LAUSR

287 diseases and myositis with mild to moderate symptoms [3]. A large population-based cohort study found that 79.5% of patients with anti-TIF1 antibody-positive DM had developed malignancies within one year after diagnosis, and 8% of patients with DM-associated malignancies were reported to develop two overlapping carcinomas [4]. Regarding the subtypes of anti-TIF1 antibodies, 98.7% of anti-TIF1 antibody-positive cases were anti-TIF1 (and ) antibody-positive and 1.3% were anti-TIF1 antibody-positive only, characterized by mild myositis and a lower incidence of malignancy compared to those with anti-TIF1 antibody [5]. To date, only one anti-TIF1 antibody-positive DM patient has been described with triple malignancies [6]. The mechanism underlying the simultaneous development of multiple malignancies in a single patient remains unknown. TIF1 acts as a tumour suppressor via WNT/ -catenin signalling and epithelial-mesenchymal transition [7], and mutations in TIF1 genes have been reported in tumours of patients with DM [8]. These mutant TIF1 genes encode abnormal TIF1 proteins that act as neoantigens to trigger the production of autoantibodies against TIF1 , which may result in the development of DM symptoms [7]. It is unclear, however, whether anti-TIF1 antibodies affect TIF1 in tumours or generate malignant neoplasms. To investigate the association between cancer and anti-TIF1 antibody, we immunostained TIF1 protein in cancers of the oesophagus (figure 1G, H), pharynx (figure 1I), and larynx (figure 1J) from Patient 1, and oesophagus (figure 1K) and lung (figure 1L) from Patient 2. All tissues revealed TIF1 , implying an association between these cancers and anti-TIF1 antibodies. These tissues showed no evidence of HPV infection. Further research is needed, however, to determine whether the two early-stage malignancies in each patient resulted from genetic mutations or were triggered by inhibition of tumour suppression by anti-TIF1 antibodies.