Evidence map›Paper›PMID 38035101›Full record

ReviewFrontiers in immunology2023

Tumor-associated macrophages: an effective player of the tumor microenvironment.

Udit Basak, Tania Sarkar, Sumon Mukherjee, Sourio Chakraborty, Apratim Dutta, Saikat Dutta, Debadatta Nayak, Subhash Kaushik, Tanya Das, Gaurisankar Sa

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 239 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
239citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

239 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
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  7. The M1/M2 Test System for Determining Macrophage Phenotypes.International journal of molecular sciences · 2026
    Review
  8. Article
  9. Emerging Immune-Based Therapeutic Strategies in Hepatocellular Carcinoma.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
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179 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

10 authors.

Udit BasakDivision of Molecular Medicine, Bose Institute, Kolkata, India.
Tania SarkarDivision of Molecular Medicine, Bose Institute, Kolkata, India.
Sumon MukherjeeDivision of Molecular Medicine, Bose Institute, Kolkata, India.
Sourio ChakrabortyDivision of Molecular Medicine, Bose Institute, Kolkata, India.
Apratim DuttaDivision of Molecular Medicine, Bose Institute, Kolkata, India.
Saikat DuttaDivision of Molecular Medicine, Bose Institute, Kolkata, India.
Debadatta NayakCentral Council for Research in Homeopathy (CCRH), New Delhi, India.
Subhash KaushikCentral Council for Research in Homeopathy (CCRH), New Delhi, India.
Tanya DasDivision of Molecular Medicine, Bose Institute, Kolkata, India.
Gaurisankar SaDivision of Molecular Medicine, Bose Institute, Kolkata, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer progression is primarily caused by interactions between transformed cells and the components of the tumor microenvironment (TME). TAMs (tumor-associated macrophages) make up the majority of the invading immune components, which are further categorized as anti-tumor M1 and pro-tumor M2 subtypes. While M1 is known to have anti-cancer properties, M2 is recognized to extend a protective role to the tumor. As a result, the tumor manipulates the TME in such a way that it induces macrophage infiltration and M1 to M2 switching bias to secure its survival. This M2-TAM bias in the TME promotes cancer cell proliferation, neoangiogenesis, lymphangiogenesis, epithelial-to-mesenchymal transition, matrix remodeling for metastatic support, and TME manipulation to an immunosuppressive state. TAMs additionally promote the emergence of cancer stem cells (CSCs), which are known for their ability to originate, metastasize, and relapse into tumors. CSCs also help M2-TAM by revealing immune escape and survival strategies during the initiation and relapse phases. This review describes the reasons for immunotherapy failure and, thereby, devises better strategies to impair the tumor-TAM crosstalk. This study will shed light on the understudied TAM-mediated tumor progression and address the much-needed holistic approach to anti-cancer therapy, which encompasses targeting cancer cells, CSCs, and TAMs all at the same time.

Indexed as

Tumor-Associated MacrophagesTumor MicroenvironmentHumansMacrophagesNeovascularization, PathologicRecurrenceanticancer therapycancer stem cellsimmunosuppressionimmunotherapymacrophage reprogrammingpro-tumor immunitytumor-associated macrophagestumor microenvironment

Identifiers

PMID38035101
PMCPMC10687432

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Registered trials

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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.