Cell culture models widely used in cancer research do not reflect metabolism in tumors; by altering culture systems to better model tumor metabolism we find that environmental cystine promotes tumor glutamine metabolism.
The percentage of a tumor’s genome with alterations in copy number is correlated with increased mortality across a range of tumor types and can be measured using a clinically approved sequencing assay.
The nutrients available in some tumors and the factors that influence tumor nutrient availability are characterized, which provides insight into the metabolic constraints of the tumor microenvironment.
A major consequence of ductal-to-squamous lineage transition in pancreatic cancer cells is to augment inflammation, which may explain the exceptionally poor clinical outcomes of squamous-subtype tumors.
MYC and Twist1 drive metastasis by a novel non-cell-autonomous transcriptional mechanism of eliciting a cytokinome that mediates the crosstalk between cancer cells and macrophages, and its therapeutic blockade inhibits metastasis.