Evidence map›Paper›PMID 29941600›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

Fatty acid metabolism complements glycolysis in the selective regulatory T cell expansion during tumor growth.

Ilenia Pacella, Claudio Procaccini, Chiara Focaccetti, Stefano Miacci, Eleonora Timperi, Deriggio Faicchia, Martina Severa, Fabiana Rizzo, Eliana Marina Coccia, Fabrizia Bonacina and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 226 papers.

0numbers the graph read from it
0cells of the map it votes in
226citing papers in PubMed
11.4field-weighted citation impact, top 1% 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

226 citing papers in PubMed, 323 citations in OpenAlex.

  1. Review
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  9. Regulatory T cells in cancer and inflammation.Signal transduction and targeted therapy · 2026
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166 more citing papers are in PubMed but not listed here.

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

20 authors at 9 institutions in 3 countries.

Ilenia PacellaDipartimento di Medicina Interna e Specialità Mediche, Sapienza Università di Roma, 00161 Rome, Italy.
Claudio ProcacciniLaboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, 80131 Naples, Italy.
Chiara FocaccettiDipartimento di Medicina Interna e Specialità Mediche, Sapienza Università di Roma, 00161 Rome, Italy.
Stefano MiacciDipartimento di Medicina Interna e Specialità Mediche, Sapienza Università di Roma, 00161 Rome, Italy.
Eleonora TimperiDipartimento di Medicina Interna e Specialità Mediche, Sapienza Università di Roma, 00161 Rome, Italy.
Deriggio FaicchiaLaboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, 80131 Naples, Italy.
Martina SeveraDepartment of Infectious Diseases, Istituto Superiore di Sanità, 00161 Rome, Italy.
Fabiana RizzoDepartment of Infectious Diseases, Istituto Superiore di Sanità, 00161 Rome, Italy.
Eliana Marina CocciaDepartment of Infectious Diseases, Istituto Superiore di Sanità, 00161 Rome, Italy.
Fabrizia BonacinaDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, 20122 Milan, Italy.
Nico MitroDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, 20122 Milan, Italy.
Giuseppe Danilo NorataDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, 20122 Milan, Italy.
Grazisa RossettiIstituto Nazionale Genetica Molecolare Romeo ed Enrica Invernizzi, 20122 Milan, Italy.ORCID 0000-0001-6361-311X
Valeria RanzaniIstituto Nazionale Genetica Molecolare Romeo ed Enrica Invernizzi, 20122 Milan, Italy.
Massimiliano PaganiIstituto Nazionale Genetica Molecolare Romeo ed Enrica Invernizzi, 20122 Milan, Italy.
Ezio GiordaImmunology Research Area, Ospedale Pediatrico Bambino Gesù Istituto di Ricovero e Cura a Carattere Scientifico, 00146 Rome, Italy.
Yu WeiLaboratoire de Pathogenèse des Virus de l'Hépatite B, Institut Pasteur, 75015 Paris, France.
Giuseppe MatareseLaboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, 80131 Naples, Italy; giuseppe.matarese@unina.it vincenzo.barnaba@uniroma1.it silvia.piconese@uniroma1.it.ORCID 0000-0001-9429-0616
Vincenzo BarnabaDipartimento di Medicina Interna e Specialità Mediche, Sapienza Università di Roma, 00161 Rome, Italy; giuseppe.matarese@unina.it vincenzo.barnaba@uniroma1.it silvia.piconese@uniroma1.it.
Silvia PiconeseDipartimento di Medicina Interna e Specialità Mediche, Sapienza Università di Roma, 00161 Rome, Italy; giuseppe.matarese@unina.it vincenzo.barnaba@uniroma1.it silvia.piconese@uniroma1.it.
Sapienza University of Rome · ITUniversity of Milan · ITInstitute for Experimental Endocrinology and Oncology · ITIstituto Superiore di Sanità · ITIstituto Nazionale Genetica Molecolare · ITBambino Gesù Children's Hospital · ITInstitut Pasteur · FRIstituto Pasteur · ITItalian Institute of Technology · IT

Funding

Cancer Research UK 26813European Research Council 310496
6 · The paper itself

Abstract

The tumor microenvironment restrains conventional T cell (Tconv) activation while facilitating the expansion of Tregs. Here we showed that Tregs' advantage in the tumor milieu relies on supplemental energetic routes involving lipid metabolism. In murine models, tumor-infiltrating Tregs displayed intracellular lipid accumulation, which was attributable to an increased rate of fatty acid (FA) synthesis. Since the relative advantage in glucose uptake may fuel FA synthesis in intratumoral Tregs, we demonstrated that both glycolytic and oxidative metabolism contribute to Tregs' expansion. We corroborated our data in human tumors showing that Tregs displayed a gene signature oriented toward glycolysis and lipid synthesis. Our data support a model in which signals from the tumor microenvironment induce a circuitry of glycolysis, FA synthesis, and oxidation that confers a preferential proliferative advantage to Tregs, whose targeting might represent a strategy for cancer treatment.

Indexed as

AnimalsCell Line, TumorFatty AcidsFatty Acid Synthase, Type IGlycolysisHumansMiceMice, TransgenicNeoplasm ProteinsNeoplasms, ExperimentalOxidation-ReductionT-Lymphocytes, RegulatoryTumor MicroenvironmentFASN protein, humanFatty AcidsFatty Acid Synthase, Type INeoplasm Proteinsfatty acid synthesisglycolysisox40Tregtumor microenvironment

Identifiers

PMID29941600
PMCPMC6048537
OpenAlexW2810786508

What OpenQuestion holds

Textmetadata
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.