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Enhancement of anti-DNA topoisomerase I autoantibody response after lung cancer in patients with systemic sclerosis: A report of two cases

✍ Scribed by Masataka Kuwana; Takao Fujii; Tsuneyo Mimori; Junichi Kaburaki


Publisher
John Wiley and Sons
Year
1996
Tongue
English
Weight
496 KB
Volume
39
Category
Article
ISSN
0004-3591

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✦ Synopsis


A Report of Two Cases MASATAKA KUWANA, TAKA0 FUJII, TSUNEYO MIMORI, and JUNICHI KABURAKI Anti-DNA topoisomerase I (anti-topo I) antibody profiles were compared before and after lung cancer in 2 patients with systemic sclerosis (SSc). Both patients developed adenocarcinoma of the lung late in the course of SSc and died of the cancer. Anti-top0 I antibody levels, determined by double immunodiffusion and enzyme-linked immunosorbent assay, increased markedly at the time of diagnosis of lung cancer. Furthermore, patients' sera obtained after lung cancer reacted with multiple epitopes on the entire top0 I molecule, some of which had not previously been recognized. These results further support the concept that anti-topo I antibody production in SSc patients is due to an antigen-driven process.

DNA topoisomerase I (topo I), a nuclear enzyme that catalyzes the relaxation of supercoiled DNA, is one of the major targets of the autoantibody response in some patients with systemic sclerosis (SSc, or scleroderma) (1). Serum anti-top0 I antibody is associated with a subset of SSc patients who have diffuse cutaneous involvement and pulmonary interstitial fibrosis (1,2). One recent report described the association of anti-top0 I antibody with cancer, especially with lung cancer (3). Interestingly, the expression of top0 I has been shown to be elevated in certain


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## Abstract ## Objective Fibroblasts play a crucial role in the development of systemic sclerosis (SSc), and antifibroblast antibodies (AFAs) capable of inducing a proinflammatory phenotype in fibroblasts have been detected in the sera of SSc patients. This study examined the prevalence of AFAs in