TP53 and neoplasm: As the independent EAC clones may grow into each other to form a single tumor mass or seed different metastatic lesions, both intratumor and primary/metastasis oncogenic amplification heterogeneity that is seen in advanced EAC58 may be the inherent outcome of chromosomal instability after p53 loss that could have been initiated in precancer BE cells and persist after transformation (Fig. 9).