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

doi:10.1016/j.ccr.2005.03.023

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

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

Cancer cell - 1 Apr 2005

Levine Ross L, Wadleigh Martha, Cools Jan, Ebert Benjamin L, Wernig Gerlinde, Huntly Brian J P, Boggon Titus J, Wlodarska Iwona, Clark Jennifer J, Moore Sandra, Adelsperger Jennifer, Koo Sumin, Lee Jeffrey C, Gabriel Stacey, Mercher Thomas, D'Andrea Alan, Fröhling Stefan, Döhner Konstanze, Marynen Peter, Vandenberghe Peter, Mesa Ruben A, Tefferi Ayalew, Griffin James D, Eck Michael J, Sellers William R, Meyerson Matthew, Golub Todd R, Lee Stephanie J, Gilliland D Gary

Abstract excerpt

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...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Granulocytes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Janus Kinase 2

Share to Mitosis

Share to Mouth Mucosa

Share to Polycythemia Vera

Share to Primary Myelofibrosis

Share to Protein-Tyrosine Kinases

Share to Thrombocythemia, Essential

Source

Open in PubMed

Identifiers

PMID: 15837627
DOI: 10.1016/j.ccr.2005.03.023

Genes

JAK2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.PMID 15837627Read ↗

Advances in Molecular Understanding of Polycythemia Vera, Essential Thrombocythemia, and Primary Myelofibrosis: Towards Precision MedicineSemantic proximity Read ↗

The diagnosis and management of polycythemia vera, essential thrombocythemia, and primary myelofibrosis in the JAK2 V617F era.Semantic proximity Read ↗

Classification, Diagnosis and Management of Myeloproliferative Disorders in the JAK2V617F EraSemantic proximity Read ↗

Molecular Characterization of Polycythemia VeraSemantic proximity Read ↗

JAK2 and MPL mutations in myeloproliferative neoplasms: discovery and science.Semantic proximity Read ↗

Narrative review: Thrombocytosis, polycythemia vera, and JAK2 mutations: The phenotypic mimicry of chronic myeloproliferation.Semantic proximity Read ↗

A role for JAK2 mutations in myeloproliferative diseases.Semantic proximity Read ↗

Polycythemia vera.Semantic proximity Read ↗

JAK2 ex13InDel drives oncogenic transformation and is associated with chronic eosinophilic leukemia and polycythemia veraSemantic proximity Read ↗

Genetic basis of MPN: Beyond JAK2-V617F.Semantic proximity Read ↗

Molecular and genetic bases of myeloproliferative disorders: questions and perspectives.Semantic proximity Read ↗

Novel JAK2 Exon 14 Mutations L611S or N622Y in cis with JAK2V617F Are Associated with Distinct Clinical Phenotype of Polycythemia Vera and Concurrent Eosinophilia.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.