cqvip:Background: The hyperproliferative keratinocytic lesions encompass a wide ran ge of non-tumorigenic, pretumorigenic, and tumorigenic conditions. The aim of this work was to examine the expression patterns of apoptosis-linked molecules (bcl-2 and p53) in these lesions. Methods: Immunoperoxidase staining methods were applied to analyze p53 and bcl- 2 protein expression in a total of 66 case s, including 12 squamous cell carcinomas (both in situ and invasive SCC), 11 act inic keratoses(AK), 13 psoriasis vulgaris(PV), eight verruca vulgaris(VV), six c hronic dermatitis(CD), five seborrheic keratosis(SK), four lichen planus(LP),thr ee epidermodysplasia verruciformis (EDV), two condyloma acuminata(CA),two lichen simplex chronicus (LSC), and 10 specimens from normal skin. Results: As compare d to normal skin (0.70 ± 0.26), the bcl- 2 average weighted scores in the non -tumorigenic (0.76 ± 0.16), pretumorigenic (1.45 ± 0.28), and tumorigenic lesions (2.83 ± 0.50 and 2.92 ± 0.50 for in situ and invasive SCC, respectiv ely) showed significant up-regulation (P = 0.001). In the non-tumorigenic lesions, the bcl- 2 expression values decreased in the following order: SK > EDV > CD > LP > CA > PV > VV (1.40 ± 0. 24 > 1.33 ± 0.67 > 0.83 ± 0.40 > 0.67 ± 0.21 > 0.50 ± 0.20 > 0.46 ± 0. 22 > 0.13 ± 0.01, respectively). As compared to normal skin (1.10 ± 0.23), t he p53 average weighted scores in the non-tumorigenic (1.86 ± 0.18), pretumo rigenic (3.64 ± 0.53), and tumorigenic lesions (5.00 ± 1.00 and 5.08 ± 0.8 6 for in situ and invasive SCC, respectively) showed significant up-regulation (P = 0.021). In the non-tumorigenic lesions, p53 average weighted scores decr eased in the following order: SK > PV > CA > LP > CD > VV > EDV (3.20 ± 0.49 > 2.38 ± 0.27 > 2.0 ± 0.0 > 1.83 ± 0.48 > 1.0 ± 0.37 > 1.0 ± 0.33 > 1.0 ± 0.0, respectively). There was a positive correlation between bcl- 2 and p5 3 protein expression in normal skin (r=0.966, P=0.0001), non-tumorigenic (r=0. 775, P= 0.0001), pretumorigenic (r=0.830, P=0.001), and tumorigenic lesions (r=0 .757, P=0.003). Conclusions: Bcl- 2 and p53 proteins are altered in the keratin ocytic hyperproliferative lesions. Determination of whether these al-terations reflect underlying gene mutations will require further investigations.
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