FC 03-02The role of the antileukoprotease secretory leukocyte protease inhibitor (SLPI) in squamous cell carcinoma of the vulva in relation to HPV-infection and smoking habit of the patients

24. Vulvar diseases and neoplasia
E.S. Quabius 1, D. Haaser 1, J. Loehr 1, T. Görögh 1, V. Günther 2, I. Alkatout 2, M. Hoffmann 1.
1Department of Otorhinolaryngology, Head and Neck Surgery, Christian-Albrechts-University Kiel, Kiel, Germany (Germany), 2Department of Gynecology and Obstetrics , Christian-Albrechts-Univresity Kiel, Kiel , Germany. (Germany)

Background / Objectives

It was previously shown that protein and mRNA expression of the antileukoproteinase SLPI was significantly inverse correlated with HPV-infection in HNSCC and led to the suggestion that elevated expression of SLPI protects against HPV-infection in HNSCC. In addition we could show that SLPI expression was upregulated in HNSCC patients reporting a smoking habit. Here we investigate whether this inverse correlation between HPV-infection smoking habit and SLPI expression could also be found in other HPV-driven cancers, namely vulvar squamous cell carcinoma (VSCC).


Methods

FFPE samples of 116 VSCC were analyzed by PCR and RT-qPCR for HPV-DNA-, and SLPI mRNA-expression and data were correlated. Data correlating HPV- and SLPI-expression with smoking habit are so far preliminary since at present only 68 patients files are complete. The same holds true for Kaplan-Meyer-analysis correlating HPV-status and SLPI-expression with overall (OS) and progression free survival (PFS).


Results

Of the analyzed 116 VSCC 10 (8.6%) are HPV-DNA positive (Genotyping by Sanger sequencing is ongoing, followed by HPV-RNA-analysis). Of the 68 patients with complete files 24 (35.3%) reported a smoking habit and of these patients 3 (12.5%) were HPV-positive. So far 3 further HPV-positive patients were identified as non-smokers and for the remaining 4 at present no data are available. SLPI-expression however, was independent of the smoking habit, 4.0-fold lower in HPV-positive than HPV-negative patients. Smoking on the other hand resulted, independent of the HPV-status of the patients, in 5.6-fold higher SLPI expression. HPV-positivity and low SLPI-expression are associated with better PSF (analysis of OS data is ongoing).


Conclusion

The data presented here indicate that SLPI plays a pivotal role in HPV-infection not only in HNSCC but also in VSCC and possibly also in other HPV-driven cancers. This however, needs to be analyzed in future studies. Furthermore these data lead to the hypothesis that the smoking induced SLPI-increase is systemic rather than local, as assumed based on the HNSCC data.


References