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Correlation between Bcl‐2 and Bax in atrophic and hypertrophic type of actinic keratosis
Author(s) -
Tomas D,
Krušlin B,
Čupič H,
Stanimirovič A,
Bošnjak B,
Lovričevič I,
Belicza M
Publication year - 2006
Publication title -
journal of the european academy of dermatology and venereology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.655
H-Index - 107
eISSN - 1468-3083
pISSN - 0926-9959
DOI - 10.1111/j.1468-3083.2005.01364.x
Subject(s) - medicine , immunohistochemistry , actinic keratosis , immunoperoxidase , polyclonal antibodies , pathology , antibody , monoclonal antibody , basal cell , immunology
Background Recent investigations consider actinic keratosis (AK) as an earliest visible pattern of squamous cell carcinoma (SCC). We have analysed the expression of apoptosis‐related proteins TP53, Bcl‐2 and Bax in 30 atrophic and 30 hypertrophic AK cases. Material and methods Immunohistochemical analysis was performed following microwave streptavidin immunoperoxidase protocol on DAKO TechMate TM Horizon automated immunostainer (DAKO, Copenhagen, Denmark). Monoclonal antibody for TP53 and Bcl‐2 and polyclonal antibody for Bax (DAKO, Copenhagen, Denmark) were used. Results Expression of TP53 showed no significant differences between two analysed groups (χ 2 ‐test, P = 0.35636) whereas expression of Bcl‐2 and Bax protein was significantly higher in atrophic compared to hypertrophic AK (χ 2 ‐test, P = 0.01458 and P = 0.00358, respectively). Comparison of Bcl‐2 : Bax ratio in two analysed AK showed significantly higher value in hypertrophic compared to atrophic AK (Mann–Whitney U test, P = 0.02272). Statistical analysis did not show any correlation between patient's sex and age, localization and size of the lesion with expression of investigated oncoproteins ( anova , P > 0.05). Conclusions Our results may indicate higher resistance of keratinocytes on apoptotic stimuli in hypertrophic compared to atrophic AK. Thus, we suppose that keratinocytes in hypertrophic AK live longer and probably have higher propensity for additional mutations and conversion to overt SCC.