AMACR and colon adenoma: Through the use of a comprehensive panel of immunostained-laser-capture-microdissected (iLCM) clinical samples comprising the entire colon adenoma-carcinoma sequence, we now report that the deregulation of AMACR during colon carcinogenesis involves non-random events, resulting in a double-deletion at CG3 and CG10, and alterations in the frequencies of deletion of CG12-16 in a newly identified CpG island (CGI) located within the core promoter of AMACR. We also identified deletion of CG12-16 as a putative regulatory polymorphism and the double-deletion at CG3 and 10 as a somatic lesion.