Evidence map›Paper›PMID 27009330›Full record

ArticleJournal of translational medicine2016

Single nucleotide polymorphisms in apoptosis pathway are associated with response to imatinib therapy in chronic myeloid leukemia.

Qiaoli Zheng, Jiang Cao, Nada Hamad, Hyeoung-Joon Kim, Joon Ho Moon, Sang Kyun Sohn, Chul Won Jung, Jeffrey H Lipton, Dennis Dong Hwan Kim

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

5 citing papers in PubMed, 11 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

9 authors at 6 institutions in 3 countries.

Qiaoli ZhengDepartment of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, China.
Jiang CaoClinical Research Center, The Second Affiliated Hospital, School of Medicine, Zhejiang University, 88 Jiefang Road, Hangzhou, 310009, Zhejiang Province, China. caoj@zju.edu.cn.ORCID http://orcid.org/0000-0001-9542-5279
Nada HamadDepartment of Medical Oncology and Hematology, Princess Margaret Cancer Centre, University Health Network, University of Toronto, Toronto, Canada.
Hyeoung-Joon KimDepartment of Hematology/Oncology, Chonnam National University Hwasun Hospital, Chonnam National University, Hwasun, South Korea.
Joon Ho MoonDepartment of Hematology/Oncology, Kyungpook National University Hospital, Kyungpook National University, Daegu, South Korea.
Sang Kyun SohnDepartment of Hematology/Oncology, Kyungpook National University Hospital, Kyungpook National University, Daegu, South Korea.
Chul Won JungDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea. leukemia1@skku.edu.
Jeffrey H LiptonDepartment of Medical Oncology and Hematology, Princess Margaret Cancer Centre, University Health Network, University of Toronto, Toronto, Canada.
Dennis Dong Hwan KimDepartment of Medical Oncology and Hematology, Princess Margaret Cancer Centre, University Health Network, University of Toronto, Toronto, Canada.
University Health Network · CAKyungpook National University Hospital · KRChonnam National University Hwasun Hospital · KRSamsung Medical Center · KRSecond Affiliated Hospital of Zhejiang University · CNSir Run Run Shaw Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe mechanism of action of imatinib is known to involve the Fas-mediated apoptosis pathway. Consequently inter-individual variations in this apoptosis pathway might be associated with imatinib response or resistance.

methodsThis study attempted to focus on eight genotypes in the apoptosis pathway including FAS (rs1800682, rs2229521, rs2234767 and rs2234978), FASLG (rs763110), CASP10 (rs13006529), and APAF1 (rs1439123, rs2288713) and analyzed their association with treatment outcomes including molecular response with 4.5 log reduction (MR4.5), following imatinib therapy in 187 Korean CML patients.

resultsThe GG/GA genotype in FAS (rs2234767) showed a higher rate of MR4.5 than the AA genotype (at 5 years 59.7 vs 37.4 %, p = 0.013). Using a bootstrap procedure for internal validation we confirmed that FAS (rs2234767) correlates with MR4.5 (p = 0.050). Multivariate analysis confirmed that the FAS genotype (rs2234767) is an independent surrogate for MR4.5 (p = 0.019, HR 0.43, 95 % CI [0.22-0.87]).

conclusionsThe Fas/FasL signaling pathway may represent the major pathway that mediates apoptosis in CML treated with imatinib. SNP markers in the apoptosis pathway including FAS genotype (rs2234767) can be potential surrogates for predicting deeper molecular response after imatinib therapy.

Indexed as

AdolescentAdultAgedAged, 80 and overApoptosisChildDemographyFemaleGenotypeHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMiddle AgedMultivariate AnalysisPolymorphism, Single NucleotideImatinib MesylateApoptosis pathwayChronic myeloid leukemiaImatinibSingle nucleotide polymorphisms

Identifiers

PMID27009330
PMCPMC4806489
OpenAlexW2307668285

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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.