Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2009 Dec;41(3):162-4.

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?

Mustafa Atasoy  1 , Rana Anadolu-Braise  2 , Ibrahim Pirim  3 , Hasan Dogan  3 , Mevlüt Ikbal  4
Affiliations

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?

Mustafa Atasoy et al. Eurasian J Med. 2009 Dec.

Abstract
in English, Turkish

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.

Amaç: Aktinik Keratoz (AK) solar ultraviole radyasyon hasarıyla uyarılan epidermise özel neoplastik kerotinositlerin proliferasyonudur. Neoplastik kerotinositler papiller retiküler dermise yayıldığında oluşan lezyon SCC olarak adlandırılır Çalışmamızın hedefi HLA sınıf-I ve sınıf-II antijen dağılımını 3 hasta grubunda karşılaştırmaktır. Bunlar AK(n:31) (geçmişlerinde ve halihazırda invaziv SCC olmayanlar, invaziv SCC (n: 38) ve AK den kaynaklanan SCC li hastalar(n: 11).

Gereç ve yöntem: PCR–SSP yöntemiyle düşük rezolusyonu (2 digit) HLA-A, B, C ve HLA-DR/DQ doku tiplendirilmesi yapıldı.

Bulgular: Bu 3 grubun HLA sınıf-I ve sınıf-II sonuçları sağlıklı kontrol grubu (n: 100) ile de karşılaştırıldı. AK grubunda HLA sınıf-I ve sınıf-II dağılımıyla kontrol grubu arasında fark bulunamadı. Fakat HLA-A2 alleli (% 60,52, p=0,016, OR=2,726, % 95 CI=1,265–5,876) ve HLA-B60 (% 13,15, p=0,025, OR=7,424, % 95 CI=1,375–40,099) allelleri SCC grubunda daha yüksekti. HLA-B51 aleli (% 72,72, p=0,008, OR=6,853, % 95 CI=1,696–27,720) kontrol grubuna göre AK den kaynaklanan SCC grubunda daha yaygındı.

Sonuç: AK premalignant olarak değerlendirilmektedir, bununla beraber AK ve SCC nin birlikte aynı hastalık prosesinin farklı basamaklarından geliştiği düşünülmektedir. Klinik ve histopatolojik olarak AK in nerede bittiğini ve invaziv SCC nin nerede başladığını saptamak zordur. Dermatolojik acıdan, AK açıkça SCC in-situ dur. Bununla birlikte Kafkaslarda yaygın lezyon olmasına rağmen, bütün AK ler invaziv SCC ye dönüşmez. Çünkü bir kısmı aynı biyolojik temelden oluşmamaktadır. Çalışmamızın sonunda, AK ve SCC lu hastaların genetic acıdan HLA sınıf I ve II dağılımlarının SCC gelişimine bir katıkısının olmadığı gösterilmiştir.

Keywords: Actinic keratoses; HLA; Squamous cell carcinoma.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

References

    1. Arnaiz-Villena A, Vargas-Alarcon G, Granados J, et al. HLA genes in Mexican Mazate-cans, the people of the Americas and the uniqueness of Amerindians. Tissue Antigens. 2000;56:405–16. - PubMed
    1. Anjos S, Polychronakos C. Mechanisms of genetic susceptibility to type1 diabetes: beyond HLA. Mol Genet Metab. 2004;81:187–95. - PubMed
    1. MacDonald DM, Markey AC, Churchill LJ. Altered expression of major histocompatibility complex (MHC) antigens by epidermal tumours. J Cutan Pathol. 1990;17:65–71. - PubMed
    1. Houck JR, Sexton FM, Zajdel HLA class I and class II antigen expression on squamous cell carcinoma of the head and neck. Arch Otolaryngol Head Neck Surg. 1990;116:1181–5. - PubMed
    1. Dehaghani AS, Amirzargar A, Farjadıan S, et al. HLA-DQBI alleles and susceptibility to cervical squamous cell carcinoma in South-hern Iranin patients. Pathol Oncol Res. 2002;8:58–61. - PubMed

LinkOut - more resources