Discover Community Create You

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

Article

Convergent mechanisms of somatic mutations in polycythemia vera.

Discovery medicine - 1 Jul 2011

Wang Kai, Swierczek Sabina, Hickman Kimberly, Hakonarson Hakon, Prchal Josef T

Abstract excerpt

Polycythemia vera (PV) is an acquired blood disorder, with variable increase of clonal myeloid cells (erythrocytes, granulocytes and platelets) and mostly normal polyclonal T lymphocytes. Most patients have a somatic V617F gain-of-function mutation in JAK2 associated with acquired uniparental disomy (UPD) on chromosome 9p. Yet, the JAK2 V617F mutation is not a PV-initiating event and the family clustering of PV...

Read the complete abstract on PubMed

Topics

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

Share to Amino Acid Substitution
Share to JAK2 gene
Share to Janus Kinase 2

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Loss of Heterozygosity

Share to Models, Biological

Share to Mutation

Share to Polycythemia Vera

Share to Polymorphism, Single Nucleotide

Source

Open in PubMed Open full text

Identifiers

PMID: 21794206
PMCID: PMC4347892

Genes

JAK2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Convergent mechanisms of somatic mutations in polycythemia vera.PMID 21794206Read ↗

Genetic Background of Polycythemia Vera.Semantic proximity Read ↗

JAK2 V617F allele burden in polycythemia vera: burden of proof.Semantic proximity Read ↗

Clonal hematopoiesis in familial polycythemia vera suggests the involvement of multiple mutational events in the early pathogenesis of the disease.Semantic proximity Read ↗

JAK2V617F homozygosity drives a phenotypic switch in myeloproliferative neoplasms, but is insufficient to sustain disease.Semantic proximity Read ↗

Prospective identification of high-risk polycythemia vera patients based on JAK2(V617F) allele burden.Semantic proximity Read ↗

Germ line variants predispose to both JAK2 V617F clonal hematopoiesis and myeloproliferative neoplasms.Semantic proximity Read ↗

A germline JAK2 SNP is associated with predisposition to the development of JAK2(V617F)-positive myeloproliferative neoplasms.Semantic proximity Read ↗

Whole-exome sequencing identifies novel candidate predisposition genes for familial polycythemia vera.Semantic proximity Read ↗

Features and Allele Frequency of JAK2 Exon 12-Mutated Polycythemia Vera in Comparison with JAK2V617F-Mutated Disease.Semantic proximity Read ↗

Hematopoietic clonal dominance, stem cell mutations, and evolutionary pattern of JAK2V617F allele burden in polycythemia vera.Semantic proximity Read ↗

The Mutational Landscape in Polycythemia Vera: Phenotype, Genotype, and Prognostic Correlates.Semantic proximity Read ↗

A molecular signature predicts hematologic evolution in polycythemia vera patients.Semantic proximity Read ↗

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