Evidence map›Paper›PMID 28331812›Full record

ArticleBBA clinical2017

The plasma lipidome in acute myeloid leukemia at diagnosis in relation to clinical disease features.

Thomas Pabst, Linda Kortz, Georg M Fiedler, Uta Ceglarek, Jeffrey R Idle, Diren Beyoğlu

Open access · hybridAbstract read
In one paragraph

Article in BBA clinical, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

45 citing papers in PubMed, 67 citations in OpenAlex.

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  6. Metabolic Signature ofJournal of personalized medicine · 2025
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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

6 authors at 3 institutions in 2 countries.

Thomas PabstDepartment of Medical Oncology, Inselspital Bern, Switzerland.
Linda KortzInstitute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, University Hospital Leipzig, Germany.
Georg M FiedlerInstitute of Clinical Chemistry, Inselspital Bern, Switzerland.
Uta CeglarekInstitute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, University Hospital Leipzig, Germany.
Jeffrey R IdleHepatology Research Group, Department of Clinical Research, University of Bern, Switzerland.
Diren BeyoğluHepatology Research Group, Department of Clinical Research, University of Bern, Switzerland.
University Hospital Leipzig · DEUniversity Hospital of Bern · CHUniversity of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEarly studies established that certain lipids were lower in acute myeloid leukemia (AML) cells than normal leukocytes. Because lipids are now known to play an important role in cell signaling and regulation of homeostasis, and are often perturbed in malignancies, we undertook a comprehensive lipidomic survey of plasma from AML patients at time of diagnosis and also healthy blood donors.

methodsPlasma lipid profiles were measured using three mass spectrometry platforms in 20 AML patients and 20 healthy blood donors. Data were collected on total cholesterol and fatty acids, fatty acid amides, glycerolipids, phospholipids, sphingolipids, cholesterol esters, coenzyme Q10 and eicosanoids.

resultsWe observed a depletion of plasma total fatty acids and cholesterol, but an increase in certain free fatty acids with the observed decline in sphingolipids, phosphocholines, triglycerides and cholesterol esters probably driven by enhanced fatty acid oxidation in AML cells. Arachidonic acid and precursors were elevated in AML, particularly in patients with high bone marrow (BM) or peripheral blasts and unfavorable prognostic risk. PGF2α was also elevated, in patients with low BM or peripheral blasts and with a favorable prognostic risk. A broad panoply of lipid classes is altered in AML plasma, pointing to disturbances of several lipid metabolic interconversions, in particular in relation to blast cell counts and prognostic risk.

conclusionsThese data indicate potential roles played by lipids in AML heterogeneity and disease outcome. GENERAL SIGNIFICANCE: Enhanced catabolism of several lipid classes increases prognostic risk while plasma PGF2α may be a marker for reduced prognostic risk in AML.

Indexed as

12-HEPE, 12-hydroxy-5Z,8Z,10E,14Z,17Z-eicosapentaenoic acid12-LOX, 12-lipoxygenase2HG, (R)-2-hydroxyglutarate2OG, 2-oxoglutarate8,9-DHET, 8,9-dihydroxy-5Z,11Z,14Z-eicosatrienoic acidAA, arachidonic acidAcute myeloid leukemiaALL, acute lymphoblastic leukemiaAML, acute myeloid leukemiaBlast cell numberCE, cholesterol esterCer, ceramideCML, chronic myelogenous leukemiaCoQ10, coenzyme Q10CPT1a, carnitine palmitate transferase 1aDG, diacylglycerolDGLA, dihomo-γ-linoleic acidDIC, disseminated intravascular coagulationEicosanoidsEPA, eicosapentaenoic acid (20:5;5Z,8Z,11Z,14Z,17Z)ESI-, electrospray ionization negative modeESI +,  electrospray ionization positive modeFAA, fatty acid amideFAB, French-American-British classificationFAME, fatty acid methyl esterFAO, fatty acid oxidationFatty acidsFLC-QqLIT-MS, fast liquid chromatography-quadrupole linear ion-trap mass spectrometryGCMS, gas chromatography–mass spectrometryLipidomicsLPC, lysophosphatidylcholineLPE, lysophosphatidylethanolamineMG, monoacylglycerolmPGES-1, microsomal prostaglandin E synthase-1MRM, multiple reactions monitoringMUFA, monounsaturated fatty acidOPLS-DA, orthogonal PLS-DAPCA, principal components analysisPC, phosphatidylcholinePE, phosphatidylethanolaminePGE2, prostaglandin E2PGF1α, prostaglandin 1αPGF2α, prostaglandin F2αPGH2, prostaglandin H2PLS-DA, projection to latent structures-discriminant analysisPOEA, palmitoleoyl ethanolamidePrognostic riskPUFA, polyunsaturated fatty acidSCD1, stearoyl CoA desaturase 1SM, sphingomyelinTG, triacylglycerol (triglyceride)TxA2, thromboxane A2TxB2, thromboxane B2UPLC-ESI-QTOFMS, ultraperformance liquid chromatography-electrospray ionization-quadrupole time-of-flight mass spectrometry

Identifiers

PMID28331812
PMCPMC5357680
OpenAlexW2592804355

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.