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

논문 기본 정보

자료유형
학술저널
저자정보
저널정보
대한생화학·분자생물학회 Experimental and Molecular Medicine Experimental and Molecular Medicine 제50권
발행연도
2018.1
수록면
1 - 7 (7page)

이용수

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

초록· 키워드

오류제보하기
FOXM1 (Forkhead box M1) is a key regulator of tumorigenesis. Previous studies demonstrated that FOXM1 overexpression was strongly correlated with poor prognosis in various cancers, including hepatocellular carcinoma (HCC). In this study, we examined an association between the gene expression signature of FOXM1 and HCC patient outcome. The co-expressed gene set of FOXM1, which is significantly associated with the prognosis of HCC patients, was identified by analyzing the gene expression profiles of 100 patients with HCC, and this gene set was validated in two independent HCC patient cohorts (n=573). In multivariate analysis, the co-expressed gene set of FOXM1 was the most significant prognostic factor for overall survival in patients with HCC (hazard ratio=1.706, 95% confidence intervals=1.176–2.475, P=0.005). We also analyzed different types of cancer, including pancreatic adenocarcinoma, lung adenocarcinoma, breast carcinoma and bladder urothelial carcinoma, to verify the association between the co-expressed gene set of FOXM1 and patient prognosis, and we found a consistent prognostic significance, regardless of tumor type. Finally, we identified a putative signaling pathway in which miR-34a acts as an upstream regulator of the FOXM1-MYC signaling network; this pathway may be ultimately responsible for the poor prognosis of HCC patients. The prognostic subgroups defined by the gene expression signature of FOXM1 could help predict high-risk patients and may guide selection of the best treatment strategy.

목차

등록된 정보가 없습니다.

참고문헌 (0)

참고문헌 신청

함께 읽어보면 좋을 논문

논문 유사도에 따라 DBpia 가 추천하는 논문입니다. 함께 보면 좋을 연관 논문을 확인해보세요!

이 논문의 저자 정보

최근 본 자료

전체보기

댓글(0)

0