Evidence map›Paper›PMID 17252012›Full record

ArticleLeukemia2007

Molecular signature of CD34(+) hematopoietic stem and progenitor cells of patients with CML in chronic phase.

E Diaz-Blanco, I Bruns, F Neumann, J C Fischer, T Graef, M Rosskopf, B Brors, S Pechtel, S Bork, A Koch and 7 more

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Leukemia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.

  1. Chronic myeloid leukemia: an update of concepts and management recommendations of European LeukemiaNet.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2009
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25 more citing papers are in PubMed but not listed here.

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

17 authors at 3 institutions in 2 countries.

E Diaz-BlancoDepartment of Hematology, Oncology and Clinical Immunology, University of Duesseldorf, Duesseldorf, Germany.
I Bruns
F Neumann
J C Fischer
T Graef
M Rosskopf
B Brors
S Pechtel
S Bork
A Koch
A Baer
U-P Rohr
G Kobbe
A von Haeseler
N Gattermann
R Haas
R Kronenwett
Heinrich Heine University Düsseldorf · DEHeidelberg University · DEMax Perutz Labs · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we provide a molecular signature of highly enriched CD34+ cells from bone marrow of untreated patients with chronic myelogenous leukemia (CML) in chronic phase in comparison with normal CD34+ cells using microarrays covering 8746 genes. Expression data reflected several BCR-ABL-induced effects in primary CML progenitors, such as transcriptional activation of the classical mitogen-activated protein kinase pathway and the phosphoinositide-3 kinase/AKT pathway as well as downregulation of the proapoptotic gene IRF8. Moreover, novel transcriptional changes in comparison with normal CD34+ cells were identified. These include upregulation of genes involved in the transforming growth factorbeta pathway, fetal hemoglobin genes, leptin receptor, sorcin, tissue inhibitor of metalloproteinase 1, the neuroepithelial cell transforming gene 1 and downregulation of selenoprotein P. Additionally, genes associated with early hematopoietic stem cells (HSC) and leukemogenesis such as HoxA9 and MEIS1 were transcriptionally activated. Differential expression of differentiation-associated genes suggested an altered composition of the CD34+ cell population in CML. This was confirmed by subset analyses of chronic phase CML CD34+ cells showing an increase of the proportion of megakaryocyte-erythroid progenitors, whereas the proportion of HSC and granulocyte-macrophage progenitors was decreased in CML. In conclusion, our results give novel insights into the biology of CML and could provide the basis for identification of new therapeutic targets.

Indexed as

Gene Expression ProfilingGene Expression Regulation, LeukemicAntigens, CD34ApoptosisCell AdhesionCell DifferentiationCell DivisionDNA, ComplementaryDNA, NeoplasmFusion Proteins, bcr-ablHematopoietic Stem CellsHumansIntercellular Signaling Peptides and ProteinsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLeukemia, Myeloid, Chronic-PhaseNeoplasm ProteinsAntigens, CD34DNA, ComplementaryDNA, NeoplasmFusion Proteins, bcr-ablIntercellular Signaling Peptides and ProteinsNeoplasm ProteinsReceptors, Cell SurfaceReceptors, Growth FactorReceptors, LeptinRNA, MessengerRNA, Neoplasm

Identifiers

PMID17252012
OpenAlexW2564723484

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.