Evidence map›Paper›PMID 26275051›Full record

ArticlePloS one2015

Microarray and Proteomic Analyses of Myeloproliferative Neoplasms with a Highlight on the mTOR Signaling Pathway.

Vladan P Čokić, Pascal Mossuz, Jing Han, Nuria Socoro, Bojana B Beleslin-Čokić, Olivera Mitrović, Tijana Subotički, Miloš Diklić, Danijela Leković, Mirjana Gotić and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  14. Loss ofMolecular and cellular biology · 2022
    Article
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  18. PDE4 subtypes in cancer.Oncogene · 2020
    Review
  19. Article
  20. CDK6 coordinatesBlood · 2019
    Article
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

13 authors at 7 institutions in 4 countries.

Vladan P ČokićInstitute for Medical Research, University of Belgrade, Belgrade, Serbia.
Pascal MossuzDépartement d'Hématologie, Institut de Biologie et Pathologie, CHU Grenoble, Grenoble, France.
Jing HanTumor vaccines and Biotechnology Branch, Division of Cellular and Gene Therapies, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD, United States of America.
Nuria SocoroLaboratoire TIMC IMAG, Faculté de Médecine de Grenoble, La Tronche Cedex, Grenoble, France.
Bojana B Beleslin-ČokićClinic of Endocrinology, Diabetes and Diseases of Metabolism, Clinical Center of Serbia, Belgrade, Serbia.
Olivera MitrovićInstitute for Medical Research, University of Belgrade, Belgrade, Serbia.
Tijana SubotičkiInstitute for Medical Research, University of Belgrade, Belgrade, Serbia.
Miloš DiklićInstitute for Medical Research, University of Belgrade, Belgrade, Serbia.
Danijela LekovićClinic of Hematology, Clinical Center of Serbia, Belgrade, Serbia.
Mirjana GotićClinic of Hematology, Clinical Center of Serbia, Belgrade, Serbia; Medical Faculty, University of Belgrade, Belgrade, Serbia.
Raj K PuriTumor vaccines and Biotechnology Branch, Division of Cellular and Gene Therapies, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD, United States of America.
Constance Tom NoguchiMolecular Medicine Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States of America.
Alan N SchechterMolecular Medicine Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States of America.
University of Belgrade · RSCentar za Promociju Nauke · RSCenter for Biologics Evaluation and Research · USCentre Hospitalier Universitaire de Grenoble · FRNational Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · USTranslational Innovation in Medicine and Complexity · FR

Funding

Globin Gene Expression And Treatment Of Sickle Cell AnemiaZIADK025021 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI NOGUCHI, CONSTANCE · 2009 to 2025
$6.3M
Pharmacological Control Of Human Hemoglobin Gene ExpressionZIADK025016 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI SCHECHTER, ALAN · 2009 to 2025
$2.5M
Intramural NIH HHS
6 · The paper itself

Abstract

The gene and protein expression profiles in myeloproliferative neoplasms (MPNs) may reveal gene and protein markers of a potential clinical relevance in diagnosis, treatment and prediction of response to therapy. Using cDNA microarray analysis of 25,100 unique genes, we studied the gene expression profile of CD34+ cells and granulocytes obtained from peripheral blood of subjects with essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF). The microarray analyses of the CD34+ cells and granulocytes were performed from 20 de novo MPN subjects: JAK2 positive ET, PV, PMF subjects, and JAK2 negative ET/PMF subjects. The granulocytes for proteomic studies were pooled in 4 groups: PV with JAK2 mutant allele burden above 80%, ET with JAK2 mutation, PMF with JAK2 mutation and ET/PMF with no JAK2 mutation. The number of differentially regulated genes was about two fold larger in CD34+ cells compared to granulocytes. Thirty-six genes (including RUNX1, TNFRSF19) were persistently highly expressed, while 42 genes (including FOXD4, PDE4A) were underexpressed both in CD34+ cells and granulocytes. Using proteomic studies, significant up-regulation was observed for MAPK and PI3K/AKT signaling regulators that control myeloid cell apoptosis and proliferation: RAC2, MNDA, S100A8/9, CORO1A, and GNAI2. When the status of the mTOR signaling pathway related genes was analyzed, PI3K/AKT regulators were preferentially up-regulated in CD34+ cells of MPNs, with down-regulated major components of the protein complex EIF4F. Molecular profiling of CD34+ cells and granulocytes of MPN determined gene expression patterns beyond their recognized function in disease pathogenesis that included dominant up-regulation of PI3K/AKT signaling.

Indexed as

Gene Expression Regulation, NeoplasticSignal TransductionFemaleHematologic NeoplasmsHumansMaleMyeloid CellsMyeloproliferative DisordersNeoplasm ProteinsOligonucleotide Array Sequence AnalysisProteomicsTOR Serine-Threonine KinasesMTOR protein, humanNeoplasm ProteinsTOR Serine-Threonine Kinases

Identifiers

PMID26275051
PMCPMC4537205
OpenAlexW1419336099

What OpenQuestion holds

Textmetadata
LicenceCC0
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.