| Theme | Update on laterally spreading tumor (LST) | |
|---|---|---|
| Title | Specific correlation of CpG island methylation status and K-ras mutation with endoscopic features of colorectal adenomas, especially laterally spreading tumors | |
| Publish Date | 2006/09 | |
| Author | Sakiko Hiraoka | Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences |
| Author | Jun Kato | Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences |
| Author | Yasushi Shiratori | Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences |
| [ Summary ] | Out of 108 sporadic colorectal adenomas larger than 1 cm, the CpG island methylator phenotype (CIMP) was determined by examination of methylation status at p16, MINT 1, 2, 12, and 31 loci. K-ras codon 12 and 13 point mutations were also examined. The relationship between macroscopic appearance and CIMP status or K-ras mutations was analyzed. CpG island methylation, involving two or more loci out of five regions examined (CIMP-high) was more likely to be observed in the LST granular type (14 / 23 ; 61 %) than in conventional protruded-type adenomas (18 / 73 ; 25 %) (p = 0.002). The prevalence of K-ras mutations in the LST granular type (18 / 23 ; 78 %) was significantly higher than that in the protruded-type adenomas (18 / 73 ; 25 %) (p < 0.0001). Moreover, the prevalence of CIMP-high and K-ras mutations in the LST granular type, located in the proximal colon, was much higher (11 / 13 ; 85 %, and 12 / 13 ; 92 %, respectively). In contrast, the LST non-granular type exhibited a low prevalence for CIMP-high (1 / 12 ; 8 %) and K-ras mutations (2 / 12 ; 17 %). The high prevalence of CIMP-high and K-ras mutations in the LST granular type, especially in the proximal colon, could strongly suggest that the LST granular type appearance is associated with a unique genetic and epigenetic carcinogenic pathway. | |