eISSN: 2299-0046
ISSN: 1642-395X
Advances in Dermatology and Allergology/Postępy Dermatologii i Alergologii
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vol. 25

Original paper
Expression of Ki-67 and β-catenine in nodular and superficial form of basal cell carcinoma

Cezary Jochymski
Aleksandra Lesiak
Małgorzata Słowik-Rylska
Wojciech Kozłowski
Anna Sysa-Jędrzejowska
Michał Rogowski-Tylman
Joanna Narbutt

Post Dermatol Alergol 2008; XXV, 6: 269–275
Online publish date: 2009/01/12
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Introduction: Basal cell carcinoma (BCC) is the most common form of skin cancer in white populations. Growing BCC incidence results in numerous studies on its pathogenesis and treatment. Exposure to ultraviolet radiation leading to dysregulation of cell-cycle-related proteins and intracellular adhesion molecules expression plays a key role in skin carcinogenesis development. BCCs are divided into subtypes, depending on their clinical picture, localization, histology and recurrences. The main groups are superficial (sBCC) and nodular (nBCC) ones. Aim: To determine Ki-67 antigen and b-catenine expression in superficial and nodular form of BCC.
Material and methods: The study group consisted of 22 Caucasians with histologically confirmed superficial (group 1, n=11) or nodular (group 2, n=11) BCC form. In all BCC specimens the mean number of Ki-67 and b-catenine (+) cells was counted (immunohistochemistry). Additionally, 4 skin samples taken from healthy volunteers served as controls (group 3).
Results: The mean number of Ki-67 (+) cells was significantly higher both in sBCC and nBCC when compared to the control group (p<0.001 for both comparisons). β-catenine (+) cell count was significantly lower in sBCC and nBCC than in the control group (p<0.05 for both comparisons). No significant differences were found in expression of analyzed proteins between the two histological BCC subtypes (p>0.05 for both comparisons).
Conclusions: The obtained results indicated that observed dysregulation of Ki-67 and β-catenine expression in BCC may be involved in its pathogenesis. The lack of differences in their expression between the two BCC forms eliminated them as molecular biomarkers for differentiation of these BCC subtypes.

basal cell carcinoma (BCC), clinical subtypes of BCC, Ki-67, β-catenine, pathogenesis

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