Evidence map›Paper›PMID 20179710›Full record

ArticleBritish journal of cancer2010

Influence of pharmacogenetics on response and toxicity in breast cancer patients treated with doxorubicin and cyclophosphamide.

J Bray, J Sludden, M J Griffin, M Cole, M Verrill, D Jamieson, A V Boddy

Registry-linked trialOpen access · hybridAbstract readEvaluation Study
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04581967 (Pharmacogenetic Risk Factors of Doxorubicin-Cyclophosphamide Chemotherapy Related Toxicities in Breast Cancer Patients), which is not on this map. Cited by 83 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 3 pooled it
7.3field-weighted citation impact, top 2% 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.

NCT04581967 unknown statusnot on this mapstarted 2020, after this paper: background citation

Pharmacogenetic Risk Factors of Doxorubicin-Cyclophosphamide Chemotherapy Related Toxicities in Breast Cancer Patients

TypeobservationalSponsorDamanhour UniversityRan2020 to 2021Enrolled100ConditionsBreast Cancer PatientsArmspolymorphism analysis, Doxorubicin-Cyclophosphamide regimen
3 · Its place in the literature

Who cites it

83 citing papers in PubMed, 3 syntheses or guidelines pooled it, 180 citations in OpenAlex.

  1. Pooled it
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  8. NbRSC advances · 2026
    Article
  9. Article
  10. Resistance to neoadjuvant chemotherapy in breast cancers: a metabolic perspective.Journal of experimental & clinical cancer research : CR · 2025
    Review
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23 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

J BrayNorthern Institute for Cancer Research, Medical School, Newcastle University, Newcastle upon Tyne, UK.
J Sludden
M J Griffin
M Cole
M Verrill
D Jamieson
A V Boddy
Newcastle University · GBFreeman Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDoxorubicin and cyclophosphamide (AC) therapy is an effective treatment for early-stage breast cancer. Doxorubicin is a substrate for ABCB1 and SLC22A16 transporters. Cyclophosphamide is a prodrug that requires oxidation to 4-hydroxycyclophosphamide, which yields a cytotoxic alkylating agent. The initial oxidation is catalysed by cytochrome P450 enzymes including CYP2B6, CYP2C9, CYP2C19 and CYP3A5. Polymorphic variants of the genes coding for these enzymes and transporters have been identified, which may influence the systemic pharmacology of the two drugs. It is not known whether this genetic variation has an impact on the efficacy or toxicity of AC therapy.

methodsGerm line DNA samples from 230 patients with breast cancer on AC therapy were genotyped for the following SNPs: ABCB1 C1236T, G2677T/A and C3435T, SLC22A16 A146G, T312C, T755C and T1226C, CYP2B6*2, *8, *9, *3, *4 and *5, CYP2C9*2 and *3, CYP3A5*3 and CYP2C19*2. Clinical data on survival, toxicity, demographics and pathology were collated.

resultsA lower incidence of dose delay, indicative of less toxicity, was seen in carriers of the SLC22A16 A146G, T312C, T755C variants. In contrast, a higher incidence of dose delay was seen in carriers of the SLC22A16 1226C, CYP2B6*2 and CYP2B6*5 alleles. The ABCB1 2677A, CYP2B6*2, CYP 2B6*8, CYP 2B6*9, CYP 2B6*4 alleles were associated with a worse outcome.

conclusionVariant alleles in the ABCB1, SLC22A16 and CYP2B6 genes are associated with response to AC therapy in the treatment of breast cancer.

Indexed as

PharmacogeneticsAntineoplastic Combined Chemotherapy ProtocolsAryl Hydrocarbon HydroxylasesATP Binding Cassette Transporter, Subfamily BATP Binding Cassette Transporter, Subfamily B, Member 1Biomarkers, PharmacologicalBiomarkers, TumorBreast NeoplasmsCarcinoma, Ductal, BreastCyclophosphamideCytochrome P-450 CYP2B6DoxorubicinDrug-Related Side Effects and Adverse ReactionsDrug Resistance, NeoplasmFemaleGene FrequencyABCB1 protein, humanAryl Hydrocarbon HydroxylasesATP Binding Cassette Transporter, Subfamily BATP Binding Cassette Transporter, Subfamily B, Member 1Biomarkers, PharmacologicalBiomarkers, TumorCyclophosphamideCYP2B6 protein, humanCytochrome P-450 CYP2B6DoxorubicinOrganic Cation Transport ProteinsOxidoreductases, N-DemethylatingSLC22A16 protein, human

Identifiers

PMID20179710
PMCPMC2844036
OpenAlexW2076489368

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.