ISSN 1308-8734 | E-ISSN 1308-8742
Original Article
HLA Antigen Profile Differences in Patients with SCC (Squamous Cell Carcinoma) In-Situ /Actinic Keratosis and Invasive SCC: Is There a Genetic Succeptibility for Invasive SCC Development?
1 Ataturk University, Faculty of Medicine, Department of Dermatology, Erzurum, Turkey  
2 Ankara University, Faculty of Medicine, Department of Dermatology, Ankara, Turkey  
3 Atatürk University, Faculty of Medicine, Department of Medical Biology, Erzurum, Turkey  
4 Karadeniz Teknik University, Faculty of Medicine, Department of Medical Biology, Erzurum, Turkey  
Eurasian J Med 2009; 41: 162-164

Key Words: Actinic keratoses, Squamous cell carcinoma, HLA
Abstract

 

Objective: Actinic keratoses (AK) are proliferation of neoplastic keratinocytes confined to the epidermis induced by damaging solar ultraviolet radiation (UVR). When the neoplastic keratinocytes extend in to papillary -reticular dermis, then the lesion termed as squamous cell carcinoma (SCC). We have compared HLA class I and II antigen profiles in three patient groups namely: AK (n: 31) (patients without past or present invasive SCC), invasive SCC (n: 38), and SCC derived from / inconjuction with AK (n: 11).

 

Materials and Methods: Low-resolution typing for the HLA-A, B, C and HLA-DR/DQ was performed by means of the PCR-sequence specific primer (PCR-SSP) method using SSP HLA class I generic DNA Typing Tray.

Results: HLA results of these three groups were compared with the healthy control group (n: 100). There were not significant difference in HLA class I and II antigen profiles in AK group compared to the control. Whereas HLA-A2 allele (60.52%, p=0.016, OR=2.726, 95%CI=1.265-5.876), HLA-B60 (13.15%, p=0.025, OR=7.424, 95%CI=1.375-40.099) were higher in SCC group than the control. HLA-B51 allele (72.72%, p=0.008, OR=6.853, 95%CI=1.696-27.720) distribution were more common in SCC derived from AK than the control.

Conclusions: Historically, AKs have been characterized as premalignant. It has, however, been considered that AK and SCC represent the same disease process at the different stages of evaluation. Clinically, and histopathologically it is difficult to determine where AK ends and invasive SCC begins. From dermatopathological point of view AK is clearly SCC in-situ, however although AK is a common lesion in Caucasians, not all AKs develop in to invasive SCC, at least not with the same biological pace. We concluded that genetic differences such as HLA class I and II distribution between AK and SCC may not seem to play susceptibility role for invasive SCC development.

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