E-MTAB-9903
Single Cell RNA-seq from Prostate Cancer Patient Derived Xenografts and LNCaP Cells
Comprehensive molecular cancer studies have extensively characterized most primary and some metastatic tumor types over the last decade. In prostate cancer, the most common tumor type in men, genomic studies have been most notably conducted for primary and metastatic tumors that had progressed under androgen deprivation therapies (ADT) to castration-resistant disease (CRPC). More recent studies have also looked at genetic alterations in a smaller number of prostate cancers frequently associated with neuroendocrine trans-differentiation.  For this tumor type, it's becoming clear that the complexity of genomic alterations does not allow an accurate assessment of the transformed phenotype.  To overcome these hurdles, we show in patient-derived xenograft models how disease progression emerges at single-cell resolution and how pharmacologic perturbation can revert this process. Given this approach, we were able to investigate disease progression and androgen independence at single cell level: in our xenograft models, we show how tumor cell subpopulation progress along the trajectory from androgen-sensitive to insensitive disease.
Comprehensive molecular cancer studies have extensively characterized most primary and some metastatic tumor types over the last decade. In prostate cancer, the most common tumor type in men, genomic studies have been most notably conducted for primary and metastatic tumors that had progressed under androgen deprivation therapies (ADT) to castration-resistant disease (CRPC). More recent studies have also looked at genetic alterations in a smaller number of prostate cancers frequently associated with neuroendocrine trans-differentiation.  For this tumor type, it's becoming clear that the complexity of genomic alterations does not allow an accurate assessment of the transformed phenotype.  To overcome these hurdles, we show in patient-derived xenograft models how disease progression emerges at single-cell resolution and how pharmacologic perturbation can revert this process. Given this approach, we were able to investigate disease progression and androgen independence at single cell level: in our xenograft models, we show how tumor cell subpopulation progress along the trajectory from androgen-sensitive to insensitive disease.