
Contributions
Abstract: PB2134
Type: Publication Only
Background
The main histocompatibility complex plays an important biological role, participating in the regulation of the immune response. There is some information in the literature about the relationship of specific HLA-specificities to various diseases, including oncohematological ones. In multiple myeloma (MM) the malignant clone develops from B-lymphocyte precursor cells, retaining the ability to produce pathological monoclonal immunoglobulins (the most common immunochemical variants are IgG, IgA) or light chains of immunoglobulins (the Bence-Jones variant). It is of interest to investigate the dependence of the onset of MM and its immunochemical variants on the specificity of the genes of the HLA system.
Aims
Identify the dependence of the occurrence of MM variants on the characteristics of patients HLA-genotypes.
Methods
The results of typing the HLA-genes of loci A, B, DRB1, DQA1, DQB1 by the SSP method were analyzed in 134 MM patients: 78 (58.2%) with variant G, 26 (19.4%) with A, 26 (19,4%) - with Bence-Jones. The frequency of occurrence of HLA-genes in patients with various forms of MM was compared with the frequency of these genes in healthy residents of the region – donors of blood components.
Results
It was found that in the general group of patients with MM this alleles were revealed significantly more often than in a healthy population: A*19 (21.6% vs 13.1% in healthy persons, p <0.05, RR = 2.0), B*16 (13.4% vs 7.7% in healthy subjects, p <0.05, RR = 2.0) and the DRB1*09 (10.9% vs 1.5%, p <0.01; RR = 8.4). The HLA-B*05 gene, on the contrary, was less common than in healthy individuals (5.2% vs 11.6%, p <0.05, RR = 0.3), which indicates its preventive effect.
A detailed analysis of the distribution of HLA-genes revealed specific genes for each immunochemical variant of MM. The HLA-A*19 gene (23.1% vs 13.1% in healthy p <0.05, RR = 2.1) and B*16 (17.9% vs 7, 7%, p <0.01, RR = 2.5) predisposed to the immunochemical variant with IgG secretion. In the variant with the secretion of pathological IgA, the specificity of HLA-A*03 was detected 3 times less frequently than in healthy individuals (11.6% vs 33.7%, p <0.05, RR = 0.3). For Bence-Jones myeloma, there was an increase in the occurrence of HLA-A*10 and B*18, often heritarily linked (HLA-A*10 - 38.5% vs 16.3%, p <0.01, RR = 3.7; HLA-B*18 - 30.8% vs 11.3%, p <0.01, RR = 3.9).
The DRB1 * 09 gene was detected in 1.5% of a healthy population, while in the variant with IgA secretion - in 4.8%, IgG - in 7.5% of patients (the differences did not reach statistical significance). In patients with the Bence-Jones variant, the DRB1 * 09 frequency was 28.0% (p <0.001, RR = 22.7).
Conclusion
To the development of MM predispose the genes A*19, B *16, DRB1*09; to the variant G - A*19, B*16; to the light chain variant - A*10, B*18, DRB*09. Protective to the development of MM is the gene B*05, to the development of variant IgA - A*03.
Session topic: 13. Myeloma and other monoclonal gammopathies – Biology & Translational Research
Keyword(s): HLA, Multiple Myeloma
Abstract: PB2134
Type: Publication Only
Background
The main histocompatibility complex plays an important biological role, participating in the regulation of the immune response. There is some information in the literature about the relationship of specific HLA-specificities to various diseases, including oncohematological ones. In multiple myeloma (MM) the malignant clone develops from B-lymphocyte precursor cells, retaining the ability to produce pathological monoclonal immunoglobulins (the most common immunochemical variants are IgG, IgA) or light chains of immunoglobulins (the Bence-Jones variant). It is of interest to investigate the dependence of the onset of MM and its immunochemical variants on the specificity of the genes of the HLA system.
Aims
Identify the dependence of the occurrence of MM variants on the characteristics of patients HLA-genotypes.
Methods
The results of typing the HLA-genes of loci A, B, DRB1, DQA1, DQB1 by the SSP method were analyzed in 134 MM patients: 78 (58.2%) with variant G, 26 (19.4%) with A, 26 (19,4%) - with Bence-Jones. The frequency of occurrence of HLA-genes in patients with various forms of MM was compared with the frequency of these genes in healthy residents of the region – donors of blood components.
Results
It was found that in the general group of patients with MM this alleles were revealed significantly more often than in a healthy population: A*19 (21.6% vs 13.1% in healthy persons, p <0.05, RR = 2.0), B*16 (13.4% vs 7.7% in healthy subjects, p <0.05, RR = 2.0) and the DRB1*09 (10.9% vs 1.5%, p <0.01; RR = 8.4). The HLA-B*05 gene, on the contrary, was less common than in healthy individuals (5.2% vs 11.6%, p <0.05, RR = 0.3), which indicates its preventive effect.
A detailed analysis of the distribution of HLA-genes revealed specific genes for each immunochemical variant of MM. The HLA-A*19 gene (23.1% vs 13.1% in healthy p <0.05, RR = 2.1) and B*16 (17.9% vs 7, 7%, p <0.01, RR = 2.5) predisposed to the immunochemical variant with IgG secretion. In the variant with the secretion of pathological IgA, the specificity of HLA-A*03 was detected 3 times less frequently than in healthy individuals (11.6% vs 33.7%, p <0.05, RR = 0.3). For Bence-Jones myeloma, there was an increase in the occurrence of HLA-A*10 and B*18, often heritarily linked (HLA-A*10 - 38.5% vs 16.3%, p <0.01, RR = 3.7; HLA-B*18 - 30.8% vs 11.3%, p <0.01, RR = 3.9).
The DRB1 * 09 gene was detected in 1.5% of a healthy population, while in the variant with IgA secretion - in 4.8%, IgG - in 7.5% of patients (the differences did not reach statistical significance). In patients with the Bence-Jones variant, the DRB1 * 09 frequency was 28.0% (p <0.001, RR = 22.7).
Conclusion
To the development of MM predispose the genes A*19, B *16, DRB1*09; to the variant G - A*19, B*16; to the light chain variant - A*10, B*18, DRB*09. Protective to the development of MM is the gene B*05, to the development of variant IgA - A*03.
Session topic: 13. Myeloma and other monoclonal gammopathies – Biology & Translational Research
Keyword(s): HLA, Multiple Myeloma