Evidence map›Paper›PMID 26474455›Full record

ArticleOncotarget2015

Genetic polymorphisms associated with increased risk of developing chronic myelogenous leukemia.

Heriberto Bruzzoni-Giovanelli, Juan R González, François Sigaux, Bruno O Villoutreix, Jean Michel Cayuela, Joëlle Guilhot, Claude Preudhomme, François Guilhot, Jean-Luc Poyet, Philippe Rousselot

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 43 citations in OpenAlex.

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  14. Di- and tripeptide transport in vertebrates: the contribution of teleost fish models.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2017
    Review
  15. Relevance of necroptosis in cancer.Immunology and cell biology · 2017
    Review
  16. Induction of K562 Cell Apoptosis by As4S4 via Down-Regulating miR181.Medical science monitor : international medical journal of experimental and clinical research · 2017
    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

10 authors at 6 institutions in 2 countries.

Heriberto Bruzzoni-GiovanelliUniversité Paris Diderot, Sorbonne Paris Cité UMRS 1160 INSERM, Paris, France.
Juan R GonzálezCentre de Recerca en Epidemiologia Ambiental (CREAL), Barcelona, Spain.
François SigauxInstitut Universitaire d'Hématologie, Université Paris Diderot, Sorbonne Paris Cité, Paris, France.
Bruno O VilloutreixUniversité Paris Diderot, Sorbonne Paris Cité UMRS 973 Inserm, Paris, France/ Inserm, U973, Paris, France.
Jean Michel CayuelaLaboratoire Central d'Hématologie, Hôpital Saint Louis, Paris, France.
Joëlle GuilhotInserm CIC 0802, CHU de Poitiers, Poitiers, France.
Claude PreudhommeLaboratoire d'Hématologie, Inserm, U837, CHRU, Lille, France/Université de Lille Nord, Institut de Recherche sur le Cancer de Lille, Lille, France.
François GuilhotInserm CIC 0802, CHU de Poitiers, Poitiers, France.
Jean-Luc PoyetUniversité Paris Diderot, Sorbonne Paris Cité UMRS 1160 INSERM, Paris, France.
Philippe RousselotService d'Hématologie et d'Oncologie, Hôpital Mignot, Université Versailles, Saint-Quentin-en-Yvelines, France.
Inserm · FRUniversité Paris Cité · FRCentro de Investigación Biomédica en Red de Epidemiología y Salud Pública · ESDélégation Paris 7 · FRHôpital Saint-Louis · FRUniversité de Versailles Saint-Quentin-en-Yvelines · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Little is known about inherited factors associated with the risk of developing chronic myelogenous leukemia (CML). We used a dedicated DNA chip containing 16 561 single nucleotide polymorphisms (SNPs) covering 1 916 candidate genes to analyze 437 CML patients and 1 144 healthy control individuals. Single SNP association analysis identified 139 SNPs that passed multiple comparisons (1% false discovery rate). The HDAC9, AVEN, SEMA3C, IKBKB, GSTA3, RIPK1 and FGF2 genes were each represented by three SNPs, the PSM family by four SNPs and the SLC15A1 gene by six. Haplotype analysis showed that certain combinations of rare alleles of these genes increased the risk of developing CML by more than two or three-fold. A classification tree model identified five SNPs belonging to the genes PSMB10, TNFRSF10D, PSMB2, PPARD and CYP26B1, which were associated with CML predisposition. A CML-risk-allele score was created using these five SNPs. This score was accurate for discriminating CML status (AUC: 0.61, 95%CI: 0.58-0.64). Interestingly, the score was associated with age at diagnosis and the average number of risk alleles was significantly higher in younger patients. The risk-allele score showed the same distribution in the general population (HapMap CEU samples) as in our control individuals and was associated with differential gene expression patterns of two genes (VAPA and TDRKH). In conclusion, we describe haplotypes and a genetic score that are significantly associated with a predisposition to develop CML. The SNPs identified will also serve to drive fundamental research on the putative role of these genes in CML development.

Indexed as

FemaleGenetic Predisposition to DiseaseHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMiddle AgedPolymorphism, Single NucleotideCMLgenetic predispositionmyeloid leukemiaSNPs

Identifiers

PMID26474455
PMCPMC4742176
OpenAlexW2113781514

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.