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

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

Content Provider	Semantic Scholar
Author	Levine, Ross L. Wadleigh, Martha Cools, Jan Ebert, Benjamin L. Wernig, Gerlinde Huntly, Brian J. P. Boggon, Titus J. Włodarska, Iwona Clark, Jennifer J. Moore, Sandra A. Adelsperger, Jennifer Lee, Jeffrey C. Gabriel, Stacey Mercher, Thomas Andrea, Alan D. D’ Fröhling, Stefan Doehner, Konstanze Marynen, Peter Vandenberghe, Peter Mesa, Ruben Tefferi, Ayalew Griffin, James Douglas Eck, Michael J. Sellers, William R. Meyerson, Matthew Golub, Todd R. Lee, Stephanie J. Gilliland, Dwight Gary
Copyright Year	2005
Abstract	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. Molecular and cytogenetic analyses demonstrated that homozygous mutations were due to duplication of the mutant allele. JAK2V617F was also identified in granulocyte DNA samples from 37 of 115 ET and 16 of 46 MMM patients, but was not observed in 269 normal individuals. In vitro analysis demonstrated that JAK2V617F is a constitutively active tyrosine kinase.
File Format	PDF HTM / HTML
DOI	10.1016/j.ccr.2005.03.023
PubMed reference number	15837627
Journal	Medline
Volume Number	7
Issue Number	4
Alternate Webpage(s)	https://core.ac.uk/download/pdf/82665478.pdf
Journal	Cancer cell
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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