Evidence map›Paper›PMID 22500049›Full record

ArticleBlood2012

Advancing the STATus of MPN pathogenesis.

Neil P Shah, Kevin Shannon

Open access · bronzeAbstract readComment
PubMed Publisher
In one paragraph

Article in Blood, 2012. 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 39% 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, 2 citations in OpenAlex.

  1. Trial
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Neil P ShahUniversity of California, San Francisco, CA, USA.
Kevin Shannon
University of California, San Francisco · US

Funding

Translational Investigation of KRas & NF1 in Myeloid LeukemiaR37CA072614 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SHANNON, KEVIN M. · 2007 to 2016
$3.4M
NCI NIH HHS R37 CA072614
6 · The paper itself

Abstract

In this issue of Blood, Yan et al and Walz et al exploit mouse genetics to investigate the contribution of signal transducer and activator of transcription 5 (STAT5) to the abnormal in vivo growth of hematopoietic cells expressing JAK2(V617F) or BCR-ABL. Eliminating STAT5 expression had dramatic effects in both contexts, and this new work and other recent studies support the therapeutic potential of targeting pathways regulated by this important signaling molecule in patients with myeloproliferative neoplasms (MPNs).

Indexed as

AnimalsGenes, ablHumansJanus Kinase 2Myeloproliferative DisordersPolycythemia VeraSTAT5 Transcription FactorJak2 protein, mouseJanus Kinase 2Stat5a protein, mouseStat5b protein, mouseSTAT5 Transcription Factor

Identifiers

PMID22500049
OpenAlexW2088233068

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.