Our single-cell atlas of SCLC patient tumors identifies plasticity changes in the form of a mixed SCLC-A/N phenotype as well as discrete intratumoral switching between canonical subtypes. We found a recurrent, pro-metastatic PLCG2-high SCLC phenotype that predicts worse overall survival and is associated with a pro-fibrotic myeloid population that is enriched in SCLC vs lung adenocarcinoma.

Our single-cell exploration of castrate-resistant prostate cancer (CRPC) in transgenic mice following RB1, TP53, and PTEN deletion identified multi-lineage infidelity through the switch from a stem-like luminal population to amphicrine, mesenchymal, and multiple neuroendocrine subtypes that show correspondence to neuroendocrine subtypes in small cell lung cancer.