지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2007.6
- 수록면
- 460 - 466 (7page)
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초록· 키워드
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Purpose: The methylation of tumor suppressor genes has been implicated in the development of breast cancer. However, the role of methylation in the progression of cancer is still unclear. In this study, the methylation stati of nine tumor suppressor genes (p14, p16, DAPK, E-cadherin, RASSF1α, TWIST, RARβ, HIN-1, cyclin D2) in normal, benign, DCIS and invasive cancer tissues were examined, and the methylation patterns in DCIS and hypermethylated genes investigated to see if a change in the methylation status would lead to the development of cancer and progression to an invasive tumor.
Methods: A total of 96 patients, who underwent surgery between March 2003 and March 2005, were retrospectively studied. DNA was extracted from tumor tissues, and the samples examined for aberrant hypermethylation using methylation-specific PCR (MSP).
Results: The total number of methylated genes in each tissue type (normal tissues; 2.97±1.74, benign tumors; 4.36 ±1.42, DCIS; 5.73±1.35, invasive cancers; 5.42±2.05) increased with tumor progression (P＜0.001). In benign tumors, HIN-1 (83%) was the most frequently methylated gene, but in DCIS, p14 (100%), RASSF (100%) and TWIST (91%) were frequently methylated. In invasive cancer, RAR β (60%) and p16 (37%) were frequently methylated compared to the other tissue types. In a multivariate study, TWIST was commonly hypermethylated in DCIS and invasive cancer; whereas, RARβ and p14 were frequently independently hypermethylated in invasive cancers.
Conclusion: Methylation induced gene silencing appears to affect multiple genes in breast tissues, which increases with cancer progression. TWIST was hypermethylated in both DCIS and invasive cancers; therefore, it was concluded that methylation of the TWIST promoter may be an early event in the development of breast cancer. The hypermethylations of RARβ and p16 are useful marker for the progression of a DCIS lesion to invasive cancer. The methylation patterns of tumor suppressor genes in DCIS were similar to those found in invasive cancer, but also showed intermediate levels of methylation between benign tumors and invasive cancers.
Methods: A total of 96 patients, who underwent surgery between March 2003 and March 2005, were retrospectively studied. DNA was extracted from tumor tissues, and the samples examined for aberrant hypermethylation using methylation-specific PCR (MSP).
Results: The total number of methylated genes in each tissue type (normal tissues; 2.97±1.74, benign tumors; 4.36 ±1.42, DCIS; 5.73±1.35, invasive cancers; 5.42±2.05) increased with tumor progression (P＜0.001). In benign tumors, HIN-1 (83%) was the most frequently methylated gene, but in DCIS, p14 (100%), RASSF (100%) and TWIST (91%) were frequently methylated. In invasive cancer, RAR β (60%) and p16 (37%) were frequently methylated compared to the other tissue types. In a multivariate study, TWIST was commonly hypermethylated in DCIS and invasive cancer; whereas, RARβ and p14 were frequently independently hypermethylated in invasive cancers.
Conclusion: Methylation induced gene silencing appears to affect multiple genes in breast tissues, which increases with cancer progression. TWIST was hypermethylated in both DCIS and invasive cancers; therefore, it was concluded that methylation of the TWIST promoter may be an early event in the development of breast cancer. The hypermethylations of RARβ and p16 are useful marker for the progression of a DCIS lesion to invasive cancer. The methylation patterns of tumor suppressor genes in DCIS were similar to those found in invasive cancer, but also showed intermediate levels of methylation between benign tumors and invasive cancers.
목차
서론
방법
결과
고찰
결론
REFERENCES
참고문헌 (24)
참고문헌 신청
1. [학술지(정기간행물)] - Widschwendter M / 2002 / DNA methylation and breast carcinogenesis / Oncogene 21 : 5462 ~ 5482
2. [학술지(정기간행물)] - Szyf M / 2004 / DNA methylation and breast cancer / Biochem Pharmacol 68 : 1187 ~ 1197
3. [학술지(정기간행물)] - Jaenisch R / 2003 / Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals / Nat Genet 300 : 489 ~ 492
4. [학술지(정기간행물)] - Soreide K / 2006 / Microsatellite instability in colorectal cancer / Br J Surg 93 : 395 ~ 406
5. [학술지(정기간행물)] - Garinis GA / 2002 / DNA hypermethylation: when tumour suppressor genes go silent / Hum Genet 111 : 115 ~ 127
2. [학술지(정기간행물)] - Szyf M / 2004 / DNA methylation and breast cancer / Biochem Pharmacol 68 : 1187 ~ 1197
3. [학술지(정기간행물)] - Jaenisch R / 2003 / Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals / Nat Genet 300 : 489 ~ 492
4. [학술지(정기간행물)] - Soreide K / 2006 / Microsatellite instability in colorectal cancer / Br J Surg 93 : 395 ~ 406
5. [학술지(정기간행물)] - Garinis GA / 2002 / DNA hypermethylation: when tumour suppressor genes go silent / Hum Genet 111 : 115 ~ 127
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UCI(KEPA) : I410-ECN-0101-2013-514-002675523