Evidence map›Paper›PMID 33090732›Full record

ArticleJournal of cachexia, sarcopenia and muscle2020

High levels of modified ceramides are a defining feature of murine and human cancer cachexia.

Pauline Morigny, Julia Zuber, Mark Haid, Doris Kaltenecker, Fabien Riols, Joanna D C Lima, Estefania Simoes, José Pinhata Otoch, Sören Fisker Schmidt, Stephan Herzig and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 4 countries.

Pauline MorignyInstitute for Diabetes and Cancer, Helmholtz Center Munich, Neuherberg, Germany.
Julia ZuberInstitute for Diabetes and Cancer, Helmholtz Center Munich, Neuherberg, Germany.
Mark HaidResearch Unit Molecular Endocrinology and Metabolism, Helmholtz Center Munich, German Research Center for Environmental Health, Neuherberg, Germany.
Doris KalteneckerInstitute for Diabetes and Cancer, Helmholtz Center Munich, Neuherberg, Germany.
Fabien RiolsResearch Unit Molecular Endocrinology and Metabolism, Helmholtz Center Munich, German Research Center for Environmental Health, Neuherberg, Germany.
Joanna D C LimaCancer Metabolism Research Group, LIM 26 HC, Medical School, University of São Paulo, São Paulo, Brazil.
Estefania SimoesCancer Metabolism Research Group, LIM 26 HC, Medical School, University of São Paulo, São Paulo, Brazil.
José Pinhata OtochCancer Metabolism Research Group, LIM 26 HC, Medical School, University of São Paulo, São Paulo, Brazil.
Sören Fisker SchmidtInstitute for Diabetes and Cancer, Helmholtz Center Munich, Neuherberg, Germany.
Stephan HerzigInstitute for Diabetes and Cancer, Helmholtz Center Munich, Neuherberg, Germany.
Jerzy AdamskiResearch Unit Molecular Endocrinology and Metabolism, Helmholtz Center Munich, German Research Center for Environmental Health, Neuherberg, Germany.
Marilia SeelaenderCancer Metabolism Research Group, LIM 26 HC, Medical School, University of São Paulo, São Paulo, Brazil.
Mauricio Berriel DiazInstitute for Diabetes and Cancer, Helmholtz Center Munich, Neuherberg, Germany.ORCID 0000-0003-4670-919X
Maria RohmInstitute for Diabetes and Cancer, Helmholtz Center Munich, Neuherberg, Germany.ORCID 0000-0003-3926-1534
Heidelberg University · DEUniversidade de São Paulo · BRHelmholtz Zentrum München · DENational University of Singapore · SG

Funding

Austrian Science Fund FWF J 4224
6 · The paper itself

Abstract

backgroundCancer cachexia (CCx) is a multifactorial energy-wasting syndrome reducing the efficiency of anti-cancer therapies, quality of life, and survival of cancer patients. In the past years, most studies focused on the identification of tumour and host-derived proteins contributing to CCx. However, there is still a lack of studies addressing the changes in bioactive lipids. The aim of this study was to identify specific lipid species as a hallmark of CCx by performing a broad range lipid analysis of plasma from well-established CCx mouse models as well as cachectic and weight stable cancer patients.

methodsPlasma from non-cachectic (PBS-injected mice, NC26 tumour-bearing mice), pre-cachectic and cachectic mice (C26 and LLC tumour-bearing mice, Apc

resultsA decrease in several lysophosphatidylcholine (LPC) species and an increase in numerous sphingolipids including sphingomyelins (SMs), ceramides (CERs), hexosyl-ceramides (HCERs) and lactosyl-ceramides (LCERs), were mutual features of CCx in both mice and cancer patients. Notably, sphingolipid levels gradually increased during cachexia development. Key enzymes involved in ceramide synthesis were elevated in liver but not in adipose, muscle, or tumour tissues, suggesting that ceramide turnover in the liver is a major contributor to elevated sphingolipid levels in CCx. LPC(16:1), LPC(20:3), SM(16:0), SM(24:1), CER(16:0), CER(24:1), HCER(16:0), and HCER(24:1) were the most consistently affected lipid species between mice and humans and correlated negatively (LPCs) or positively (SMs, CERs and HCERs) with the severity of body weight loss.

conclusionsHigh levels of sphingolipids, specifically ceramides and modified ceramides, are a defining feature of murine and human CCx and may contribute to tissue wasting and skeletal muscle atrophy through the inhibition of anabolic signals. The progressive increase in sphingolipids during cachexia development supports their potential as early biomarkers for CCx.

Indexed as

CachexiaCeramidesNeoplasmsAnimalsHumansMiceMuscular AtrophyQuality of LifeCeramidesCancer cachexiaCeramidesLipidomicsSignalling lipidsSphingolipids

Identifiers

PMID33090732
PMCPMC7749558
OpenAlexW3092325902

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.