Evidence map›Paper›PMID 18301416›Full record

ArticleThe pharmacogenomics journal2009

Genome-wide approaches to identify pharmacogenetic contributions to adverse drug reactions.

M R Nelson, S-A Bacanu, M Mosteller, L Li, C E Bowman, A D Roses, E H Lai, M G Ehm

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In one paragraph

Article in The pharmacogenomics journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
–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

50 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  7. HLA-B*44 Alleles and HLA-DQA1*03:01 as Genetic Risk Factors for Drug-Induced Liver Injury due to Fluoroquinolones.Liver international : official journal of the International Association for the Study of the Liver · 2026
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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

8 authors.

M R NelsonPharmacogenetics, GlaxoSmithKline, Research Triangle Park, NC 27709-3398, USA. matthew.r.nelson@gsk.com
S-A Bacanu
M Mosteller
L Li
C E Bowman
A D Roses
E H Lai
M G Ehm

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adverse drug reactions (ADRs) have a major impact on patients, physicians, health care providers, regulatory agencies and pharmaceutical companies. Identifying the genetic contributions to ADR risk may lead to a better understanding of the underlying mechanisms, identification of patients at risk and a decrease in the number of events. Technological advances have made the routine monitoring and investigation of the genetic basis of ADRs during clinical trials possible. We demonstrate through simulation that genome-wide genotyping, coupled with the use of clinically matched or population controls, can yield sufficient statistical power to permit the identification of strong genetic predictors of ADR risk in a prospective manner with modest numbers of ADR cases. The results of a 500,000 single nucleotide polymorphism analysis of abacavir-associated hypersensitivity reaction suggest that the known HLA-B gene region could be identified with as few as 15 cases and 200 population controls in a sequential analysis.

Indexed as

Genome, HumanPolymorphism, Single NucleotideAbacavirClinical Trials as TopicDideoxynucleosidesDNADrug HypersensitivityDrug-Related Side Effects and Adverse ReactionsHLA-B AntigensHumansPharmacogeneticsAbacavirDideoxynucleosidesDNAHLA-B Antigens

Identifiers

PMID18301416

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.