Evidence map›Paper›PMID 19647224›Full record

ArticleCancer cell2009

Persistence of leukemia-initiating cells in a conditional knockin model of an imatinib-responsive myeloproliferative disorder.

Katherine I Oravecz-Wilson, Steven T Philips, Omer H Yilmaz, Heather M Ames, Lina Li, Brendan D Crawford, Alice M Gauvin, Peter C Lucas, Kajal Sitwala, James R Downing and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 70 citations in OpenAlex.

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  16. Current Progresses of Single Cell DNA Sequencing in Breast Cancer Research.International journal of biological sciences · 2017
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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 2 institutions in 1 country.

Katherine I Oravecz-WilsonDepartment of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Steven T Philips
Omer H Yilmaz
Heather M Ames
Lina Li
Brendan D Crawford
Alice M Gauvin
Peter C Lucas
Kajal Sitwala
James R Downing
Sean J Morrison
Theodora S Ross
University of Michigan–Ann Arbor · USSt. Jude Children's Research Hospital · US

Funding

Training Program in Tumor MicroenvironmentT32CA009676 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Maria G Castro, Analisa Virginia DiFeo · 1992 to 2026
$7.3M
Huntington Interacting Protein-1(HIP1) and the Promotion of NeoplasiaR01CA098730 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI ROSS, THEODORA S · 2003 to 2012
$2.6M
MECHANISM OF TRANSFORMATION BY HIP1/PDGFBRR01CA082363 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ROSS, THEODORA S · 2000 to 2004
$1.3M
Howard Hughes Medical InstituteNCI NIH HHS CA009676NCI NIH HHS R01 CA082363NCI NIH HHS R01 CA098730NCI NIH HHS R01 CA098730-01NCI NIH HHS R01 CA82363-03NCI NIH HHS T32 CA009676
6 · The paper itself

Abstract

Despite remarkable responses to the tyrosine kinase inhibitor imatinib, CML patients are rarely cured by this therapy perhaps due to imatinib refractoriness of leukemia-initiating cells (LICs). Evidence for this is limited because of poor engraftment of human CML-LICs in NOD-SCID mice and nonphysiologic expression of oncogenes in retroviral transduction mouse models. To address these challenges, we generated mice bearing conditional knockin alleles of two human oncogenes: HIP1/PDGFbetaR (H/P) and AML1-ETO (A/E). Unlike retroviral transduction, physiologic expression of H/P or A/E individually failed to induce disease, but coexpression of both H/P and A/E led to rapid onset of a fully penetrant, myeloproliferative disorder, indicating cooperativity between these two alleles. Although imatinib dramatically decreased disease burden, LICs persisted, demonstrating imatinib refractoriness of LICs.

Indexed as

AnimalsAntineoplastic AgentsBenzamidesCore Binding Factor Alpha 2 SubunitDisease Models, AnimalDNA-Binding ProteinsDrug Resistance, NeoplasmGene Knock-In TechniquesGenotypeHematopoietic Stem CellsHumansImatinib MesylateLeukemia, Myelomonocytic, ChronicMiceMice, TransgenicMyeloproliferative DisordersAML1-ETO fusion protein, humanAntineoplastic AgentsBenzamidesCore Binding Factor Alpha 2 SubunitDNA-Binding ProteinsHIP1 protein, humanImatinib MesylateOncogene Proteins, FusionPiperazinesPyrimidinesRUNX1 Translocation Partner 1 Protein

Identifiers

PMID19647224
PMCPMC2763369
OpenAlexW2165808846

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.