Spontaneous tumour regression after high-dose therapy and autologous stem cell transplantation is associated with the aplastic anaemia-like syndrome and the presence of polyclonal autoantibodies against carbonic anhydrase I (CA I). When tumour cells were grown in vitro in the presence of patients' sera positive for anti-CA I autoantibodies, their morphological pattern was altered. These changes were accompanied by modifications in the gene expression profile. We observed downregulation of genes of the basal lamina assembly (collagen type IV alpha 4, the laminin subunit gamma 2), the extracellular matrix (collagen type I alpha 1), the cytoskeleton (keratin 14 type I), the collagen triple helix repeat containing 1 and the proto-oncogene WNT7B. On the other hand, the expression of the CA 1 gene was increased in the tumour cells. It was also noticed that the presence of anti-CA I autoantibodies did not impair tumour cell proliferation and cell viability in vitro. These findings were observed only in the presence of patients' sera positive for anti-CA I autoantibodies.
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http://dx.doi.org/10.1111/jcmm.13000 | DOI Listing |
Mediators Inflamm
January 2025
Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovakia.
Spontaneous tumor regression is a recognized phenomenon across various cancer types. Recent research emphasizes the alterations in autoantibodies against carbonic anhydrase I (CA I) (anti-CA I) levels as potential prognostic markers for various malignancies. Particularly, autoantibodies targeting CA I and II appear to induce cellular damage by inhibiting their respective protein's catalytic functions.
View Article and Find Full Text PDFAm J Med Sci
December 2023
Graduate School of Medical Science, Department of Medical Biochemistry, Karadeniz Technical University, Trabzon, Türkiye; Faculty of Medicine, Department of Medical Biochemistry, Istanbul University, Istanbul, Turkey.
Background: Carbonic anhydrases (CA) are metalloenzymes with wide tissue distribution, involved in many important physiological processes, and in some rheumatic diseases, autoantibodies are formed against these enzymes. Recent studies have suggested that oxidative stress triggers anti-CA antibody formation. In this study, we aimed to investigate the effects of modification with oxidative/nitrosative stress end products on CA antigenicity in mice and the relationship between the modified CA autoantibodies and oxidant-antioxidant status in patients with rheumatoid arthritis (RA) and Sjögren's syndrome (SjS).
View Article and Find Full Text PDFJ Neurol
June 2023
Department of Neurology, Cantonal Hospital Aarau, Tellstrasse 25, CH-5011, Aarau, Switzerland.
Medicine (Baltimore)
January 2023
Department of Rheumatology and Immunology, Beijing Key Laboratory for Rheumatism and Immune Diagnosis, Peking University People's Hospital, Beijing, China.
Primary Sjögren syndrome (pSS) is a systemic autoimmue disease featured by excessive autoantibody production. It has been demonstrated that anti-carbonic anhydrase II (anti-CA II) antibody is correlated with renal tubular acidosis in pSS; however, no further details about urinary acidification defect have been reported, and the antibody's relationship with other organ impairments remains unknown. This case-control study aimed to examine anti-CA II antibody levels in relation to various systemic complications in pSS, and evaluate its potential role as a organ-specific biomarker in a Chinese cohort.
View Article and Find Full Text PDFJ Neurol
March 2023
Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Heidelberg, Germany.
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