Fusion tyrosine kinases induce drug resistance by stimulation of homology-dependent recombination repair, prolongation of G(2)/M phase, and protection from apoptosis.

@article{Slupianek2002FusionTK,
  title={Fusion tyrosine kinases induce drug resistance by stimulation of homology-dependent recombination repair, prolongation of G(2)/M phase, and protection from apoptosis.},
  author={Artur Slupianek and Grazyna Anna Hoser and Ireneusz Majsterek and Agnieszka Bronisz and Maciej Malecki and Janusz Blasiak and Richard Fishel and Tomasz Sk{\'o}rski},
  journal={Molecular and cellular biology},
  year={2002},
  volume={22 12},
  pages={4189-201}
}
Fusion tyrosine kinases (FTKs) such as BCR/ABL, TEL/ABL, TEL/JAK2, TEL/PDGF beta R, TEL/TRKC(L), and NPM/ALK arise from reciprocal chromosomal translocations and cause acute and chronic leukemias and non-Hodgkin's lymphoma. FTK-transformed cells displayed drug resistance against the cytostatic drugs cisplatin and mitomycin C. These cells were not protected from drug-mediated DNA damage, implicating activation of the mechanisms preventing DNA damage-induced apoptosis. Various FTKs, except TEL… CONTINUE READING

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