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Although most sporadic colorectal cancers ( CRC ) are thought to develop from protruded adenomas through the adenoma–carcinoma sequence, some  CRC  develop through flat lesions, so‐called laterally spreading tumors ( LST ). We previously analyzed epigenetic aberrations in  LST  and found that  LST  are clearly classified into two molecular subtypes: intermediate‐methylation with   KRAS   mutation and low‐methylation with absence of oncogene mutation. Intermediate‐methylation  LST  were mostly granular type  LST  ( LST ‐G) and low‐methylation  LST  were mostly non‐granular  LST  ( LST ‐ NG ). In the present study, we conducted a targeted exon sequencing study including 38 candidate  CRC  driver genes to gain insight into how these genes modulate the development of  LST . We identified a mean of 11.5 suspected nonpolymorphic variants per sample, including indels and non‐synonymous mutations, although there was no significant difference in the frequency of total mutations between  LST ‐G and  LST ‐ NG . Genes associated with  RTK / RAS  signaling pathway were mutated more frequently in  LST ‐G than  LST ‐ NG  ( P  = 0.004), especially   KRAS   mutation occurring at 70% (30/43) of  LST ‐G but 26% (13/50) of  LST ‐ NG  ( P  < 0.0001). Both  LST  showed high frequency of   APC   mutation, even at adenoma stage, suggesting its involvement in the initiation stage of  LST , as it is involved at early stage of colorectal carcinogenesis via adenoma‐carcinoma sequence.   TP 53  mutation was never observed in adenomas, but was specifically detected in cancer samples.   TP 53  mutation occurred during development of intramucosal cancer in  LST ‐ NG , but during development of cancer with submucosal invasion in  LST ‐G. It is suggested that   TP 53  mutation occurs in the early stages of cancer development from adenoma in both  LST ‐G and  LST ‐ NG , but is involved at an earlier stage in  LST ‐ NG .

TP 53 mutation at early stage of colorectal cancer progression from two types of laterally spreading tumors