Gregory L. Beatty

TL;DR: It is suggested that inflammation enhances cancer progression in part by facilitating EMT and entry into the circulation and tagged cells invaded and entered the bloodstream unexpectedly early, before frank malignancy could be detected by rigorous histologic analysis.

TL;DR: These findings demonstrate a CD40-dependent mechanism for targeting tumor stroma in the treatment of cancer and demonstrate that cancer immune surveillance does not necessarily depend on therapy-induced T cells; rather, it is shown that tumor regression required macrophages but not T cells or gemcitabine.

TL;DR: It is shown that tumor-derived granulocyte-macrophage colony-stimulating factor (GM-CSF) is necessary and sufficient to drive the development of Gr-1(+) CD11b(+) cells that suppressed antigen-specific T cells in pancreatic ductal adenocarcinoma.

TL;DR: This work discusses immune escape mechanisms exploited by cancer and presents strategies for applying this knowledge to improving the efficacy of cancer immunotherapy.

TL;DR: Findings support the development of mRNA CAR-based strategies for carcinoma and other solid tumors by showing the potential of using mRNA-engineered T cells to evaluate, in a controlled manner, potential off-tumor on-target toxicities and showing that short-lived CAR T cells can induce epitope spreading and mediate antitumor activity in patients with advanced cancer.