Resting natural killer cells promote the progress of colon cancer liver metastasis (CCLM), which may be exploited for novel strategies to improve therapeutic outcomes for patients with CCLM.

The gluconeogenic enzyme PCK1 and pyrimidine nucleotide biosynthetic enzyme DHODH drive hypoxic pyrimidine nucleotide biosynthesis and liver metastatic colonization in colorectal cancer, which is therapeutically exploitable by DHODH pharmacologic inhibition.

Continuous perioperative IFNα therapy stimulates hepatic endothelial cells to build up physical vascular barrier that limits tumor cell entry into the liver and promotes long-term antitumor immunity.

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.

A photoconversion-based isolation technique enables systematic investigation of spatially distinct small metastases (microcolonies) versus large lesions (macrometastases).

Kidney-specific TFEB overexpression in transgenic mice closely recapitulates features observed in both TFEB- and TFE3-mediated human kidney tumors.

In small cell lung cancer, the transition from a neuroendocrine state to a more neuronal state endows these cancer cells with increased migration and metastatic potential.

Single-cell sequencing and functional analysis identify T cells that can be useful for marker selection and cell therapy in uveal melanoma, a disease largely unresponsive to conventional immune checkpoint therapies.

DKK2 is crucial for the development of lysozyme-expressing cancer cells with Paneth cell characteristics necessary for liver metastasized colon cancer growth.

In contrast with earlier conclusions, negative selection has a major role in cancer evolution.