Fragmentation of Small-Cell Lung Cancer Regulatory States in Heterotypic Microenvironments.

ABSTRACT: Small-cell lung cancers derive from pulmonary neuroendocrine cells, which have stem-like properties to reprogram into other cell types upon lung injury. It is difficult to uncouple transcriptional plasticity of these transformed cells from genetic changes that evolve in primary tumors or secondary metastases. Profiling of single cells is also problematic if the required sample dissociation activates injury-like signaling and reprogramming. Here we defined cell-state heterogeneities in situ through laser capture microdissection-based 10-cell transcriptomics coupled with stochastic-profiling fluctuation analysis. In labeled cells from a small-cell lung cancer mouse model initiated by neuroendocrine deletion of Rb1-Trp53, variations in transcript abundance revealed cell-t

SUBMITTER: Schaff DL 

PROVIDER: S-EPMC8137564 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature