Association of the Autoimmune Disease Scleroderma with an Immunologic Response to Cancer

Author:

Joseph Christine G.1,Darrah Erika2,Shah Ami A.2,Skora Andrew D.1,Casciola-Rosen Livia A.2,Wigley Fredrick M.2,Boin Francesco2,Fava Andrea2,Thoburn Chris3,Kinde Isaac1,Jiao Yuchen1,Papadopoulos Nickolas1,Kinzler Kenneth W.1,Vogelstein Bert1,Rosen Antony2

Affiliation:

1. Ludwig Center, the Howard Hughes Medical Institutions, and the Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.

2. Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.

3. Division of Immunology, The Johns Hopkins Sidney Kimmel Comprehensive Cancer Center, Baltimore, MD 21287, USA.

Abstract

Cancer Immunosurveillance Gone Bad? A subset of patients who develop scleroderma, a debilitating autoimmune disease, have an elevated risk of developing cancer. These patients harbor autoantibodies to RPC1, an RNA polymerase subunit encoded by the POLR3A gene. Joseph et al. (p. 152 , published online December 5; see the Perspective by Teng and Smyth ) explored whether the RPC1 autoantibodies target a “foreign” antigen derived from a mutated POLR3A gene. Sequence analysis revealed that POLR3A mutations were present in tumors from six of eight patients with RPC1 autoantibodies but in no tumors from eight control patients who lacked RPC1 autoantibodies. Cell culture data suggested that the POLR3A mutations triggered cellular and humoral immune responses in the patients. These results provide support for the “immunosurveillance” hypothesis, which posits the continual eradication of nascent tumor cells via immune responses.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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