In their study in Nature Communications, Dustin Flanagan, Owen Sansom and colleagues showed that high TGFβ expression – whose role has been described as contradictory in colorectal cancer – accelerated tumour formation in the context of KRAS and APC mutation. While linked to aggressive disease progression, mechanistically epithelial TGFβ activation stimulated growth factor signalling pathways which as a result is a promising finding for potential drug targeting strategies.
The Beatson Translational Molecular Imaging team, led by David Lewis, introduced a new, automated methodology and quality control procedure for fluorine-18 radiolabelled tetrafluoroborate, which is used to visualise cancer through nuclear imaging techniques. Application of the tracer in a lung tumour model in mice allowed the acquisition of images of high quality and improved sensitivity. [High molar activity [18F]tetrafluoroborate synthesis for sodium iodide symporter imaging by PET]
When sensing softer surroundings, such as encountered in metastatic environments, pancreatic cancer cells produced and secreted high levels of collagen IV – as detailed in recent investigations in the Journal of Cell Science by the Machesky lab. In a combination of in vitro experiments involving hydrogels of adjustable stiffness and preclinical pancreatic cancer models, the authors illustrated mechanosensitive mechanisms by which pancreatic cancer cells promote their own survival and their metastatic growth.
For further insight into their work, read the First Person Interview with former Beatson PhD student and joint first author Vasileios Papalazarou in Journal of Cell Sciences.
Beatson scientists, around Sarah Edwards and Seth Coffelt provided a comprehensive analysis of IL-17A-producing γδ T cells in healthy lung versus in the pre-metastatic setting. In response to a tumour, T cell diversity increased, marked by differentially upregulating co-inhibitory molecules such as PD-1 and TIM-3. As a result, the deletion of those cells brought about a sensitivity to anti-PD-1 and anti-TIM-3 immunotherapy.[PD-1 and TIM-3 differentially regulate subsets of mouse IL-17A–producing γδ T cells]
