메뉴 건너뛰기
.. 내서재 .. 알림
소속 기관/학교 인증
인증하면 논문, 학술자료 등을  무료로 열람할 수 있어요.
한국대학교, 누리자동차, 시립도서관 등 나의 기관을 확인해보세요
(국내 대학 90% 이상 구독 중)
로그인 회원가입 고객센터 ENG
주제분류

추천
검색

이용수

표지
📌
연구주제
📖
연구배경
🔬
연구방법
🏆
연구결과
AI에게 요청하기
추천
검색

초록· 키워드

오류제보하기
Background: The p16INK4a gene methylation has been reported to be a major tumorigenic mechanism. Methods: We evaluated the methylation status of the p16INK4a genes in 231 invasive breast cancer and 90 intraductal carcinoma specimens using a methylation-specific polymerase chain reaction and p16 protein expression using immunohistochemistry. The quantity of cell-free methylated p16INK4a DNA in the plasma samples of 200 patients with invasive breast cancer was also examined using a fluorescence-based real-time polymerase chain reaction assay. Results: The frequencies of p16INK4a methylation in invasive and intraductal tumors were 52.8% (122/231) and 57.8% (52/90),respectively. The p16 protein was overexpressed in 145 of the 231 invasive carcinomas (62.8%) and 63 of the 90 intraductal carcinomas (70%). High p16 expression in invasive carcinomas correlated significantly with a high histologic grade, a negative estrogen receptor and progesterone receptor status, p53 immunoreactivity and high Ki-67 expression with immunohistochemistry. In addition, the methylation index of p16INK4a was significantly higher in the cancer patients than the normal controls (p<0.001). Conclusions: High p16 immunoreactivity correlated with a loss of differentiation in breast carcinomas and high frequency of p16INK4a promoter methylation in both invasive and intraductal carcinomas, suggesting it maybe involved in the pathogenesis of breast cancer.

목차

등록된 정보가 없습니다.

참고문헌 (23)

참고문헌 신청

이 논문의 저자 정보

최근 본 자료

전체보기

댓글(0)

0