Piotr Dzien, Karen Blyth, David Lewis, and colleagues have published an article in Cancer & Metabolism that proposes positron emission tomography (PET) imaging of the sodium iodide symporter (NIS) as a rapid and sensitive in vivo test for metabolic treatments targeting energetic pathways. This new approach makes in vivo testing more practical, giving an immediate readout after a single dose; it reduces drug costs, animal use, and the time associated with long therapeutic studies.

In their research released on bioRxiv, Ximena Raffo-Iraolagoitia, Leo Carlin and colleagues found an increase of γδ cells in tumour bearing mice showing an altered phenotype. The findings of this study reveal a potential pro-tumour role for a less abundant γδ T cell subset in the lung. This may have implications in the design of immunotherapies for lung adenocarcinoma as it directly influences the difficult to target tumour-promoting tumour-associated macrophages.

bioRxiv has released a preprint by Esmee Vringer, Stephen Tait and colleagues who found that upon mitochondrial outer membrane permeabilization (MOMP), mitochondria are promiscuously ubiquitylated. The team found that, surprisingly, upon MOMP, autophagy is not essential for mitochondrial degradation. Their findings connect mitochondrial outer membrane integrity to direct activation of NF-κB activity, contributing to the pro-inflammatory effects of MOMP. MOMP associated inflammation can elicit anti-tumour immunity and therefore represents a therapeutic target in cancer.

Stephen Tait and colleagues at the CRUK Scotland Institute have collaborated with researchers at the Mayo Clinic, USA, and their work has been published in Nature. The team’s findings indicate that minority mitochondrial outer membrane permeabilization (miMOMP) occurs during cellular senescence and can drive the senescence-associated secretory phenotype (SASP) through the release of mitochondrial DNA (mtDNA) into the cytosol. They found that inhibition of MOMP in vivo decreases inflammatory markers and improves health span in aged mice, suggesting that inhibition of miMOMP-induced inflammation may therefore be a therapeutic route to improve health during ageing and responses to cancer therapies.

In their preprint released on bioRxiv, Robert Wiesheu, Seth Coffelt and colleagues show that immature CD27⁺Ly6C^- cells convert into mature CD27⁺Ly6C⁺ cells and these mature cells control cancer progression. The team also found that IL-27 supports the cytotoxic phenotype and function of mouse CD27⁺Ly6C⁺ cells and human Vδ1⁺ cells. These results reveal an increased complexity within IFNγ-producing γδ T cells, comprising of immature and terminally differentiated subsets, that offer new insights into unconventional T cell biology.