Evidence map›Paper›PMID 27430367›Full record

ArticleMolecular medicine reports2016

Effects of imatinib and nilotinib on the whole transcriptome of cultured murine osteoblasts.

Gyöngyi Kirschner, Bernadett Balla, Péter Horváth, Andrea Kövesdi, Gergely Lakatos, István Takács, Zsolt Nagy, Bálint Tóbiás, Kristóf Árvai, János Pál Kósa and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
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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

11 authors at 1 institution in 1 country.

Gyöngyi KirschnerFirst Department of Internal Medicine, Semmelweis University, 1083 Budapest, Hungary.
Bernadett BallaFirst Department of Internal Medicine, Semmelweis University, 1083 Budapest, Hungary.
Péter HorváthFirst Department of Internal Medicine, Semmelweis University, 1083 Budapest, Hungary.
Andrea KövesdiFirst Department of Internal Medicine, Semmelweis University, 1083 Budapest, Hungary.
Gergely LakatosSecond Department of Internal Medicine, Semmelweis University, 1083 Budapest, Hungary.
István TakácsFirst Department of Internal Medicine, Semmelweis University, 1083 Budapest, Hungary.
Zsolt NagyFirst Department of Internal Medicine, Semmelweis University, 1083 Budapest, Hungary.
Bálint TóbiásFirst Department of Internal Medicine, Semmelweis University, 1083 Budapest, Hungary.
Kristóf ÁrvaiFirst Department of Internal Medicine, Semmelweis University, 1083 Budapest, Hungary.
János Pál KósaFirst Department of Internal Medicine, Semmelweis University, 1083 Budapest, Hungary.
Péter LakatosFirst Department of Internal Medicine, Semmelweis University, 1083 Budapest, Hungary.
Semmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerous clinical observations have confirmed that breakpoint cluster region-abelson fusion oncoprotein tyrosine kinase inhibitors used in leukemia treatment alter bone physiology in a complex manner. The aim of the present study was to analyze the whole transcriptome of cultured murine osteoblasts and determine the changes following treatment with imatinib and nilotinib using Sequencing by Oligonucleotide Ligation and Detection next generation RNA sequencing. This study also aimed to identify candidate signaling pathways and network regulators by multivariate Ingenuity Pathway Analysis. Based on the right-tailed Fisher's exact test, significantly altered pathways including upstream regulators were defined for each drug. The correlation between these pathways and bone metabolism was also examined. The preliminary results suggest the two drugs have different mechanisms of action on osteoblasts, and imatinib was shown to have a greater effect on gene expression. Data also indicated the potential role of a number of genes and signaling cascades that may contribute to identifying novel targets for the treatment of metabolic bone diseases.

Indexed as

TranscriptomeAnimalsCell LineCells, CulturedCell SurvivalComputational BiologyGene Expression ProfilingGene Expression RegulationImatinib MesylateMiceOsteoblastsProtein Kinase InhibitorsPyrimidinesSignal TransductionImatinib MesylatenilotinibProtein Kinase InhibitorsPyrimidines

Identifiers

PMID27430367
PMCPMC4991674
OpenAlexW2472426767

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.