Evidence map›Paper›PMID 18922853›Full record

ArticleBlood2009

Primitive quiescent CD34+ cells in chronic myeloid leukemia are targeted by in vitro expanded natural killer cells, which are functionally enhanced by bortezomib.

Agnes S M Yong, Keyvan Keyvanfar, Nancy Hensel, Rhoda Eniafe, Bipin N Savani, Maria Berg, Andreas Lundqvist, Sharon Adams, Elaine M Sloand, John M Goldman and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 61 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 2 institutions in 1 country.

Agnes S M YongHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1202, USA. yonga@nhlbi.nih.gov
Keyvan Keyvanfar
Nancy Hensel
Rhoda Eniafe
Bipin N Savani
Maria Berg
Andreas Lundqvist
Sharon Adams
Elaine M Sloand
John M Goldman
Richard Childs
A John Barrett
National Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

Allogeneic Immunotherapy for cancer and nonmalignant hematological disordersZIAHL002345 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CHILDS, RICHARD · 2009 to 2025
$53.3M
GRAFT-VERSUS-LEUKEMIAZ01HL002342 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI BARRETT, AUSTIN JOHN · 1994 to 2008
$7.7M
Allogeneic Immunotherapy for cancer and nonmalignant hematological disordersZ01HL002345 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CHILDS, RICHARD · 2000 to 2008
$6.5M
Graft-versus-leukemiaZIAHL002342 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI BARRETT, AUSTIN JOHN · 2009 to 2010
$6.3M
Cyclosporine Inhalation Solution (CIS) treatment of Bronchiolitis ObliteransZIAHL006090 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CHILDS, RICHARD · 2010 to 2019
$3.9M
6 · The paper itself

Abstract

Primitive quiescent CD34(+) chronic myeloid leukemia (CML) cells are more biologically resistant to tyrosine kinase inhibitors than their cycling counterparts; however, graft-versus-leukemia (GVL) effects after allogeneic stem cell transplantation (SCT) probably eliminate even these quiescent cells in long-term surviving CML transplant recipients. We studied the progeny of CD34(+) cells from CML patients before SCT, which were cultured 4 days in serum-free media with hematopoietic growth factors. BCR-ABL expression was similar in both cycling and quiescent noncycling CD34(+) populations. Quiescent CD34(+) cells from CML patients were less susceptible than their cycling CD34(+) and CD34(-) counterparts to lysis by natural killer (NK) cells from their HLA-identical sibling donors. Compared with cycling populations, quiescent CD34(+) CML cells had higher surface expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptors DR4 and DR5. Bortezomib up-regulated TRAIL receptor expression on quiescent CD34(+) CML cells, and further enhanced their susceptibility to cytotoxicity by in vitro expanded donor NK cells. These results suggest that donor-derived NK cell-mediated GVL effects may be improved by sensitizing residual quiescent CML cells to NK-cell cytotoxicity after SCT. Such treatment, as an adjunct to donor lymphocyte infusions and pharmacologic therapy, may reduce the risk of relapse in CML patients who require treatment by SCT.

Indexed as

AdolescentAdultAntigens, CD34Boronic AcidsBortezomibCells, CulturedCell SeparationFemaleGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseGenotypeHumansKiller Cells, NaturalLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMiddle AgedAntigens, CD34Boronic AcidsBortezomibGEM protein, humanMonomeric GTP-Binding ProteinsPyrazinesReceptors, Death Domain

Identifiers

PMID18922853
PMCPMC2630272
OpenAlexW2092349279

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.