The lymphoma-associated NPM-ALK oncogene elicits a p16INK4a/pRb-dependent tumor-suppressive pathway.

@article{Martinelli2011TheLN,
  title={The lymphoma-associated NPM-ALK oncogene elicits a p16INK4a/pRb-dependent tumor-suppressive pathway.},
  author={Paola Martinelli and Paola Bonetti and Cristina Sironi and Giancarlo Pruneri and Caterina Fumagalli and Paola Rafaniello Raviele and Sara Volorio and Stefano A Pileri and Roberto Chiarle and Fiona Kate Elizabeth McDuff and Betsabeh Khoramian Tusi and Suzanne D Turner and Giorgio Inghirami and Pier Giuseppe Pelicci and Emanuela Colombo},
  journal={Blood},
  year={2011},
  volume={117 24},
  pages={6617-26}
}
Oncogene-induced senescence (OIS) is a barrier for tumor development. Oncogene-dependent DNA damage and activation of the ARF/p53 pathway play a central role in OIS and, accordingly, ARF and p53 are frequently mutated in human cancer. A number of leukemia/lymphoma-initiating oncogenes, however, inhibit ARF/p53 and only infrequently select for ARF or p53 mutations, suggesting the involvement of other tumor-suppressive pathways. We report that NPM-ALK, the initiating oncogene of anaplastic large… CONTINUE READING

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NPM - ALK inhibits the p 53 tumor suppressor pathway in an MDM 2 and JNK - dependent man

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