Nature Communications (Feb 2018)

Actionable perturbations of damage responses by TCL1/ATM and epigenetic lesions form the basis of T-PLL

  • A. Schrader,
  • G. Crispatzu,
  • S. Oberbeck,
  • P. Mayer,
  • S. Pützer,
  • J. von Jan,
  • E. Vasyutina,
  • K. Warner,
  • N. Weit,
  • N. Pflug,
  • T. Braun,
  • E. I. Andersson,
  • B. Yadav,
  • A. Riabinska,
  • B. Maurer,
  • M. S. Ventura Ferreira,
  • F. Beier,
  • J. Altmüller,
  • M. Lanasa,
  • C. D. Herling,
  • T. Haferlach,
  • S. Stilgenbauer,
  • G. Hopfinger,
  • M. Peifer,
  • T. H. Brümmendorf,
  • P. Nürnberg,
  • K. S. J. Elenitoba-Johnson,
  • S. Zha,
  • M. Hallek,
  • R. Moriggl,
  • H. C. Reinhardt,
  • M.-H. Stern,
  • S. Mustjoki,
  • S. Newrzela,
  • P. Frommolt,
  • M. Herling

DOI
https://doi.org/10.1038/s41467-017-02688-6
Journal volume & issue
Vol. 9, no. 1
pp. 1 – 22

Abstract

Read online

T-cell prolymphocytic leukemia (T-PLL) is a rare malignancy with a poor prognosis. Here, the authors investigate the genomic landscape, gene expression profiles and functional mechanisms in 111 patients, highlighting TCL1 overexpression and ATM aberrations as core lesions which co-operate to impair DNA damage processing.