Evidence map›Paper›PMID 24549002›Full record

ArticleClinical pharmacology and therapeutics2014

Integrating cell-based and clinical genome-wide studies to identify genetic variants contributing to treatment failure in neuroblastoma patients.

N Pinto, E R Gamazon, N Antao, J Myers, A L Stark, A Konkashbaev, H K Im, S J Diskin, W B London, S M Ludeman and 4 more

Abstract read
In one paragraph

Article in Clinical pharmacology and therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. International journal of molecular sciences · 2026
    Article
  2. Genomic Variants of Cytarabine Sensitivity Associated with Treatment-Related Mortality in Pediatric AML: A Report from the Children's Oncology Group.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Article
  3. Article
  4. Article
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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

14 authors.

N PintoSection of Pediatric Hematology/Oncology, Department of Pediatrics, The University of Chicago, Chicago, Illinois, USA.
E R GamazonSection of Genetic Medicine, Department of Medicine, The University of Chicago, Chicago, Illinois, USA.
N AntaoSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, Illinois, USA.
J MyersSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, Illinois, USA.
A L StarkSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, Illinois, USA.
A KonkashbaevSection of Genetic Medicine, Department of Medicine, The University of Chicago, Chicago, Illinois, USA.
H K ImDepartment of Health Studies, The University of Chicago, Chicago, Illinois, USA.
S J DiskinDivision of Oncology and Center for Childhood Cancer Research, The Children's Hospital of Philadelphia and Department of Pediatrics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA.
W B London1] Boston Children's Hospital/Dana Farber Harvard Cancer Center, Harvard University, Boston, Massachusetts, USA [2] Children's Oncology Group Statistics and Data Center, Arcadia, California, USA.
S M LudemanDepartment of Basic and Social Sciences, Albany College of Pharmacy and Health Sciences, Albany, New York, USA.
J M MarisDivision of Oncology and Center for Childhood Cancer Research, The Children's Hospital of Philadelphia and Department of Pediatrics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA.
N J CoxSection of Genetic Medicine, Department of Medicine, The University of Chicago, Chicago, Illinois, USA.
S L CohnSection of Pediatric Hematology/Oncology, Department of Pediatrics, The University of Chicago, Chicago, Illinois, USA.
M E DolanSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, Illinois, USA.

Funding

Whole GenomeU01GM061393 · NIGMS · UNIVERSITY OF CHICAGO · PI RATAIN, MARK J · 2000 to 2014
$39.0M
Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
Variation in Hormone and xenobiotic metabolizing enzyme genes and breast cancerP50CA125183 · NCI · UNIVERSITY OF CHICAGO · PI COX, NANCY · 2006 to 2010
$11.3M
The Genetic Basis of Neuroblastoma TumorigenesisR01CA124709 · NCI · CHILDREN'S HOSP OF PHILADELPHIA · PI MARIS, JOHN M · 2008 to 2017
$6.3M
PHARMACOLOGY OF CYCLOPHOSPHAMIDE AND OTHER ALYKLATORSR01CA016783 · NCI · JOHNS HOPKINS UNIVERSITY · PI LUDEMAN, SUSAN M · 1985 to 2009
$2.8M
Genetic determinants associated with pemetrexed response and toxicityR01CA136765 · NCI · UNIVERSITY OF CHICAGO · PI DOLAN, MARY EILEEN · 2009 to 2013
$1.6M
NCATS NIH HHS UL1 TR000430NCATS NIH HHS UL1TR000430NCI NIH HHS P50 CA125183NCI NIH HHS R01 CA 016783NCI NIH HHS R01 CA016783NCI NIH HHS R01 CA124709NCI NIH HHS R01 CA136765NIGMS NIH HHS U01 GM061393NIGMS NIH HHS U01GM61393
6 · The paper itself

Abstract

High-risk neuroblastoma is an aggressive malignancy, with high rates of treatment failure. We evaluated genetic variants associated with in vitro sensitivity to two derivatives of cyclophosphamide for association with clinical response in a separate replication cohort of neuroblastoma patients (n = 2,709). To determine sensitivity, lymphoblastoid cell lines (LCLs) were exposed to increasing concentrations of 4-hydroperoxycyclophosphamide (4HC; n = 422) and phosphoramide mustard (PM; n = 428). Genome-wide association studies were performed to identify single-nucleotide polymorphisms (SNPs) associated with sensitivity to 4HC and PM. SNPs consistently associated with LCL sensitivity were analyzed for associations with event-free survival (EFS) in patients. Two linked SNPs, rs9908694 and rs1453560, were found to be associated with (i) sensitivity to PM in LCLs across populations and (ii) EFS in all patients (P = 0.01) and within the high-risk subset (P = 0.05). Our study highlights the value of cell-based models to identify candidate variants that may predict response to treatment in patients with cancer.

Indexed as

Genome-Wide Association StudyAntineoplastic Agents, AlkylatingBrain NeoplasmsCell Line, TumorChildCohort StudiesCyclohexylaminesCyclophosphamideDisease-Free SurvivalDrug Resistance, NeoplasmGenetic Predisposition to DiseaseGenetic VariationHumansNeuroblastomaPhenotypePolymorphism, Single NucleotideAntineoplastic Agents, AlkylatingCyclohexylaminesCyclophosphamideperfosfamideRNA, Small Interfering

Identifiers

PMID24549002
PMCPMC4029857

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Registered trials

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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.