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declare that they have no competing interests. Authors’ contributions MK, HO, SH, DS, HT and RH performed experiments and data analysis. DK, CT, SY, TF, GN, HS, MK, MF and YK collected cases and clinical Carnitine palmitoyltransferase II data. MK and SN conceived and designed the study, and prepared the initial manuscript. YK supervised the project. All authors contributed to the final manuscript. All authors read and approved the final manuscript.”
“Background Colorectal cancer (CRC), a disease arising from complex and heterogeneous etiological factors and pathogenetic mechanisms, develops in a multi-step manner from normal epithelium, through a pre-malignant lesion (adenoma), into a malignant lesion (carcinoma) [1]. Histopathological evaluation of early stage CRC in many cases reveals areas of adenomatous mucosa, but the presence of tissue with histological features ranging from pure tubular to pure villous adenomas accompanied by dysplasia is also frequently detected in invasive colorectal cancer [1,2]. Although individuals with syndromes that strongly predispose to adenomas, e.g. familial adenomatous polyposis (FAP), invariably develop CRC by the third to fifth decade of life if these lesions are not removed [3], most adenomas (not FAP) have a low risk of progressing into cancer (about 5%) if not resected.