Targeting dendritic cells to drive PDAC immunotherapy response.

Pancreatic adenocarcinoma (PDAC) has been historically unresponsive to immunotherapy, predominantly due to lower antigen loads and a lack of tumor-infiltrating dendritic cells (DCs) and T cells. A recent study by Mahadevan and colleagues demonstrates that increasing DC infiltration through use of an engineered DC1 vaccine can sensitize PDAC to immunotherapy.

Stromal reprogramming overcomes resistance to RAS-MAPK inhibition to improve pancreas cancer responses to cytotoxic and immune therapy.

Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy that is often resistant to therapy. An immune suppressive tumor microenvironment (TME) and oncogenic mutations in have both been implicated as drivers of resistance to therapy. Mitogen-activated protein kinase (MAPK) inhibition has not yet shown clinical efficacy, likely because of rapid acquisition of tumor-intrinsic resistance.

Mapping the Fate of Hypoxic Cells Using an Irreversible Fluorescent Switch.

Hypoxia has been reported to promote tumor progression and metastasis in murine models, and patients with hypoxic tumors have a worse prognosis. Besides its effect on cancer, normal processes like embryogenesis, or other pathologies such as ischemia, depend on hypoxia-regulated mechanisms. Given the degradable nature of HIF-1/2α in the presence of oxygen, defining the role of hypoxia in modeling biological processes becomes challenging when a cell enters oxygen-rich regions within a tissue.