Evidence map›Paper›PMID 16007127›Full record

ArticleOncogene2005

JAK the trigger.

François-Xavier Mahon

Open access · bronzeAbstract readComment
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

François-Xavier MahonLaboratoire d'hématopoïèse leucémique et cible thérapeutique, Université Victor Segalen Bordeaux 2, INSERM E0217, 33076 Bordeaux Cedex, France. francois-xavier.mahon@umr5540.u-bordeaux2.fr
Université de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A somatic mutation that leads to activation of the JAK2 tyrosine kinase has recently been identified as a recurrent genetic abnormality in several different myeloproliferative disorders. A translocation generating the constitutively activated fusion protein PCM1-JAK2 has also been recently found in atypical chronic myelogenous leukemia and acute leukemia. This recent spate of independent studies (one of which is published in this issue of Oncogene) establish abnormal JAK2 activation as the underlying defect in a significant number of cases of myeloproliferative disease, and JAK2 as an important new therapeutic target.

Indexed as

Amino Acid SubstitutionAutoantigensCell Cycle ProteinsChromosomes, Human, Pair 8Chromosomes, Human, Pair 9Enzyme ActivationHumansJanus Kinase 2LeukemiaLeukemia, Myelogenous, Chronic, BCR-ABL PositiveOncogene Proteins, FusionPhenylalanineProtein Structure, TertiaryProtein-Tyrosine KinasesProto-Oncogene ProteinsTranslocation, GeneticAutoantigensCell Cycle ProteinsJAK2 protein, humanJanus Kinase 2Oncogene Proteins, FusionPCM1 protein, humanPhenylalanineProtein-Tyrosine KinasesProto-Oncogene Proteins

Identifiers

PMID16007127
OpenAlexW2005640051

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.