These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: The clinicopathological and prognostic impact of 14-3-3 sigma expression on vulvar squamous cell carcinomas.
    Author: Wang Z, Tropè CG, Suo Z, Trøen G, Yang G, Nesland JM, Holm R.
    Journal: BMC Cancer; 2008 Oct 24; 8():308. PubMed ID: 18950492.
    Abstract:
    BACKGROUND: 14-3-3 sigma promotes G2/M cell cycle arrest by sequestering cyclin B1-CDC2 complex in cytoplasm. Down-regulation of 14-3-3sigma, which has been demonstrated in various carcinomas, may contribute to malignant transformation. However, the exact role of 14-3-3sigma in the pathogenesis of vulvar carcinoma is not fully characterized, and the prognostic impact of 14-3-3sigma protein expression is still unknown. METHODS: We investigated the 14-3-3sigma expression in a series of 302 vulvar squamous cell carcinomas using immunohistochemistry and its associations with clinicopathological factors and clinical outcome. RESULTS: In cytoplasm, nucleus and cytoplasm/nucleus of vulvar carcinomas high 14-3-3sigma protein expression was found in 72%, 59% and 75% of the carcinomas, respectively, and low levels in 28%, 41% and 25% of the cases, respectively. High level of 14-3-3sigma in cytoplasm, nucleus and cytoplasm/nucleus was significantly correlated to large tumor diameter (p = 0.001, p = 0.002 and p = 0.001, respectively) and deep invasion (p = 0.01, p = 0.001 and p = 0.007, respectively). Variations of 14-3-3sigma protein expression were not associated to disease-specific survival. CONCLUSION: Our results indicate that 14-3-3sigma may be involved in the development of a subset of vulvar squamous cell carcinomas by down-regulation of 14-3-3sigma protein. Neither cytoplasmic nor nuclear level of 14-3-3sigma expression was associated with prognosis.
    [Abstract] [Full Text] [Related] [New Search]