Evidence map›Paper›PMID 23642027›Full record

ArticleMolecular cancer2013

Gene expression profiling of chronic myeloid leukemia with variant t(9;22) reveals a different signature from cases with classic translocation.

Francesco Albano, Antonella Zagaria, Luisa Anelli, Nicoletta Coccaro, Luciana Impera, Crescenzio Francesco Minervini, Angela Minervini, Antonella Russo Rossi, Giuseppina Tota, Paola Casieri and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

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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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  3. Molecular Pathogenesis ofFrontiers in oncology · 2021
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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.

Francesco AlbanoDepartment of Emergency and Organ Transplantation-Hematology Section, University of Bari, Bari, Italy. francesco.albano@uniba.it
Antonella Zagaria
Luisa Anelli
Nicoletta Coccaro
Luciana Impera
Crescenzio Francesco Minervini
Angela Minervini
Antonella Russo Rossi
Giuseppina Tota
Paola Casieri
Giorgina Specchia
University of Bari Aldo Moro · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe t(9;22)(q34;q11) generating the BCR/ABL1 fusion gene represents the cytogenetic hallmark of chronic myeloid leukemia (CML). About 5-10% of CML cases show variant translocations with the involvement of other chromosomes in addition to chromosomes 9 and 22. The molecular bases of biological differences between CML patients with classic and variant t(9;22) have never been clarified.

findingsIn this study, we performed gene expression microarray analysis to compare CML patients bearing variant rearrangements and those with classic t(9;22)(q34;q11). We identified 59 differentially expressed genes significantly associated with the two analyzed groups. The role of specific candidate genes such as TRIB1 (tribbles homolog 1), PTK2B (protein tyrosine kinase 2 beta), and C5AR1 (complement component 5a receptor 1) is discussed.

conclusionsOur results reveal that in CML cases with variant t(9;22) there is an enhancement of the MAPK pathway deregulation and show that kinases are a common target of molecular alterations in hematological disorders.

Indexed as

Gene Expression ProfilingGene Expression Regulation, LeukemicTranslocation, GeneticChromosomes, Human, Pair 22Chromosomes, Human, Pair 9Cluster AnalysisGene Regulatory NetworksHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMitogen-Activated Protein KinasesPhosphotransferasesProto-Oncogene Proteins p21(ras)Signal TransductionMitogen-Activated Protein KinasesPhosphotransferasesProto-Oncogene Proteins p21(ras)

Identifiers

PMID23642027
PMCPMC3658885
OpenAlexW2106225476

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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.