During my postdoctoral training, I expanded my expertise into in vivo models to investigate how cellular mechanotype influences each step of the metastatic cascade. I developed stable subpopulations of breast cancer cells with distinct mechanical properties via microfluidic mechanical sorting, then implanted these cells into an orthotopic mouse model of metastasis. I found that stiffer, larger cells (high strain energy, HSE) form slower-growing primary tumors and metastasize less frequently than their softer, smaller (low strain energy, LSE) counterparts. However, only the stiffer subpopulation successfully  colonizes bone, suggesting a critical role for mechanotype in organotropic metastasis. This work, supported  by an NIH F32 postdoctoral fellowship (for which I serve as PI), provides the first direct evidence that mechanical phenotype contributes causally to metastatic potential and organ-specific dissemination.