Evidence map›Paper›PMID 26101462›Full record

ArticleMediators of inflammation2015

Modulation of Acid Sphingomyelinase in Melanoma Reprogrammes the Tumour Immune Microenvironment.

Emma Assi, Davide Cervia, Laura Bizzozero, Annalisa Capobianco, Sarah Pambianco, Federica Morisi, Clara De Palma, Claudia Moscheni, Paolo Pellegrino, Emilio Clementi and 1 more

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Sphingolipid metabolism and regulated cell death in malignant melanoma.Apoptosis : an international journal on programmed cell death · 2024
    Review
  4. Article
  5. Acid Sphingomyelinase Deficiency: A Clinical and Immunological Perspective.International journal of molecular sciences · 2021
    Review
  6. Article
  7. Article
  8. Effect of 1α,25(OH)Cancers · 2020
    Article
  9. Review
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  11. 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

11 authors at 4 institutions in 1 country.

Emma AssiScientific Institute IRCCS Eugenio Medea, 23842 Bosisio Parini, Italy ; Division of Molecular Oncology, San Raffaele Scientific Institute, 20132 Milan, Italy.
Davide CerviaUnit of Clinical Pharmacology, National Research Council-Institute of Neuroscience, Department of Biomedical and Clinical Sciences "Luigi Sacco" (DIBIC), University Hospital "Luigi Sacco", Università di Milano, 20157 Milan, Italy ; Department for Innovation in Biological, Agro-Food and Forest Systems (DIBAF), Università della Tuscia, 01100 Viterbo, Italy.
Laura BizzozeroScientific Institute IRCCS Eugenio Medea, 23842 Bosisio Parini, Italy ; Department of Oncology, Università di Torino and Laboratory of Neurovascular Biology, Candiolo Cancer Institute, 10060 Candiolo, Italy.
Annalisa CapobiancoDivision of Regenerative Medicine, San Raffaele Scientific Institute, 20132 Milan, Italy.ORCID 0000-0002-0271-6323
Sarah PambiancoUnit of Clinical Pharmacology, National Research Council-Institute of Neuroscience, Department of Biomedical and Clinical Sciences "Luigi Sacco" (DIBIC), University Hospital "Luigi Sacco", Università di Milano, 20157 Milan, Italy.
Federica MorisiUnit of Clinical Pharmacology, National Research Council-Institute of Neuroscience, Department of Biomedical and Clinical Sciences "Luigi Sacco" (DIBIC), University Hospital "Luigi Sacco", Università di Milano, 20157 Milan, Italy.
Clara De PalmaUnit of Clinical Pharmacology, National Research Council-Institute of Neuroscience, Department of Biomedical and Clinical Sciences "Luigi Sacco" (DIBIC), University Hospital "Luigi Sacco", Università di Milano, 20157 Milan, Italy.
Claudia MoscheniUnit of Morphology, Department of Biomedical and Clinical Sciences "Luigi Sacco" (DIBIC), Università di Milano, 20157 Milan, Italy.
Paolo PellegrinoUnit of Clinical Pharmacology, National Research Council-Institute of Neuroscience, Department of Biomedical and Clinical Sciences "Luigi Sacco" (DIBIC), University Hospital "Luigi Sacco", Università di Milano, 20157 Milan, Italy.
Emilio ClementiScientific Institute IRCCS Eugenio Medea, 23842 Bosisio Parini, Italy ; Unit of Clinical Pharmacology, National Research Council-Institute of Neuroscience, Department of Biomedical and Clinical Sciences "Luigi Sacco" (DIBIC), University Hospital "Luigi Sacco", Università di Milano, 20157 Milan, Italy.ORCID 0000-0001-7333-8270
Cristiana PerrottaUnit of Clinical Pharmacology, National Research Council-Institute of Neuroscience, Department of Biomedical and Clinical Sciences "Luigi Sacco" (DIBIC), University Hospital "Luigi Sacco", Università di Milano, 20157 Milan, Italy.ORCID 0000-0001-6680-4536
Luigi Sacco Hospital · ITCandiolo Cancer Institute · ITSan Raffaele University of Rome · ITUniversità degli Studi della Tuscia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The inflammatory microenvironment induces tumours to acquire an aggressive and immunosuppressive behaviour. Since acid sphingomyelinase (A-SMase) downregulation in melanoma was shown to determine a malignant phenotype, we aimed here to elucidate the role of A-SMase in the regulation of tumour immunogenic microenvironment using in vivo melanoma models in which A-SMase was either downregulated or maintained at constitutively high levels. We found high levels of inflammatory factors in low A-SMase expressing tumours, which also displayed an immunosuppressive/protumoural microenvironment: high levels of myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes (Tregs), as well as low levels of dendritic cells (DCs). In contrast, the restoration of A-SMase in melanoma cells not only reduced tumour growth and immunosuppression, but also induced a high recruitment at tumour site of effector immune cells with an antitumoural function. Indeed, we observed a poor homing of MDSCs and Tregs and the increased recruitment of CD8(+) and CD4(+) T lymphocytes as well as the infiltration of DCs and CD8(+)/CD44(high) T lymphocytes. This study demonstrates that change of A-SMase expression in cancer cells is sufficient per se to tune in vivo melanoma growth and that A-SMase levels modulate immune cells at tumour site. This may be taken into consideration in the setting of therapeutic strategies.

Indexed as

Cellular ReprogrammingTumor MicroenvironmentAnimalsCD8-Positive T-LymphocytesCell ProliferationFemaleImmune ToleranceMelanoma, ExperimentalMiceMice, Inbred C57BLSphingomyelin PhosphodiesteraseSphingomyelin Phosphodiesterase

Identifiers

PMID26101462
PMCPMC4460251
OpenAlexW1594494382

What OpenQuestion holds

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LicenceCC BY
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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.