Evidence map›Paper›PMID 15863514›Full record

ArticleThe Journal of biological chemistry2005

Identification of an acquired JAK2 mutation in polycythemia vera.

Runxiang Zhao, Shu Xing, Zhe Li, Xueqi Fu, Qingshan Li, Sanford B Krantz, Zhizhuang Joe Zhao

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 236 papers.

0numbers the graph read from it
0cells of the map it votes in
236citing papers in PubMed
34.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

236 citing papers in PubMed, 615 citations in OpenAlex.

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  6. Lenalidomide plus prednisone results in durable clinical, histopathologic, and molecular responses in patients with myelofibrosis.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2009
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  10. A Scalable Design for Proximity-Inducing Molecules.bioRxiv : the preprint server for biology · 2026
    Article
  11. Macrophages in Hematopoiesis and Related Blood Diseases.Genomics, proteomics & bioinformatics · 2025
    Review
  12. Review
  13. Review
  14. Review
  15. Article
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  17. Polycythemia Vera: Thinking Beyond the Hematocrit.Journal of the advanced practitioner in oncology · 2023
    Review
  18. Article
  19. Review
  20. Article

176 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Runxiang ZhaoHematology/Oncology Division, Department of Medicine, Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee 37232, USA.
Shu Xing
Zhe Li
Xueqi Fu
Qingshan Li
Sanford B Krantz
Zhizhuang Joe Zhao
Jilin University · CNVanderbilt University · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Tyrosine Phosphatase in Signal TransductionR01HL076309 · NHLBI · VANDERBILT UNIVERSITY · PI ZHAO, ZHIZHUANG JOE · 2004 to 2007
$1.3M
ERYTHROPOIETIN &REGULATION OF ERYTHROPOIESISR01DK015555 · NIDDK · VANDERBILT UNIVERSITY · PI KRANTZ, SANFORD B · 1986 to 2003
$864k
NCI NIH HHS P30 CA068485NHLBI NIH HHS HL076309NHLBI NIH HHS R01 HL076309NHLBI NIH HHS R01 HL076309-01NIDDK NIH HHS DK-15555
6 · The paper itself

Abstract

Polycythemia vera (PV) is a human clonal hematological disorder. The molecular etiology of the disease has not been identified. PV hematopoietic progenitor cells exhibit hypersensitivity to growth factors and cytokines, suggesting possible abnormalities in protein-tyrosine kinases and phosphatases. By sequencing the entire coding regions of cDNAs of candidate enzymes, we identified a G:C--> T:A point mutation of the JAK2 tyrosine kinase in 20 of 24 PV blood samples but none in 12 normal samples. The mutation has varying degrees of heterozygosity and is apparently acquired. It changes conserved Val(617) to Phe in the pseudokinase domain of JAK2 that is known to have an inhibitory role. The mutant JAK2 has enhanced kinase activity, and when overexpressed together with the erythropoietin receptor in cells, it caused hyperactivation of erythropoietin-induced cell signaling. This gain-of-function mutation of JAK may explain the hypersensitivity of PV progenitor cells to growth factors and cytokines. Our study thus defines a molecular defect of PV.

Indexed as

MutationAmino Acid SequenceAnimalsBase SequenceCytokinesDNA, ComplementaryDNA Mutational AnalysisErythropoietinHeLa CellsHeterozygoteHumansImmunoblottingJanus Kinase 2Molecular Sequence DataPhenylalaninePoint MutationCytokinesDNA, ComplementaryErythropoietinJAK2 protein, humanJanus Kinase 2PhenylalanineProtein-Tyrosine KinasesProto-Oncogene ProteinsReceptors, ErythropoietinTyrosineValine

Identifiers

PMID15863514
PMCPMC1201515
OpenAlexW2105949419

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.