Evidence map›Paper›PMID 33077904›Full record

ReviewCellular & molecular immunology2021

Implications of metabolism-driven myeloid dysfunctions in cancer therapy.

Laura Strauss, Valentina Guarneri, Alessandra Gennari, Antonio Sica

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular & molecular immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

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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

4 authors at 3 institutions in 2 countries.

Laura StraussDepartment of Immunopharmacology and Immuno Oncology, EMD Serono Research & Development Institute, Inc., 801195 45A Middlesex Turnpike, Billerica, MA, 01821, USA.
Valentina GuarneriDepartment of Surgery, Oncology and Gastroenterology, University of Padova, Padova, Italy.
Alessandra GennariDivision of Oncology, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy.
Antonio SicaDepartment of Pharmaceutical Sciences, University of Eastern Piedmont, A. Avogadro, via Bovio 6, Novara, Italy. antonio.sica@uniupo.it.ORCID http://orcid.org/0000-0002-8342-7442
Università degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITOno Pharmaceutical (United States) · USUniversity of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune homeostasis is maintained by an adequate balance of myeloid and lymphoid responses. In chronic inflammatory states, including cancer, this balance is lost due to dramatic expansion of myeloid progenitors that fail to mature to functional inflammatory neutrophils, macrophages, and dendritic cells (DCs), thus giving rise to a decline in the antitumor effector lymphoid response. Cancer-related inflammation orchestrates the production of hematopoietic growth factors and cytokines that perpetuate recruitment and activation of myeloid precursors, resulting in unresolved and chronic inflammation. This pathologic inflammation creates profound alterations in the intrinsic cellular metabolism of the myeloid progenitor pool, which is amplified by competition for essential nutrients and by hypoxia-induced metabolic rewiring at the tumor site. Therefore, persistent myelopoiesis and metabolic dysfunctions contribute to the development of cancer, as well as to the severity of a broad range of diseases, including metabolic syndrome and autoimmune and infectious diseases. The aims of this review are to (1) define the metabolic networks implicated in aberrant myelopoiesis observed in cancer patients, (2) discuss the mechanisms underlying these clinical manifestations and the impact of metabolic perturbations on clinical outcomes, and (3) explore new biomarkers and therapeutic strategies to restore immunometabolism and differentiation of myeloid cells towards an effector phenotype to increase host antitumor immunity. We propose that the profound metabolic alterations and associated transcriptional changes triggered by chronic and overactivated immune responses in myeloid cells represent critical factors influencing the balance between therapeutic efficacy and immune-related adverse effects (irAEs) for current therapeutic strategies, including immune checkpoint inhibitor (ICI) therapy.

Indexed as

Metabolic Networks and PathwaysMyelopoiesisAnimalsCell DifferentiationHumansImmunotherapyMyeloid CellsNeoplasmsCancer therapyMetabolismMyeloid-derived suppressor cellsMyelopoiesisTumor-associated macrophages

Identifiers

PMID33077904
PMCPMC7570408
OpenAlexW3093421028

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.