Evidence map›Paper›PMID 24562423›Full record

ArticleNature methods2014

Identification of small molecules that support human leukemia stem cell activity ex vivo.

Caroline Pabst, Jana Krosl, Iman Fares, Geneviève Boucher, Réjean Ruel, Anne Marinier, Sébastien Lemieux, Josée Hébert, Guy Sauvageau

Abstract read
PubMed Publisher
In one paragraph

Article in Nature methods, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
–field-weighted citation impact
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

69 citing papers in PubMed.

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9 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

9 authors.

Caroline PabstInstitute for Research in Immunology and Cancer, University of Montreal, Montreal, Quebec, Canada.
Jana KroslInstitute for Research in Immunology and Cancer, University of Montreal, Montreal, Quebec, Canada.
Iman FaresInstitute for Research in Immunology and Cancer, University of Montreal, Montreal, Quebec, Canada.
Geneviève BoucherInstitute for Research in Immunology and Cancer, University of Montreal, Montreal, Quebec, Canada.
Réjean RuelInstitute for Research in Immunology and Cancer, University of Montreal, Montreal, Quebec, Canada.
Anne Marinier1] Institute for Research in Immunology and Cancer, University of Montreal, Montreal, Quebec, Canada. [2] Chemistry Department, University of Montreal, Montreal, Quebec, Canada.
Sébastien Lemieux1] Institute for Research in Immunology and Cancer, University of Montreal, Montreal, Quebec, Canada. [2] Department of Computer Science and Operations Research, University of Montreal, Montreal, Quebec, Canada.
Josée Hébert1] Institute for Research in Immunology and Cancer, University of Montreal, Montreal, Quebec, Canada. [2] Leukemia Cell Bank of Quebec, Maisonneuve-Rosemont Hospital, Montreal, Quebec, Canada. [3] Division of Hematology-Oncology, Maisonneuve-Rosemont Hospital, Montreal, Quebec, Canada. [4] Department of Medicine, University of Montreal, Montreal, Quebec, Canada.
Guy Sauvageau1] Institute for Research in Immunology and Cancer, University of Montreal, Montreal, Quebec, Canada. [2] Leukemia Cell Bank of Quebec, Maisonneuve-Rosemont Hospital, Montreal, Quebec, Canada. [3] Division of Hematology-Oncology, Maisonneuve-Rosemont Hospital, Montreal, Quebec, Canada. [4] Department of Medicine, University of Montreal, Montreal, Quebec, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leukemic stem cells (LSCs) are considered a major cause of relapse in acute myeloid leukemia (AML). Defining pathways that control LSC self-renewal is crucial for a better understanding of underlying mechanisms and for the development of targeted therapies. However, currently available culture conditions do not prevent spontaneous differentiation of LSCs, which greatly limits the feasibility of cell-based assays. To overcome these constraints we conducted a high-throughput chemical screen and identified small molecules that inhibit differentiation and support LSC activity in vitro. Similar to reports with cord blood stem cells, several of these compounds suppressed the aryl-hydrocarbon receptor (AhR) pathway, which we show to be inactive in vivo and rapidly activated ex vivo in AML cells. We also identified a compound, UM729, that collaborates with AhR suppressors in preventing AML cell differentiation. Together, these findings provide newly defined culture conditions for improved ex vivo culture of primary human AML cells.

Indexed as

AdenineCell Culture TechniquesCulture Media, Serum-FreeDrug Screening Assays, AntitumorHumansIndolesLeukemiaLeukemia, Myeloid, AcuteMolecular StructureNeoplastic Stem CellsPyrimidinesAdenineCulture Media, Serum-FreeIndolesPyrimidinesUM729 compound

Identifiers

PMID24562423

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.