Evidence map›Paper›PMID 25434823›Full record

ArticleStem cell reports2015

Oxymetholone therapy of fanconi anemia suppresses osteopontin transcription and induces hematopoietic stem cell cycling.

Qing-Shuo Zhang, Eric Benedetti, Matthew Deater, Kathryn Schubert, Angela Major, Carl Pelz, Soren Impey, Laura Marquez-Loza, R Keaney Rathbun, Shigeaki Kato and 2 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 29 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

12 authors at 4 institutions in 2 countries.

Qing-Shuo ZhangOregon Stem Cell Center, Department of Pediatrics, Oregon Health & Science University, Portland, OR 97239, USA. Electronic address: zhangqi@ohsu.edu.
Eric BenedettiOregon Stem Cell Center, Department of Pediatrics, Oregon Health & Science University, Portland, OR 97239, USA.
Matthew DeaterOregon Stem Cell Center, Department of Pediatrics, Oregon Health & Science University, Portland, OR 97239, USA.
Kathryn SchubertOregon Stem Cell Center, Department of Pediatrics, Oregon Health & Science University, Portland, OR 97239, USA.
Angela MajorDepartment of Pathology, Texas Children's Hospital, Houston, TX 77030, USA.
Carl PelzOregon Stem Cell Center, Department of Pediatrics, Oregon Health & Science University, Portland, OR 97239, USA.
Soren ImpeyOregon Stem Cell Center, Department of Pediatrics, Oregon Health & Science University, Portland, OR 97239, USA.
Laura Marquez-LozaOregon Stem Cell Center, Department of Pediatrics, Oregon Health & Science University, Portland, OR 97239, USA.
R Keaney RathbunNW VA Cancer Research Center, VA Medical Center Portland, Portland, OR 97239, USA.
Shigeaki KatoInstitute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo 113-0032, Japan.
Grover C BagbyNW VA Cancer Research Center, VA Medical Center Portland, Portland, OR 97239, USA.
Markus GrompeOregon Stem Cell Center, Department of Pediatrics, Oregon Health & Science University, Portland, OR 97239, USA.
Oregon Health & Science University · USPortland VA Medical Center · USTexas Children's Hospital · USThe University of Tokyo · JP

Funding

Xenograft CoreP01HL048546 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI FLEMING, WILLIAM H · 1994 to 2020
$36.4M
NHLBI NIH HHS P01 HL048546
6 · The paper itself

Abstract

Androgens are widely used for treating Fanconi anemia (FA) and other human bone marrow failure syndromes, but their mode of action remains incompletely understood. Aged Fancd2(-/-) mice were used to assess the therapeutic efficacy of oxymetholone (OXM) and its mechanism of action. Eighteen-month-old Fancd2(-/-) mice recapitulated key human FA phenotypes, including reduced bone marrow cellularity, red cell macrocytosis, and peripheral pancytopenia. As in humans, chronic OXM treatment significantly improved these hematological parameters and stimulated the proliferation of hematopoietic stem and progenitor cells. RNA-Seq analysis implicated downregulation of osteopontin as an important potential mechanism for the drug's action. Consistent with the increased stem cell proliferation, competitive repopulation assays demonstrated that chronic OXM therapy eventually resulted in stem cell exhaustion. These results expand our knowledge of the regulation of hematopoietic stem cell proliferation and have direct clinical implications for the treatment of bone marrow failure.

Indexed as

AnimalsBlood Cell CountBone MarrowCell CycleCell ProliferationDisease Models, AnimalFanconi AnemiaFanconi Anemia Complementation Group D2 ProteinGene Expression RegulationHematopoiesisHematopoietic Stem CellsHumansMiceMice, KnockoutOsteopontinOxymetholoneFanconi Anemia Complementation Group D2 ProteinOsteopontinOxymetholone

Identifiers

PMID25434823
PMCPMC4297866
OpenAlexW2034553446

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.