Evidence map›Paper›PMID 24146202›Full record

ReviewCurrent hematologic malignancy reports2013

Preclinical models for drug selection in myeloproliferative neoplasms.

Niccolò Bartalucci, Costanza Bogani, Alessandro M Vannucchi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hematologic malignancy reports, 2013. 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
–field-weighted citation impact, top 94% 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. Hi-Frontiers in medicine · 2020
    Review
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

3 authors at 1 institution in 1 country.

Niccolò BartalucciDepartment of Experimental and Clinical Medicine, University of Florence, Florence, Italy.
Costanza Bogani
Alessandro M Vannucchi
University of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The discovery that an abnormally activated JAK-STAT signaling pathway is central to the pathogenesis of myeloproliferative neoplasms has promoted the clinical development of small-molecule JAK2 inhibitors. These agents have shown remarkable efficacy in disease control, but do not induce molecular remission; on the other hand, interferon holds the promise to target the putative hematopoietic progenitor cell initiating the disease. The presence of additional molecular abnormalities indicates a high molecular complexity of myeloproliferative neoplasms, and the need for simultaneously targeting different targets. Several drugs are currently under study as single agents and in combination. This review briefly describes the several in vitro and in vivo models of myeloproliferative neoplasms that are being used as preclinical models for drug development.

Indexed as

AnimalsAntineoplastic AgentsDisease Models, AnimalDrug Evaluation, PreclinicalGATA1 Transcription FactorGene Knock-In TechniquesHematologic NeoplasmsHumansJanus Kinase 2MiceMice, TransgenicMolecular Targeted TherapyMyeloproliferative DisordersProtein Kinase InhibitorsAntineoplastic AgentsGATA1 Transcription FactorJanus Kinase 2Protein Kinase Inhibitors

Identifiers

PMID24146202
OpenAlexW1984237722

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.