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Anti-ANP32A antibodies in systemic sclerosis
  1. Rachel Wallwork,
  2. Livia Casciola-Rosen,
  3. Ami A Shah
  1. Department of Medicine/Rheumatology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA
  1. Correspondence to Dr Ami A Shah, Medicine/Rheumatology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA; Ami.Shah{at}jhmi.edu

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Numerous studies have identified autoantibody status as an important biomarker of cancer risk around the time of systemic sclerosis (SSc) onset. For example, anti-RNA polymerase III antibody positivity associates with increased cancer risk near SSc onset, while the presence of anticentromere or anti-Th/To antibodies may be protective.1–4

In this context, we selected serum from a well-characterised patient with SSc with squamous cell skin cancer and a short cancer–scleroderma interval to discover cancer-associated autoantibodies. Immunoprecipitations performed with this serum using 624 melanoma cell lysates were subjected to on bead digestion and liquid chromatography tandem mass spectrometry peptide sequencing. This identified antibodies targeting the tumour suppressor gene, acidic leucine-rich nuclear phosphoprotein (ANP32A), which migrates on SDS-polyacrylamide gels at ~28.5 kDa. Antibodies against ANP32A were validated in this serum by immunoprecipitation using 35S-methionine labelled ANP32A generated by in vitro transcription/translation from DNA (Origene) as described.5

To further explore the association between anti-ANP32A antibodies and cancer in patients with SSc, sera from patients with (n=213) and without cancer (n=190) were randomly selected from the Johns Hopkins Scleroderma Center Research Registry for anti-ANP32A antibody testing. The Registry prospectively collects demographic information, cancer diagnoses and longitudinal disease metrics. …

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Footnotes

  • Handling editor Josef S Smolen

  • Contributors All authors were involved in drafting the letter and revising it critically for intellectual content, and all authors approved the final version to be published. Study conception and design were done by LC-R and AAS. Acquisition of data was done by LC-R and AAS. RW, LC-R and AAS were involved in analysis and interpretation of data.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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