Evidence map›Paper›PMID 18552208›Full record

ArticleBlood2008

Quantitative trait loci associated with susceptibility to therapy-related acute murine promyelocytic leukemia in hCG-PML/RARA transgenic mice.

Ryan K Funk, Taylor J Maxwell, Masayo Izumi, Deepa Edwin, Friederike Kreisel, Timothy J Ley, James M Cheverud, Timothy A Graubert

Open access · greenAbstract read
In one paragraph

Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Mouse models of myelodysplastic syndromes.Hematology/oncology clinics of North America · 2010
    Review
  7. Therapy-related myelodysplastic syndrome: models and genetics.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2010
    Review
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 2 institutions in 1 country.

Ryan K FunkDepartment of Internal Medicine, Division of Oncology, Stem Cell Biology Section, Washington University School of Medicine, St Louis, MO 63110, USA.
Taylor J Maxwell
Masayo Izumi
Deepa Edwin
Friederike Kreisel
Timothy J Ley
James M Cheverud
Timothy A Graubert
Washington University in St. Louis · USThe University of Texas Health Science Center at Houston · US

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN · 2001 to 2026
$128.0M
Specimen Acquistition and Expression ProfilingP01CA101937 · NCI · WASHINGTON UNIVERSITY · PI LEY, TIMOTHY J. · 2003 to 2023
$58.8M
Trans-NIDDK Short-Term Training for Medical StudentsT35DK074375 · NIDDK · WASHINGTON UNIVERSITY · PI BARANSKI, THOMAS JOHN · 2006 to 2015
$891k
NCI NIH HHS P01 CA101937NCI NIH HHS P30 CA091842NCI NIH HHS P30 CA91842NIDDK NIH HHS T35 DK074375
6 · The paper itself

Abstract

Therapy-related acute myelogenous leukemia (t-AML) is an important late adverse effect of alkylator chemotherapy. Susceptibility to t-AML has a genetic component, yet specific genetic variants that influence susceptibility are poorly understood. We analyzed an F(2) intercross (n = 282 mice) between mouse strains resistant or susceptible to t-AML induced by the alkylator ethyl-N-nitrosourea (ENU) to identify genes that regulate t-AML susceptibility. Each mouse carried the hCG-PML/RARA transgene, a well-characterized initiator of myeloid leukemia. In the absence of ENU treatment, transgenic F(2) mice developed leukemia with higher incidence (79.4% vs 12.5%) and at earlier time points (108 days vs 234 days) than mice in the resistant background. ENU treatment of F(2) mice further increased incidence (90.4%) and shortened median survival (171 vs 254 days). We genotyped F(2) mice at 384 informative single nucleotide polymorphisms across the genome and performed quantitative trait locus (QTL) analysis. Thirteen QTLs significantly associated with leukemia-free survival, spleen weight, or white blood cell count were identified on 8 chromosomes. These results suggest that susceptibility to ENU-induced leukemia in mice is a complex trait governed by genes at multiple loci. Improved understanding of genetic risk factors should lead to tailored treatment regimens that reduce risk for patients predisposed to t-AML.

Indexed as

Oncogene Proteins, FusionQuantitative Trait LociAlkylating AgentsAnimalsDisease-Free SurvivalDisease Models, AnimalGenetic Predisposition to DiseaseGenomeHumansIncidenceLeukemia, MyeloidLeukemia, Promyelocytic, AcuteLeukocyte CountMiceMice, TransgenicNeoplasms, Second PrimaryAlkylating AgentsOncogene Proteins, Fusionpromyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein

Identifiers

PMID18552208
PMCPMC2515115
OpenAlexW1991814251

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.