Melanomas resist T-cell therapy through inflammation-induced reversible dedifferentiation

Jennifer Landsberg, Judith Kohlmeyer, Marcel Renn, Tobias Bald, Meri Rogava, Mira Cron, Martina Fatho, Volker Lennerz, Thomas Wölfel, Michael Hölzel and Thomas Tüting ()
Additional contact information
Jennifer Landsberg: Laboratory of Experimental Dermatology, University of Bonn, D-53105 Bonn, Germany
Judith Kohlmeyer: Laboratory of Experimental Dermatology, University of Bonn, D-53105 Bonn, Germany
Marcel Renn: Laboratory of Experimental Dermatology, University of Bonn, D-53105 Bonn, Germany
Tobias Bald: Laboratory of Experimental Dermatology, University of Bonn, D-53105 Bonn, Germany
Meri Rogava: Laboratory of Experimental Dermatology, University of Bonn, D-53105 Bonn, Germany
Mira Cron: Laboratory of Experimental Dermatology, University of Bonn, D-53105 Bonn, Germany
Martina Fatho: Haematology/Oncology/Pneumology, University Medical Centre of the Johannes Gutenberg University, D-55101 Mainz, Germany
Volker Lennerz: Haematology/Oncology/Pneumology, University Medical Centre of the Johannes Gutenberg University, D-55101 Mainz, Germany
Thomas Wölfel: Haematology/Oncology/Pneumology, University Medical Centre of the Johannes Gutenberg University, D-55101 Mainz, Germany
Michael Hölzel: Unit for RNA Biology, University of Bonn, D-53105 Bonn, Germany
Thomas Tüting: Laboratory of Experimental Dermatology, University of Bonn, D-53105 Bonn, Germany

Nature, 2012, vol. 490, issue 7420, 412-416

Abstract: A genetically engineered mouse model is used to determine the mechanism of acquired resistance to adoptive therapy with cytotoxic T cells specific for a melanocytic differentiation antigen; tumour necrosis factor (TNF)-α is identified as a crucial factor that causes reversible dedifferentiation of mouse and human melanoma cells.

Date: 2012
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DOI: 10.1038/nature11538

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