Evidence map›Paper›PMID 26175407›Full record

ArticleCancer cell2015

Targeting the Inactive Conformation of JAK2 in Hematological Malignancies.

Olli Silvennoinen, Stevan R Hubbard

Open access · bronzeAbstract readComment
PubMed Publisher
In one paragraph

Article in Cancer cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

5 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Frontiers in cell and developmental biology · 2022
    Review
  3. Article
  4. Article
  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Olli SilvennoinenSchool of Medicine, University of Tampere, Biokatu 8, 33014 Tampere, Finland; Clinical Hematology, Department of Internal Medicine, Tampere University Hospital, Medisiinarinkatu 3, 33520 Tampere, Finland. Electronic address: olli.silvennoinen@uta.fi.
Stevan R HubbardKimmel Center for Biology and Medicine at the Skirball Institute and Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA.
New York University · USTampere University · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activating JAK2 mutants cause hematological malignancies. Current clinical type I JAK2 inhibitors effectively relieve symptoms but fail to resolve the disease. In this issue of Cancer Cell, two articles by Wu and colleagues and Meyer and colleagues characterize a type II JAK2 inhibitor that is effective in preclinical models of JAK2-dependent myeloproliferative neoplasms and B cell acute lymphoblastic leukemia.

Indexed as

AminopyridinesAnimalsAntineoplastic AgentsBenzimidazolesDexamethasoneDrug Resistance, NeoplasmHumansJanus Kinase 2Myeloproliferative DisordersPrecursor Cell Lymphoblastic Leukemia-LymphomaProtein Kinase InhibitorsAminopyridinesAntineoplastic AgentsBenzimidazolesDexamethasoneJanus Kinase 2Protein Kinase Inhibitors

Identifiers

PMID26175407
OpenAlexW1532557615

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.