Evidence map›Paper›PMID 19322209›Full record

ArticleLeukemia2009

PML-RARalpha initiates leukemia by conferring properties of self-renewal to committed promyelocytic progenitors.

S Wojiski, F C Guibal, T Kindler, B H Lee, J L Jesneck, A Fabian, D G Tenen, D G Gilliland

Open access · greenAbstract read
In one paragraph

Article in Leukemia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

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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

8 authors at 5 institutions in 1 country.

S WojiskiDivision of Hematology, Brigham and Women's Hospital, Boston, MA 02115, USA.
F C Guibal
T Kindler
B H Lee
J L Jesneck
A Fabian
D G Tenen
D G Gilliland
Harvard University · USHoward Hughes Medical Institute · USBrigham and Women's Hospital · USBroad Institute · USHarvard Stem Cell Institute · US

Funding

TYROSINE KINASE ONCOGENESIS IN MYELOID LEUKEMIAP01CA066996 · NCI · DANA-FARBER CANCER INSTITUTE · PI SCOTT A ARMSTRONG · 1996 to 2026
$52.5M
SIGNAL TRANSDUCTION PATHWAYS IN STABLE PHASE CHRONIC MYELOID LEUKEMIA CELLSP01DK050654 · NIDDK · DANA-FARBER CANCER INSTITUTE · PI D'ANDREA, ALAN DAVID · 1996 to 2006
$10.3M
Howard Hughes Medical InstituteNCI NIH HHS CA66996NCI NIH HHS P01 CA066996NIDDK NIH HHS DK50654NIDDK NIH HHS P01 DK050654
6 · The paper itself

Abstract

Acute promyelocytic leukemia (APL) is characterized by hyperproliferation of promyelocytes, progenitors that are committed to terminal differentiation into granulocytes, making it an ideal disease in which to study the transforming potential of less primitive cell types. We utilized a murine model of APL in which the PML-RARalpha oncogene is expressed from the endogenous cathepsin G promoter to test the hypothesis that leukemia stem cell (LSC) activity resides within the differentiated promyelocyte compartment. We prospectively purified promyelocytes from transgenic mice at various stages of disease and observed that PML-RARalpha-expressing promyelocytes from young preleukemic mice had acquired properties of self-renewal both in vitro and in vivo. Progression to acute leukemia was associated with an expansion of the promyelocyte compartment at the expense of other stem, progenitor and terminally differentiated populations. Leukemic promyelocytes exhibited properties of self-renewal, and were capable of engendering leukemia in secondary recipient mice. These data indicate that PML-RARalpha alone can confer properties of self-renewal to committed hematopoietic progenitors before the onset of disease. These findings are consistent with the hypothesis that cancer stem cells may arise from committed progenitors that lack stem cell properties, provided that the initiating mutation in cancer progression activates programs that confer properties of self-renewal.

Indexed as

AnimalsAntineoplastic AgentsBone Marrow TransplantationCathepsin GCathepsinsCell DivisionGranulocyte Precursor CellsGranulocytesHematopoietic Stem CellsHumansLeukemia, Promyelocytic, AcuteMiceMice, Inbred C57BLNeoplastic Stem CellsOncogene Proteins, FusionPreleukemiaAntineoplastic AgentsCathepsin GCathepsinsCTSG protein, humanCtsg protein, mouseOncogene Proteins, Fusionpromyelocytic leukemia-retinoic acid receptor alpha fusion oncoproteinRecombinant Fusion ProteinsSerine EndopeptidasesTretinoin

Identifiers

PMID19322209
PMCPMC2914549
OpenAlexW1998572012

What OpenQuestion holds

Textmetadata
LicenceTDM
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.