes such as proliferation, self-renewal, tumorigenicity and response to chemotherapy. Interestingly, we have identified the cytokines midkine and pleiotrophin as the main ligands activating ALK. Importantly, this receptor can be targeted using clinically-approved compounds, such as crizotinib and ensartinib, representing a promising therapeutic strategy for PDAC.

You can also find the full-texts in our publications section!!

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