Field Cancerization in Sporadic Colon Cancer
Gut and Liver
;
: 773-780, 2016.
Artículo
en Inglés
| WPRIM
| ID: wpr-179850
ABSTRACT
BACKGROUND/AIMS:
Aberrant DNA methylation has a specific role in field cancerization. Certain molecular markers, including secreted frizzled-related protein 2 (SFRP2), tissue factor pathway inhibitor 2 (TFPI2), N-Myc downstream-regulated gene 4 (NDRG4) and bone morphogenic protein 3 (BMP3), have previously been shown to be hypermethylated in colorectal cancer (CRC). We aim to examine field cancerization in CRC based on the presence of aberrant DNA methylation in normal-appearing tissue from CRC patients.METHODS:
We investigated promoter methylation in 34 CRC patients and five individuals with normal colonoscopy results. CRC patients were divided into three tissue groups tumor tissue, adjacent and nonadjacent normal-appearing tissue. The methylation status (positive methylation level >20%) of SFRP2, TFPI2, NDRG4, and BMP3 promoters was investigated using methylation-specific PCR.RESULTS:
The methylation frequencies of the SFRP2, TFPI2, NDRG4 and BMP3 promoters in tumor/adjacent/nonadjacent normal-appearing tissue were 79.4%/63.0%/70.4%, 82.4%/53.6%/60.7%, 76.5%/61.5%/69.2%, 41.2%/35.7%/50.0%, respectively. The methylation levels of the SFRP,TFPI2, NDRG4 and BMP3 promoters in tumor tissues were significantly higher than those in normal-appearing tissue (SFRP2, p=0.013; TFPI2, p<0.001; NDRG4, p=0.003; BMP3, p=0.001). No significant correlation was observed between the methylation levels of the promoters and the clinicopathological variables.CONCLUSIONS:
The field effect is present in CRC and affects both the adjacent and nonadjacent normal-appearing mucosa.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Tromboplastina
/
Neoplasias Colorrectales
/
Reacción en Cadena de la Polimerasa
/
Colonoscopía
/
Colon
/
Neoplasias del Colon
/
Metilación de ADN
/
Epigenómica
/
Metilación
/
Membrana Mucosa
Límite:
Humanos
Idioma:
Inglés
Revista:
Gut and Liver
Año:
2016
Tipo del documento:
Artículo
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