Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.

@article{Levine2005ActivatingMI,
  title={Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.},
  author={Ross L. Levine and Martha Wadleigh and Jan Cools and Benjamin L. Ebert and Gerlinde Wernig and Brian J P Huntly and Titus J Boggon and Iwona Wlodarska and Jennifer J Clark and Sandra Moore and Jennifer Adelsperger and Sumin Helen Koo and Jeffrey C. Lee and Stacey Gabriel and Thomas Mercher and Alan D'andrea and Stefan Fr{\"o}hling and Konstanze Doehner and Peter Marynen and Peter Vandenberghe and Ruben A. Mesa and Ayalew Tefferi and James D Griffin and Michael J. Eck and William R Sellers and Matthew Meyerson and Todd R. Golub and Stephanie J Lee and Dwight Gary Gilliland},
  journal={Cancer cell},
  year={2005},
  volume={7 4},
  pages={387-97}
}
Polycythemia vera (PV), essential thrombocythemia (ET), and myeloid metaplasia with myelofibrosis (MMM) are clonal disorders arising from hematopoietic progenitors. An internet-based protocol was used to collect clinical information and biological specimens from patients with these diseases. High-throughput DNA resequencing identified a recurrent somatic missense mutation JAK2V617F in granulocyte DNA samples of 121 of 164 PV patients, of which 41 had homozygous and 80 had heterozygous mutations… CONTINUE READING
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