Abstract
Objective:Cancer, one of the principal causes of death, is a global social health problem. Autoantibodies developed against the organism’s self-antigens are detected in the sera of subjects with cancer. In recent years carbonic anhydrase (CA) I and II autoantibodies have been shown in some autoimmune diseases and carcinomas, but the mechanisms underlying this immune response have not yet been explained. The aim of this study was to evaluate CA I and II autoantibodies in patients with acute myeloid leukemia (AML) and to provide a novel perspective regarding the autoimmune basis of the disease.Materials and Methods:Anti-CA I and II antibody levels were investigated using ELISA in serum samples from 30 patients with AML and 30 healthy peers.Results:Anti-CA I and II antibody titers in the AML group were significantly higher compared with the control group (p=0.0001 and 0.018, respectively). A strong positive correlation was also determined between titers of anti-CA I and II antibodies (r=0.613, p=0.0001).Conclusion:Our results suggest that these autoantibodies may be involved in the pathogenesis of AML. More extensive studies are now needed to reveal the entire mechanism.
Highlights
Cancer is the second most important cause of mortality and a major public health problem worldwide [1]
Anti-carbonic anhydrase (CA) I and II antibody titers in the acute myeloid leukemia (AML) group were significantly higher compared with the control group (p=0.0001 and 0.018, respectively)
There was no significant difference in terms of mean age between the study and control groups
Summary
Cancer is the second most important cause of mortality and a major public health problem worldwide [1]. Acute myeloid leukemia (AML) is a complex and heterogeneous clonal disease involving arrest of differentiation in the myeloid lineage along with deposition of immature progenitors in bone marrow, concluding in hematopoietic failure [2]. The pathogenesis of AML involves various disorders, such as mutations in transcription factors or epigenetic modifiers, aberrant signaling pathways, excessive expression of the gene involved in multidrug resistance, abnormal immune function, and abnormalities in the bone marrow microenvironment [3]. Autoantibodies can be observed in the sera of patients with solid tumors and hematological malignancies [4,5]. These autoantibodies are regarded as early biomarkers for some types of cancer [6,7,8]
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