Artikel
Meningioma – is there an association with human leukocyte antigens (HLA)?
Untersuchungen zur HLA-Assoziation von zerebralen Meningeomen
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Autoren
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M. Tschigrjai
- Interbranch HLA Laboratory/Department GHATT, Institute of Medical Immunology, Martin-Luther University, Halle
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H. K. G. Machulla
- Interbranch HLA Laboratory/Department GHATT, Institute of Medical Immunology, Martin-Luther University, Halle
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F. Steinborn
- Interbranch HLA Laboratory/Department GHATT, Institute of Medical Immunology, Martin-Luther University, Halle
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J. Langner
- Interbranch HLA Laboratory/Department GHATT, Institute of Medical Immunology, Martin-Luther University, Halle
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N. G. Rainov
- University of Liverpool, Department of Neurological Sciences, Liverpool/UK
| Veröffentlicht: | 4. Mai 2005 |
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Gliederung
Text
Objective
The expression of HLA alleles plays an important role in the development and recurrence of benign and malignant diseases. Association of single HLA alleles or haplotypes with neoplastic processes has been investigated previously, and correlation between HLA and solid tumors, such as head and neck cancers or uterine cervical squamous epithelial lesions, were reported. However, there is no published data on the influence of the HLA system on the development of symptomatic cerebral meningioma, a mostly benign intracranial tumor of mesenchymal origin in adults. The aim of the present study was to find out correlations between HLA markers and meningioma as a further brain tumor.
Methods
The present investigation is comparing the frequency of single HLA alleles and haplotypes in 81 adult Caucasian patients with symptomatic CNS meningiomas to that of 157 area- and race matched healthy controls. Both standard serologic and molecular genetic (PCR) techniques were used for HLA typing.
Results
Our results suggest an association between single HLA alleles and occurrence of clinically symptomatic meningioma. Patients with HLA-A*02 had a 2.5-fold increased risk of meningioma (p=0.02), and those with HLA-DQB1*05 a 1.8-fold increased risk of meningioma (p=0.05). Conversely, HLA-A*01, -B*08 and -DRB1*03 were associated with a 0.4-, 0.5-, and 0.5-fold, respectively, decreased risk of meningioma (p=0.008; p=0.05, and p=0.04). Moreover, the occurrence rate of combinations and estimated haplotypes containing the above HLA alleles was strikingly different in meningioma patients compared with controls: significantly increased for the haplotypes HLA-A*02:DRB1*04 (p=0.02, RR=2.5) and HLA-A*02:DRB1*04:DQB1*0302,DQB1*05 (p=0.03, RR=7.5), and significantly decreased for the haplotype HLA-A*01:B*08:DRB1*03 (p=0.01, RR=0.2).
Conclusions
In conclusion, these data suggest that some single HLA alleles and haplotypes may protect from or predispose to developing symptomatic CNS meningioma during adult life. These associations may be indicative of the involvement of the immune system in the host antitumor surveillance, recognition, and destruction of de novo arising human tumor cells.
