These transitional populations often retain partial adenocarcinoma identity while acquiring neuroendocrine or basal-like features, consistent with a model in which early genomic alterations, such as concurrent TP53 and RB1 loss, create a permissive chromatin landscape that facilitates subsequent epigenetic and transcriptional reprogramming mediated by regulators such as PRC2 and NOTCH signaling. This evidence concerns the gene TP53 and adenocarcinoma.