Evidence map›Paper›PMID 28117416›Full record

ReviewNature reviews. Clinical oncology2017

Tumour-associated macrophages as treatment targets in oncology.

Alberto Mantovani, Federica Marchesi, Alberto Malesci, Luigi Laghi, Paola Allavena

Abstract readReview
In one paragraph

Review in Nature reviews. Clinical oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2,424 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2,424citing papers in PubMed, 2 pooled it
120.2field-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

2,424 citing papers in PubMed, 2 syntheses or guidelines pooled it, 3,920 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Omega-3 fatty acids reprogram tumor-associated macrophage cytokine signaling and suppress pancreatic cancer growth.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  17. Granzyme B PET Imaging Reveals LgmnAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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2,364 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

5 authors at 2 institutions in 1 country.

Alberto MantovaniIstituto Clinico Humanitas, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Via A. Manzoni 113, 20089 Rozzano, Milan, Italy.
Federica MarchesiIstituto Clinico Humanitas, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Via A. Manzoni 113, 20089 Rozzano, Milan, Italy.
Alberto MalesciIstituto Clinico Humanitas, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Via A. Manzoni 113, 20089 Rozzano, Milan, Italy.
Luigi LaghiIstituto Clinico Humanitas, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Via A. Manzoni 113, 20089 Rozzano, Milan, Italy.
Paola AllavenaIstituto Clinico Humanitas, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Via A. Manzoni 113, 20089 Rozzano, Milan, Italy.
Istituti di Ricovero e Cura a Carattere Scientifico · ITUniversity of Milan · IT

Funding

European Research Council 669415
6 · The paper itself

Abstract

Macrophages are crucial drivers of tumour-promoting inflammation. Tumour-associated macrophages (TAMs) contribute to tumour progression at different levels: by promoting genetic instability, nurturing cancer stem cells, supporting metastasis, and taming protective adaptive immunity. TAMs can exert a dual, yin-yang influence on the effectiveness of cytoreductive therapies (chemotherapy and radiotherapy), either antagonizing the antitumour activity of these treatments by orchestrating a tumour-promoting, tissue-repair response or, instead, enhancing the overall antineoplastic effect. TAMs express molecular triggers of checkpoint proteins that regulate T-cell activation, and are targets of certain checkpoint-blockade immunotherapies. Other macrophage-centred approaches to anticancer therapy are under investigation, and include: inhibition of macrophage recruitment to, and/or survival in, tumours; functional re-education of TAMs to an antitumour, 'M1-like' mode; and tumour-targeting monoclonal antibodies that elicit macrophage-mediated extracellular killing, or phagocytosis and intracellular destruction of cancer cells. The evidence supporting these strategies is reviewed herein. We surmise that TAMs can provide tools to tailor the use of cytoreductive therapies and immunotherapy in a personalized medicine approach, and that TAM-focused therapeutic strategies have the potential to complement and synergize with both chemotherapy and immunotherapy.

Indexed as

Antineoplastic AgentsHumansMacrophage ActivationMacrophagesMolecular Targeted TherapyNeoplasmsAntineoplastic Agents

Identifiers

PMID28117416
PMCPMC5480600
OpenAlexW2582686270

What OpenQuestion holds

Textmetadata
LicenceTDM
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.