Send to

Choose Destination
See comment in PubMed Commons below
Gynecol Oncol. 2007 Sep;106(3):567-71. Epub 2007 Jun 8.

The role of angiogenesis and COX-2 expression in the evolution of vulvar lichen sclerosus to squamous cell carcinoma of the vulva.

Author information

Department of Human Pathology and Oncology, School of Medicine University of Florence, Viale G.B. Morgagni, 85. 50134 Florence, Italy.



We aimed to determine whether premalignant changes in vulvar lichen sclerosus (LS) could be identified by analysing markers of angiogenesis and the expression of the enzyme cyclooxygenase-2 (COX-2).


Eight cases of histologically diagnosed vulvar LS, which showed an evolution to carcinoma of the vulva histologically documented, were compared to 10 cases of vulvar LS, for which follow-up information was available for at least 9 years, and to 10 cases of LS adjacent to squamous cell carcinoma (SCC) of the vulva. The microvessel density (MVD), and the expression of vascular endothelial growth factor (VEGF) and of COX-2 were analysed.


Difference of MVD between unchanged LS cases and LS cases evolving to SCC and LS adjacent to SCC cases was statistically significant (P=0.008, Wilcoxon Mann-Whitney test). Difference of VEGF and COX-2 expression between unchanged LS cases and LS cases evolving to SCC and LS adjacent to SCC cases were statistically significant (P=0.007 and P=0.01, respectively; Fisher's exact test).


Our study addresses the possibility that immunohistochemical studies may add information to permit the identification of LS as a precursor lesion that has a greater potential to evolve into SCC. These data may identify characteristics of vulvar LS disclosing alterations that indicate the further development to cancer; therefore, it may allow the identification of a group of LS patients who need a careful follow-up and adjunctive biopsies.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center