In their recent article in Neuro-Oncology Advances, Dominik Koessinger, David Novo and colleagues identify an inter-cellular communication tool where p53-mutant glioblastoma cells release podocalyxin-containing extracellular vesicles. This stimulates neighbouring brain cells to secrete factors creating an environment favourable to cell invasion and ultimately promoting cancer cell infiltration in the brain. Investigating the tumour microenvironment in this study has potentially highlighted a druggable target for a cancer type with particularly poor prognosis.

In Cancer Immunology Research, scientists working with Seth Coffelt and Toshi Suzuki show that bowel cancer downregulates factors called butyrophilin-like (BTNL) molecules that usually attract cancer-killing immune cells to the gut. Targeting pathways regulating BTNL offers a potential avenue to re-sensitise the immune system to cancer cell detection and therefore stop colorectal cancer from growing.

A team of Glasgow scientists, led by Saverio Tardito, reveal that triple negative breast cancer cells can secrete a factor that protects them from iron-dependent cell death, a process called ferroptosis. In their study, released on BioRxiv, mass spectrometry-based lipodomic analysis identifies monosaturated fatty acid(MUFA)-containing lipids as the pro-survival signalling molecule and the authors suggest that diets lacking MUFA could enhance the effects of drug treatments that target ferroptosis.

Using a genetic model of mesothelioma, Beatson scientists, Pooyeh Farahmand and Daniel Murphy show that asbestos exposure, although not required for its development, speeds up cancer growth dramatically. On a cellular level, the presence of asbestos leads to increased infiltration of macrophages, however, no effects on survival are observed when these immune cells are targeted pharmacologically. [Asbestos accelerates disease onset in a genetic model of malignant pleural mesothelioma]