Telomere dysfunction drives aberrant hematopoietic differentiation and myelodysplastic syndrome.

@article{Colla2015TelomereDD,
  title={Telomere dysfunction drives aberrant hematopoietic differentiation and myelodysplastic syndrome.},
  author={Simona Colla and Derrick Sek Tong Ong and Yamini Ogoti and Matteo Marchesini and Nipun A. Mistry and Karen Clise-Dwyer and Sonny A Ang and Paola Storti and Andrea Viale and Nicola Giuliani and Kathryn E. Ruisaard and Irene Ganan Gomez and Christopher Aaron Bristow and Marcos R. H. Estecio and David C. Weksberg and Yan Wing Ho and Baoli Hu and Giannicola Genovese and Piergiorgio Francesco Pettazzoni and Asha S Multani and Shan Jiang and Sujun Hua and Michael C. Ryan and Alessandro Carugo and L Nezi and Yue Wei and Hui Yang and Marianna D'Anca and Li Zhang and Sarah Gaddis and Ting Gong and James W. Horner and Timothy Paul Heffernan and Philip M. Jones and Laurence J. N. Cooper and Han Liang and Hagop M Kantarjian and Y. Alan Wang and Lynda Chin and Carlos E Bueso-Ramos and Guillermo Garcia-Manero and Ronald A. Depinho},
  journal={Cancer cell},
  year={2015},
  volume={27 5},
  pages={644-57}
}
Myelodysplastic syndrome (MDS) risk correlates with advancing age, therapy-induced DNA damage, and/or shorter telomeres, but whether telomere erosion directly induces MDS is unknown. Here, we provide the genetic evidence that telomere dysfunction-induced DNA damage drives classical MDS phenotypes and alters common myeloid progenitor (CMP) differentiation by repressing the expression of mRNA splicing/processing genes, including SRSF2. RNA-seq analyses of telomere dysfunctional CMP identified… CONTINUE READING
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