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- W2997056384 abstract "Abstract Anti-transcription intermediary factor 1 (TIF1)-γ autoantibodies are robustly linked with cancer-associated DM in adults. This review aims to give an overview of the physiological context of TIF1-γ and to determine whether there is a pathophysiological link between anti-TIF1-γ autoantibodies and the occurrence of cancer. Detection of anti-TIF1-γ autoantibodies has a high sensitivity and specificity for cancer-associated DM in adults and is therefore useful for both diagnosis and cancer risk stratification. The function of the autoantigen, TIF1-γ, may provide insight into the mechanism behind this association. TIF1-γ is a ubiquitously present protein involved in various biological pathways, including TGF-β signalling. In cancer, it can act either as a tumour suppressor or promoter, depending on the cellular context and cancer stage. Evolving data provide pathophysiological insights, linking anti-TIF1-γ autoantibodies to both the anti-tumour response and to muscle and skin damage. TIF1-γ expression is increased in muscle and skin tissue of patients with DM. Mutations or loss-of-heterozygosity in TIF1-γ alleles in malignant tissue may result in the expression of tumour-specific neo-antigens stimulating autoantibody production. The newly formed autoantibodies are hypothesized to cross-react with antigens in muscle and skin, driving the development of DM. Based on the current evidence, anti-TIF1-γ autoantibodies should be considered warning lights of a potential tumour autoantigen and should alert the physician to the possibility of an underlying cancer." @default.
- W2997056384 created "2020-01-10" @default.
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- W2997056384 creator A5071488467 @default.
- W2997056384 creator A5078671381 @default.
- W2997056384 date "2019-12-28" @default.
- W2997056384 modified "2023-10-11" @default.
- W2997056384 title "Anti-TIF1-γ autoantibodies: warning lights of a tumour autoantigen" @default.
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- W2997056384 doi "https://doi.org/10.1093/rheumatology/kez572" @default.
- W2997056384 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31883334" @default.
- W2997056384 hasPublicationYear "2019" @default.
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