Abstract
Pancreatic ductal adenocarcinoma is one of the most aggressive and deadliest carcinomas worldwide. Despite modest response rates and extremely low cure rates, gemcitabine-based therapies still represent standard of care. Importantly, chemotherapeutic agents such as gemcitabine target mainly highly proliferative and differentiated cells, while cancer stem cells (CSCs) as the most aggressive and chemoresistant cells in the tumor are regularly spared. CSCs are capable of self-renewing and giving rise to more differentiated progenies, representing the bulk of cancer cells. Thus, CSCs represent the root of the tumor and are considered the source of disease relapse. To actually achieve long-term progression-free survival, treatment regimens should also target CSCs, either by directly eliminating them or inducing their differentiation rendering them more susceptible to chemotherapy. Intriguingly, our recent studies revealed that the anti-malaria drug chloroquine preferentially targets CD133+ CSCs by depleting their number and self-renewal ability translating into drastically reduced in vivo tumorigenic activity. Even more importantly, chloroquine virtually abolished invasiveness of the metastatic CSC sub-population that co-expresses CD133 and CXCR4 . Thus, out data suggest that repurposing chloroquine as a CSC-targeting agent could represent a valuable and imminently available adjuvant therapy for patients with pancreatic ductal adenocarcinoma.
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