A new study co-authored by Ludwig Princeton's founding member Yibin Kang writes that metastasis is a major contributor to cancer patient mortality. Tumour cells often develop phenotypic plasticity to successfully metastasize to different target organs.

Recent progress in the study of bone metastasis has provided novel insight into the biological processes that drive the spread and growth of cancer cells in the bone. In this review, we provide a summary of how the bone marrow microenvironment promotes phenotypic plasticity of metastatic tumour cells and alters therapeutic responses. We highlight pivotal transformations in cellular status driven by plasticity, including mesenchymal-epithelial transition, acquisition of stem-like traits, and awakening from dormancy. Additionally, we describe the phenomenon of host-organ mimicry and metabolic rewiring that collectively serve as key attributes of disseminated tumour cells, enabling their successful colonization and growth within the bone marrow microenvironment.