Development and application of highly sensitive in situ transcriptomics method, Flura-seq, in identifying dynamic organ-specific transcriptomes in early stage breast cancer metastasis have been described.

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.

The ATM kinase has an unanticipated role in tumor progression through the regulation of cell migration by oxidative stress.

NIFK promotes lung cancer metastasis via Runx1-dependent repression of CK1α, which activates TCF4/β-catenin signaling.

DECR1, a rate-limiting enzyme for polyunsaturated fatty acid (PUFA) β-oxidation, is an androgen-repressed gene in prostate cancer cells that limits oxidative stress to promote cancer cell survival.

Mucins, long associated with cancer aggression, remodel the cancer glycocalyx in a way that promotes proliferation in the metastatic site by enhancing integrin-mediated adhesion and thus driving cell cycle progression.

Inactivation of a multifunctional RNA-binding protein can lead to the acquisition of pro-metastatic phenotypes, possibly by stabilizing large-scale transcriptomic changes that provide a selective advantage during cancer progression.

Editors' Summary: This Replication Study has reproduced some parts of the original paper but other parts could not be interpreted.

A combination of animal models reveal how the molecular mechanisms of exosome secretion (RalA/B-dependent) are linked to their cargo content and their function in breast cancer pre-metastatic niche formation.

The action of the collagen receptor DDR2 in CAFs regulates Rap1-Talin1 mediated Integrin mechanotransduction in breast tumors to impact tumor stiffness and metastases.