J. P. Morton

This study shows that wild-type KRAS suppresses tumour growth and metastasis in KRAS mutant colorectal cancer while enhancing resistance to MEK inhibition.

This study shows that loss of wild-type Kras enhances oncogenic Kras signaling and promotes pancreatic ductal adenocarcinoma, while also increasing sensitivity to MEK1/2 inhibitors.

This study examines DNA methylation changes in human skeletal muscle after low carbohydrate exercise under energy balance and deficit conditions, identifying hypomethylation in gene regions linked to metabolic pathways.

This study identifies βIII-tubulin as a suppressor of extrinsic apoptosis in pancreatic cancer, showing that its silencing enhances sensitivity to death signals and reduces tumor progression.

This study shows that extracellular adenosine promotes an immunosuppressive microenvironment in PDAC by enhancing myeloid cell infiltration and resistance to immunotherapy, and that blocking adenosine pathway components improves therapeutic outcomes.

This study identifies Ly6G expression levels as a marker for neutrophil maturation stages and shows spleen-derived neutrophils mature faster with distinct transcriptional profiles.

This study identifies IQSEC1 variants that spatially regulate phosphoinositide metabolism to switch cell behavior from growth to invasion, with implications for metastasis.

This study shows that KRASG12D mutant cells are outcompeted by wild-type cells in the adult pancreas, dependent on EphA2 signaling, leading to tissue clearance and reduced premalignant lesions.

This study identifies TLR2 as a key mediator of oncogene-induced senescence by promoting cell cycle arrest and regulating the senescence-associated secretory phenotype through DAMPs.

This study shows macrophages in pancreatic cancer release pyrimidines that inhibit gemcitabine therapy by competing with the drug for uptake and metabolism, and reducing macrophage burden improves treatment response.