Qian et al. show that the receptor tyrosine kinase FLT1 is highly expressed in a subset of macrophages enriched in breast cancer metastatic sites. Inhibition of this kinase reduces metastasis to the lungs by blocking signaling via focal adhesion kinase 1 to an inflammatory state in the macrophages centered on signaling from the macrophage growth factor, colony stimulating factor-1.

No abstract

Resistance to targeted therapeutics is a key issue limiting the long-term utility of these medications

Two cases of metastatic colorectal cancer with a POLE mutation, both of which were ultramutated and microsatellite stable, are presented and discussed from the standpoint of the basic biochemical mechanisms leading to a unique phenotype in POLE deficiency, the challenges faced with interpreting the genomic profiling of tumors in this important subset of patients, and the potential clinical implications.