IDEAS home Printed from https://ideas.repec.org/a/adm/journl/v7y2018i1p57-65.html
   My bibliography  Save this article

Prognostic and Clinicopathological Value of SIRT1 Expression in Female Reproductive System Cancer

Author

Listed:
  • Shuai Zhang
  • Zhe Sun
  • Yuewen Qi
  • Xiaolu Fang
  • Hong Yu

Abstract

Objective: Numerous epidemiological studies have reported the association between silent mating type information regulation 2 homolog-1 (SIRT1) and female reproductive system cancer, but the data of different reports remains controversial. To accurately evaluate the significance of SIRT1 expression in reproductive system cancer, a meta-analysis based on published studies was conducted. Methods: Relevant articles before August 2017 on SIRT1 and reproductive system cancer were searched via PubMed, Embase, Cochrane Central and Chinese National Knowledge Infrastructure databases(NCBI). The studies were chosen for the meta-analysis based on requisite criteria. The overall survival (OS) and clinical features including FIGO stage , lymph node metastasis (LNM) and tumor grade were analyzed using RevMan 5.3 software. Odds ratios (OR) , hazard ratios (HR) and their 95% corresponding confidence intervals (CI) were pooled to estimate the effect of specific associations. Results: A total of 14 eligible studies containing 1002 patients were enrolled, in which 47.9% of the patients overexpressed SIRT1. The results showed that SIRT1 overexpression significantly correlated with the risk of reproductive cancers (OR=3.92, 95% CI: 3.06–5.02, P

Suggested Citation

  • Shuai Zhang & Zhe Sun & Yuewen Qi & Xiaolu Fang & Hong Yu, 2018. "Prognostic and Clinicopathological Value of SIRT1 Expression in Female Reproductive System Cancer," International Journal of Sciences, Office ijSciences, vol. 7(01), pages 57-65, January.
  • Handle: RePEc:adm:journl:v:7:y:2018:i:1:p:57-65
    DOI: 10.18483/ijSci.1510
    as

    Download full text from publisher

    File URL: https://www.ijsciences.com/pub/article/1510
    Download Restriction: no

    File URL: https://www.ijsciences.com/pub/pdf/V72018011510.pdf
    Download Restriction: no

    File URL: https://libkey.io/10.18483/ijSci.1510?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    References listed on IDEAS

    as
    1. Shin-ichiro Imai & Christopher M. Armstrong & Matt Kaeberlein & Leonard Guarente, 2000. "Transcriptional silencing and longevity protein Sir2 is an NAD-dependent histone deacetylase," Nature, Nature, vol. 403(6771), pages 795-800, February.
    Full references (including those not matched with items on IDEAS)

    Most related items

    These are the items that most often cite the same works as this one and are cited by the same works as this one.
    1. Björn Klabunde & André Wesener & Wilhelm Bertrams & Isabell Beinborn & Nicole Paczia & Kristin Surmann & Sascha Blankenburg & Jochen Wilhelm & Javier Serrania & Kèvin Knoops & Eslam M. Elsayed & Katri, 2023. "NAD+ metabolism is a key modulator of bacterial respiratory epithelial infections," Nature Communications, Nature, vol. 14(1), pages 1-16, December.
    2. Beata Jablonska & Katrina L. Adams & Panagiotis Kratimenos & Zhen Li & Emma Strickland & Tarik F. Haydar & Katharina Kusch & Klaus-Armin Nave & Vittorio Gallo, 2022. "Sirt2 promotes white matter oligodendrogenesis during development and in models of neonatal hypoxia," Nature Communications, Nature, vol. 13(1), pages 1-20, December.
    3. Xiangkai Zhen & Xiaolong Xu & Le Ye & Song Xie & Zhijie Huang & Sheng Yang & Yanhui Wang & Jinyu Li & Feng Long & Songying Ouyang, 2024. "Structural basis of antiphage immunity generated by a prokaryotic Argonaute-associated SPARSA system," Nature Communications, Nature, vol. 15(1), pages 1-13, December.

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:adm:journl:v:7:y:2018:i:1:p:57-65. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    If CitEc recognized a bibliographic reference but did not link an item in RePEc to it, you can help with this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Staff ijSciences (email available below). General contact details of provider: .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.