The tumor microenvironment and nano-based therapies - new publication from Dr Al-Jamal’s group
Vera Silva (third-year PhD student) and her supervisor, Dr. Wafa Al-Jamal, have recently published a review article focusing on the exploitation of the tumor microenvironment using nano-therapies. The title of the review is “Exploiting the cancer niche: tumor-associated macrophages and hypoxia as promising synergistic targets for nano-based therapy” and was published in Journal of Controlled Release. The published article focused on summarizing the active role of tumor associated macrophages (TAMs) and hypoxia on tumor progression, while thoroughly discussing the development of novel therapeutics that simultaneously target both features in the tumor microenvironment. Nano-based systems have been highlighted as interesting strategies for dual modality treatments, with somewhat improved tissue extravasation. Such approach could be seen as a promising strategy to overcome drug resistance and enhance the efficacy of chemotherapy in advanced solid and metastatic tumors, especially when exploiting cell-based nano-therapies. The highlight of this review is the importance of developing combinatorial therapies. The authors also provided an in-depth opinion on the need to reevaluate the current in vitro and in vivo models to make nanomedicine clinical translation more feasible and realistic. This review should provide an interesting read for academic researchers, industrial scientist and clinician working in the area of cancer nanomedicine.
Vera’s project is funded by UEA studentship (ref. 100099479). She is grateful for UEA for providing facilities and supervision of her PhD course. Click here to read the article.
Fig 3. Nanoparticle-based therapeutics targeting TAMs and hypoxia. Drug delivery systems (DDS) have shown great promises to inhibit the effect of TAMs and hypoxia on cancer development. The main mechanisms that have been developed so far using nanoparticles to targets tumor microenvironment are: 1) inhibiting monocyte maturation, leading to a reduced accumulation of pro-tumor immune cells (M2) at the tumor site; 2) depleting the tumor from M2 macrophages; 3) shifting the polarization of M2 macrophages (pro-tumor state) to an anti-tumor M1 state; 4) downregulating HIF-1with specific inhibitors and ligands; and 5) using macrophages as trojan horses to deliver DDS to the hypoxic regions of the tumor.
Dr Wafa Al-Jamal