Although few models of prostate carcinoma exist, the diverse LNCaP substrains provide substrate for mechanistic studies to address key biological questions relating to clinically relevant biology, including DNA mismatch repair deficiency, the genesis of AR splice variants, processes driving AR amplification, consequences of TP53 inactivation, the role of Y chromosome loss, the contribution of ETS-transcription factors to prostate carcinoma pathobiology, and systemic screens to identify prostate carcinoma vulnerabilities in the context of lineage plasticity. Here, TP53 is linked to prostate carcinoma.